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Unexpected link between light drinking and dementia risk
new research suggests.
Investigators assessed dementia risk using changes in alcohol consumption over a 2-year period in nearly 4 million people in South Korea. After about 7 years, dementia was 21% less likely in mild drinkers and 17% less likely in moderate drinkers. Heavy drinking was linked to an 8% increased risk.
Other studies of the relationship between alcohol and dementia have yielded mixed results, and this study does little to clear those murky waters. Nor do the results mean that drinking is recommended, the investigators note.
But the study does offer new information on how risk changes over time as people change their drinking habits, lead investigator Keun Hye Jeon, MD, assistant professor of family medicine at Cha Gumi Medical Center at Cha University, Gumi, South Korea, told this news organization.
“Although numerous studies have shown a relationship between alcohol consumption and dementia, there is a paucity of understanding as to how the incidence of dementia changes with changes in drinking habits,” Dr. Jeon said.
“By measuring alcohol consumption at two time points, we were able to study the relationship between reducing, ceasing, maintaining, and increasing alcohol consumption and incident dementia,” he added.
The findings were published online in JAMA Network Open.
Tracking drinking habits
Researchers analyzed data from nearly 4 million individuals aged 40 years and older in the Korean National Health Insurance Service who completed questionnaires and underwent physical exams in 2009 and 2011.
Study participants completed questionnaires on their drinking habits and were assigned to one of five groups according to change in alcohol consumption during the study period. These groups consisted of sustained nondrinkers; those who stopped drinking (quitters); those who reduced their consumption of alcohol but did not stop drinking (reducers); those who maintained the same level of consumption (sustainers); and those who increased their level of consumption (increasers).
A standard drink in the United States contains 14 g of alcohol. For this study, mild drinking was defined as less than 15 g/day, or one drink; moderate consumption as 15-29.9 g/day, or one to two drinks; and heavy drinking as 30 g/day or more, or three or more drinks.
At baseline, 54.8% of participants were nondrinkers, 26.7% were mild drinkers, 11.0% were moderate drinkers, and 7.5% were heavy drinkers.
From 2009 to 2011, 24.2% of mild drinkers, 8.4% of moderate drinkers, and 7.6% of heavy drinkers became quitters. In the same period, 13.9% of nondrinkers, 16.1% of mild drinkers, and 17.4% of moderate drinkers increased their drinking level.
After a mean follow-up of 6.3 years, 2.5% of participants were diagnosed with dementia, 2.0% with Alzheimer’s disease, and 0.3% with vascular dementia.
Unexpected finding
Compared with consistently not drinking, mild and moderate alcohol consumption was associated with a 21% (adjust hazard ratio, 0.79; 95% confidence interval, 0.77-0.81) and 17% (aHR, 0.83; 95% CI, 0.79-0.88) decreased risk for dementia, respectively.
Heavy drinking was linked to an 8% increased risk (aHR, 1.08; 95% CI, 1.03-1.12).
Similar associations were found between alcohol consumption and risk for Alzheimer’s disease and vascular dementia.
Reducing drinking habits from heavy to moderate led to a reduction in risk for dementia and Alzheimer’s, and increasing drinking levels led to an increase in risk for both conditions.
But when the researchers analyzed dementia risk for nondrinkers who began drinking at mild levels during the study period, they found something unexpected – the risk in this group decreased by 7% for dementia (aHR, 0.93; 95% CI, 0.90-0.96) and by 8% for Alzheimer’s (aHR, 0.92; 95% CI, 0.89-0.95), compared with sustained mild drinkers.
“Our study showed that initiation of mild alcohol consumption leads to a reduced risk of all-cause dementia and Alzheimer’s disease, which has never been reported in previous studies,” Dr. Jeon said.
However, Dr. Jeon was quick to point out that this doesn’t mean that people who don’t drink should start.
Previous studies have shown that heavy alcohol use can triple an individual’s dementia risk, while other studies have shown that no amount of alcohol consumption is good for the brain.
“None of the existing health guidelines recommend starting alcohol drinking,” Dr. Jeon said. “Our findings regarding an initiation of mild alcohol consumption cannot be directly translated into clinical recommendations,” but the findings do warrant additional study, he added.
Risks persist
Commenting on the findings, Percy Griffin, PhD, director of scientific engagement for the Alzheimer’s Association in Chicago, agrees.
“While this study is interesting, and this topic deserves further study, no one should drink alcohol as a method of reducing risk of Alzheimer’s disease or other dementia based on this study,” said Dr. Griffin, who was not part of the study.
The exact tipping point in alcohol consumption that can lead to problems with cognition or increased dementia risk is unknown, Dr. Griffin said. Nor do researchers understand why mild drinking may have a protective effect.
“We do know, however, that excessive alcohol consumption has negative effects on heart health and general health, which can lead to problems with brain function,” he said. “Clinicians should have discussions with their patients around their alcohol consumption patterns and the risks associated with drinking in excess, including potential damage to their cognition.”
Funding for the study was not disclosed. Dr. Jeon and Dr. Griffin report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
Investigators assessed dementia risk using changes in alcohol consumption over a 2-year period in nearly 4 million people in South Korea. After about 7 years, dementia was 21% less likely in mild drinkers and 17% less likely in moderate drinkers. Heavy drinking was linked to an 8% increased risk.
Other studies of the relationship between alcohol and dementia have yielded mixed results, and this study does little to clear those murky waters. Nor do the results mean that drinking is recommended, the investigators note.
But the study does offer new information on how risk changes over time as people change their drinking habits, lead investigator Keun Hye Jeon, MD, assistant professor of family medicine at Cha Gumi Medical Center at Cha University, Gumi, South Korea, told this news organization.
“Although numerous studies have shown a relationship between alcohol consumption and dementia, there is a paucity of understanding as to how the incidence of dementia changes with changes in drinking habits,” Dr. Jeon said.
“By measuring alcohol consumption at two time points, we were able to study the relationship between reducing, ceasing, maintaining, and increasing alcohol consumption and incident dementia,” he added.
The findings were published online in JAMA Network Open.
Tracking drinking habits
Researchers analyzed data from nearly 4 million individuals aged 40 years and older in the Korean National Health Insurance Service who completed questionnaires and underwent physical exams in 2009 and 2011.
Study participants completed questionnaires on their drinking habits and were assigned to one of five groups according to change in alcohol consumption during the study period. These groups consisted of sustained nondrinkers; those who stopped drinking (quitters); those who reduced their consumption of alcohol but did not stop drinking (reducers); those who maintained the same level of consumption (sustainers); and those who increased their level of consumption (increasers).
A standard drink in the United States contains 14 g of alcohol. For this study, mild drinking was defined as less than 15 g/day, or one drink; moderate consumption as 15-29.9 g/day, or one to two drinks; and heavy drinking as 30 g/day or more, or three or more drinks.
At baseline, 54.8% of participants were nondrinkers, 26.7% were mild drinkers, 11.0% were moderate drinkers, and 7.5% were heavy drinkers.
From 2009 to 2011, 24.2% of mild drinkers, 8.4% of moderate drinkers, and 7.6% of heavy drinkers became quitters. In the same period, 13.9% of nondrinkers, 16.1% of mild drinkers, and 17.4% of moderate drinkers increased their drinking level.
After a mean follow-up of 6.3 years, 2.5% of participants were diagnosed with dementia, 2.0% with Alzheimer’s disease, and 0.3% with vascular dementia.
Unexpected finding
Compared with consistently not drinking, mild and moderate alcohol consumption was associated with a 21% (adjust hazard ratio, 0.79; 95% confidence interval, 0.77-0.81) and 17% (aHR, 0.83; 95% CI, 0.79-0.88) decreased risk for dementia, respectively.
Heavy drinking was linked to an 8% increased risk (aHR, 1.08; 95% CI, 1.03-1.12).
Similar associations were found between alcohol consumption and risk for Alzheimer’s disease and vascular dementia.
Reducing drinking habits from heavy to moderate led to a reduction in risk for dementia and Alzheimer’s, and increasing drinking levels led to an increase in risk for both conditions.
But when the researchers analyzed dementia risk for nondrinkers who began drinking at mild levels during the study period, they found something unexpected – the risk in this group decreased by 7% for dementia (aHR, 0.93; 95% CI, 0.90-0.96) and by 8% for Alzheimer’s (aHR, 0.92; 95% CI, 0.89-0.95), compared with sustained mild drinkers.
“Our study showed that initiation of mild alcohol consumption leads to a reduced risk of all-cause dementia and Alzheimer’s disease, which has never been reported in previous studies,” Dr. Jeon said.
However, Dr. Jeon was quick to point out that this doesn’t mean that people who don’t drink should start.
Previous studies have shown that heavy alcohol use can triple an individual’s dementia risk, while other studies have shown that no amount of alcohol consumption is good for the brain.
“None of the existing health guidelines recommend starting alcohol drinking,” Dr. Jeon said. “Our findings regarding an initiation of mild alcohol consumption cannot be directly translated into clinical recommendations,” but the findings do warrant additional study, he added.
Risks persist
Commenting on the findings, Percy Griffin, PhD, director of scientific engagement for the Alzheimer’s Association in Chicago, agrees.
“While this study is interesting, and this topic deserves further study, no one should drink alcohol as a method of reducing risk of Alzheimer’s disease or other dementia based on this study,” said Dr. Griffin, who was not part of the study.
The exact tipping point in alcohol consumption that can lead to problems with cognition or increased dementia risk is unknown, Dr. Griffin said. Nor do researchers understand why mild drinking may have a protective effect.
“We do know, however, that excessive alcohol consumption has negative effects on heart health and general health, which can lead to problems with brain function,” he said. “Clinicians should have discussions with their patients around their alcohol consumption patterns and the risks associated with drinking in excess, including potential damage to their cognition.”
Funding for the study was not disclosed. Dr. Jeon and Dr. Griffin report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
Investigators assessed dementia risk using changes in alcohol consumption over a 2-year period in nearly 4 million people in South Korea. After about 7 years, dementia was 21% less likely in mild drinkers and 17% less likely in moderate drinkers. Heavy drinking was linked to an 8% increased risk.
Other studies of the relationship between alcohol and dementia have yielded mixed results, and this study does little to clear those murky waters. Nor do the results mean that drinking is recommended, the investigators note.
But the study does offer new information on how risk changes over time as people change their drinking habits, lead investigator Keun Hye Jeon, MD, assistant professor of family medicine at Cha Gumi Medical Center at Cha University, Gumi, South Korea, told this news organization.
“Although numerous studies have shown a relationship between alcohol consumption and dementia, there is a paucity of understanding as to how the incidence of dementia changes with changes in drinking habits,” Dr. Jeon said.
“By measuring alcohol consumption at two time points, we were able to study the relationship between reducing, ceasing, maintaining, and increasing alcohol consumption and incident dementia,” he added.
The findings were published online in JAMA Network Open.
Tracking drinking habits
Researchers analyzed data from nearly 4 million individuals aged 40 years and older in the Korean National Health Insurance Service who completed questionnaires and underwent physical exams in 2009 and 2011.
Study participants completed questionnaires on their drinking habits and were assigned to one of five groups according to change in alcohol consumption during the study period. These groups consisted of sustained nondrinkers; those who stopped drinking (quitters); those who reduced their consumption of alcohol but did not stop drinking (reducers); those who maintained the same level of consumption (sustainers); and those who increased their level of consumption (increasers).
A standard drink in the United States contains 14 g of alcohol. For this study, mild drinking was defined as less than 15 g/day, or one drink; moderate consumption as 15-29.9 g/day, or one to two drinks; and heavy drinking as 30 g/day or more, or three or more drinks.
At baseline, 54.8% of participants were nondrinkers, 26.7% were mild drinkers, 11.0% were moderate drinkers, and 7.5% were heavy drinkers.
From 2009 to 2011, 24.2% of mild drinkers, 8.4% of moderate drinkers, and 7.6% of heavy drinkers became quitters. In the same period, 13.9% of nondrinkers, 16.1% of mild drinkers, and 17.4% of moderate drinkers increased their drinking level.
After a mean follow-up of 6.3 years, 2.5% of participants were diagnosed with dementia, 2.0% with Alzheimer’s disease, and 0.3% with vascular dementia.
Unexpected finding
Compared with consistently not drinking, mild and moderate alcohol consumption was associated with a 21% (adjust hazard ratio, 0.79; 95% confidence interval, 0.77-0.81) and 17% (aHR, 0.83; 95% CI, 0.79-0.88) decreased risk for dementia, respectively.
Heavy drinking was linked to an 8% increased risk (aHR, 1.08; 95% CI, 1.03-1.12).
Similar associations were found between alcohol consumption and risk for Alzheimer’s disease and vascular dementia.
Reducing drinking habits from heavy to moderate led to a reduction in risk for dementia and Alzheimer’s, and increasing drinking levels led to an increase in risk for both conditions.
But when the researchers analyzed dementia risk for nondrinkers who began drinking at mild levels during the study period, they found something unexpected – the risk in this group decreased by 7% for dementia (aHR, 0.93; 95% CI, 0.90-0.96) and by 8% for Alzheimer’s (aHR, 0.92; 95% CI, 0.89-0.95), compared with sustained mild drinkers.
“Our study showed that initiation of mild alcohol consumption leads to a reduced risk of all-cause dementia and Alzheimer’s disease, which has never been reported in previous studies,” Dr. Jeon said.
However, Dr. Jeon was quick to point out that this doesn’t mean that people who don’t drink should start.
Previous studies have shown that heavy alcohol use can triple an individual’s dementia risk, while other studies have shown that no amount of alcohol consumption is good for the brain.
“None of the existing health guidelines recommend starting alcohol drinking,” Dr. Jeon said. “Our findings regarding an initiation of mild alcohol consumption cannot be directly translated into clinical recommendations,” but the findings do warrant additional study, he added.
Risks persist
Commenting on the findings, Percy Griffin, PhD, director of scientific engagement for the Alzheimer’s Association in Chicago, agrees.
“While this study is interesting, and this topic deserves further study, no one should drink alcohol as a method of reducing risk of Alzheimer’s disease or other dementia based on this study,” said Dr. Griffin, who was not part of the study.
The exact tipping point in alcohol consumption that can lead to problems with cognition or increased dementia risk is unknown, Dr. Griffin said. Nor do researchers understand why mild drinking may have a protective effect.
“We do know, however, that excessive alcohol consumption has negative effects on heart health and general health, which can lead to problems with brain function,” he said. “Clinicians should have discussions with their patients around their alcohol consumption patterns and the risks associated with drinking in excess, including potential damage to their cognition.”
Funding for the study was not disclosed. Dr. Jeon and Dr. Griffin report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Nature, not nurture, the culprit in OCD
new research suggests.
This finding from a large, register-based study is particularly surprising because results from previous studies of major depression and anxiety disorder have shown a significant effect of parenting and a child’s home environment on the risk for these disorders, the investigators noted.
While the results likely won’t change patient treatment, one expert said it could alleviate concerns of some parents with OCD who fear that witnessing their obsessive behaviors might put their children at higher risk for the disorder.
“The evidence is consistent with the idea that the psychological transmission of OCD from parent to child, if it exists, is really pretty weak,” lead author Kenneth S. Kendler, MD, professor of psychiatry and director of the Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, said in an interview.
The findings were published online in JAMA Psychiatry.
Family analysis
The study is the first to include adoptive parents in an analysis of OCD transmission, which allowed investigators to answer the nature versus nurture question that is often difficult to decipher.
Working with Swedish population registries, researchers identified more than 2.4 million offspring. Of these, 27,141 individuals (1.1%) had a lifetime diagnosis of OCD.
Families were divided into four types: intact families, with kids who lived at home with their biological parents from birth to at least age 15 years; families with kids who never lived with their biological father; families with children who did not live with their biological fathers between birth and age 15 years but who lived with a stepfather for at least 10 of those years; and families with children who were adopted before the age of 5 by people with no biological connection to the child.
After analyzing data from all parent-child relationships, researchers found that genes plus rearing (odds ratio, 3.94; 95% confidence interval, 3.58-4.33) and genes only (OR, 3.34; 95% CI, 2.27-4.93) were significantly more likely to be correlated to transmission of OCD from parent to offspring than rearing alone. Rearing only (OR, 1.4; 95% CI, 0.45-4.39) was not significantly correlated with OCD transmission
“It appears from our data that the only substantial transmission that occurs is in the genes parents transmit, not by the modeling of behavior,” Dr. Kendler said.
“There’s an idea that you can learn some things from your parents from psychopathology, but we didn’t see that kids picked that up much in the case of OCD,” he added.
However, there was one outlier: Children raised by stepparents or adoptive parents with an anxiety disorder had a greater risk of developing OCD.
Given the lack of evidence of a strong rearing effect in other analyses, Dr. Kendler noted that this rogue finding could be caused by an underpowered sample; the researchers plan to study the data further.
“Psychiatric disorders, like many other conditions, are often correlated with neighboring conditions,” he said. “Our study would suggest that some of the molecular genetic variants between OCD and generalized anxiety disorder or other anxiety disorders would be shared, but some would be unique.”
Answers an old question
In a comment, Jon Grant, JD, MD, MPH, professor of psychiatry and director of the Addictive, Compulsive, and Impulsive Disorders Research Lab at the University of Chicago, said the findings fill an important gap in what is known about OCD.
“I think the findings are really answering this old question of: ‘Is OCD due to the rearing patterns in a family versus genetics?’ This was able to get at that information showing that it’s virtually all due to genetics within families, and that’s really good to know,” said Dr. Grant, who was not a part of the study.
He was also struck by the finding of a strong genetic relationship between OCD and generalized anxiety disorder (GAD).
While identifying that OCD and GAD are genetically linked likely won’t change clinical care, “I think it at least allows clinicians to know when we see that comorbidity that it may be much more genetically linked in the case of GAD,” Dr. Grant said.
The study was funded by the Swedish Research Council, as well as Avtal om Läkarutbildning och Forskning funding from Region Skåne. Dr. Kendler and Dr. Grant reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
This finding from a large, register-based study is particularly surprising because results from previous studies of major depression and anxiety disorder have shown a significant effect of parenting and a child’s home environment on the risk for these disorders, the investigators noted.
While the results likely won’t change patient treatment, one expert said it could alleviate concerns of some parents with OCD who fear that witnessing their obsessive behaviors might put their children at higher risk for the disorder.
“The evidence is consistent with the idea that the psychological transmission of OCD from parent to child, if it exists, is really pretty weak,” lead author Kenneth S. Kendler, MD, professor of psychiatry and director of the Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, said in an interview.
The findings were published online in JAMA Psychiatry.
Family analysis
The study is the first to include adoptive parents in an analysis of OCD transmission, which allowed investigators to answer the nature versus nurture question that is often difficult to decipher.
Working with Swedish population registries, researchers identified more than 2.4 million offspring. Of these, 27,141 individuals (1.1%) had a lifetime diagnosis of OCD.
Families were divided into four types: intact families, with kids who lived at home with their biological parents from birth to at least age 15 years; families with kids who never lived with their biological father; families with children who did not live with their biological fathers between birth and age 15 years but who lived with a stepfather for at least 10 of those years; and families with children who were adopted before the age of 5 by people with no biological connection to the child.
After analyzing data from all parent-child relationships, researchers found that genes plus rearing (odds ratio, 3.94; 95% confidence interval, 3.58-4.33) and genes only (OR, 3.34; 95% CI, 2.27-4.93) were significantly more likely to be correlated to transmission of OCD from parent to offspring than rearing alone. Rearing only (OR, 1.4; 95% CI, 0.45-4.39) was not significantly correlated with OCD transmission
“It appears from our data that the only substantial transmission that occurs is in the genes parents transmit, not by the modeling of behavior,” Dr. Kendler said.
“There’s an idea that you can learn some things from your parents from psychopathology, but we didn’t see that kids picked that up much in the case of OCD,” he added.
However, there was one outlier: Children raised by stepparents or adoptive parents with an anxiety disorder had a greater risk of developing OCD.
Given the lack of evidence of a strong rearing effect in other analyses, Dr. Kendler noted that this rogue finding could be caused by an underpowered sample; the researchers plan to study the data further.
“Psychiatric disorders, like many other conditions, are often correlated with neighboring conditions,” he said. “Our study would suggest that some of the molecular genetic variants between OCD and generalized anxiety disorder or other anxiety disorders would be shared, but some would be unique.”
Answers an old question
In a comment, Jon Grant, JD, MD, MPH, professor of psychiatry and director of the Addictive, Compulsive, and Impulsive Disorders Research Lab at the University of Chicago, said the findings fill an important gap in what is known about OCD.
“I think the findings are really answering this old question of: ‘Is OCD due to the rearing patterns in a family versus genetics?’ This was able to get at that information showing that it’s virtually all due to genetics within families, and that’s really good to know,” said Dr. Grant, who was not a part of the study.
He was also struck by the finding of a strong genetic relationship between OCD and generalized anxiety disorder (GAD).
While identifying that OCD and GAD are genetically linked likely won’t change clinical care, “I think it at least allows clinicians to know when we see that comorbidity that it may be much more genetically linked in the case of GAD,” Dr. Grant said.
The study was funded by the Swedish Research Council, as well as Avtal om Läkarutbildning och Forskning funding from Region Skåne. Dr. Kendler and Dr. Grant reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
This finding from a large, register-based study is particularly surprising because results from previous studies of major depression and anxiety disorder have shown a significant effect of parenting and a child’s home environment on the risk for these disorders, the investigators noted.
While the results likely won’t change patient treatment, one expert said it could alleviate concerns of some parents with OCD who fear that witnessing their obsessive behaviors might put their children at higher risk for the disorder.
“The evidence is consistent with the idea that the psychological transmission of OCD from parent to child, if it exists, is really pretty weak,” lead author Kenneth S. Kendler, MD, professor of psychiatry and director of the Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, said in an interview.
The findings were published online in JAMA Psychiatry.
Family analysis
The study is the first to include adoptive parents in an analysis of OCD transmission, which allowed investigators to answer the nature versus nurture question that is often difficult to decipher.
Working with Swedish population registries, researchers identified more than 2.4 million offspring. Of these, 27,141 individuals (1.1%) had a lifetime diagnosis of OCD.
Families were divided into four types: intact families, with kids who lived at home with their biological parents from birth to at least age 15 years; families with kids who never lived with their biological father; families with children who did not live with their biological fathers between birth and age 15 years but who lived with a stepfather for at least 10 of those years; and families with children who were adopted before the age of 5 by people with no biological connection to the child.
After analyzing data from all parent-child relationships, researchers found that genes plus rearing (odds ratio, 3.94; 95% confidence interval, 3.58-4.33) and genes only (OR, 3.34; 95% CI, 2.27-4.93) were significantly more likely to be correlated to transmission of OCD from parent to offspring than rearing alone. Rearing only (OR, 1.4; 95% CI, 0.45-4.39) was not significantly correlated with OCD transmission
“It appears from our data that the only substantial transmission that occurs is in the genes parents transmit, not by the modeling of behavior,” Dr. Kendler said.
“There’s an idea that you can learn some things from your parents from psychopathology, but we didn’t see that kids picked that up much in the case of OCD,” he added.
However, there was one outlier: Children raised by stepparents or adoptive parents with an anxiety disorder had a greater risk of developing OCD.
Given the lack of evidence of a strong rearing effect in other analyses, Dr. Kendler noted that this rogue finding could be caused by an underpowered sample; the researchers plan to study the data further.
“Psychiatric disorders, like many other conditions, are often correlated with neighboring conditions,” he said. “Our study would suggest that some of the molecular genetic variants between OCD and generalized anxiety disorder or other anxiety disorders would be shared, but some would be unique.”
Answers an old question
In a comment, Jon Grant, JD, MD, MPH, professor of psychiatry and director of the Addictive, Compulsive, and Impulsive Disorders Research Lab at the University of Chicago, said the findings fill an important gap in what is known about OCD.
“I think the findings are really answering this old question of: ‘Is OCD due to the rearing patterns in a family versus genetics?’ This was able to get at that information showing that it’s virtually all due to genetics within families, and that’s really good to know,” said Dr. Grant, who was not a part of the study.
He was also struck by the finding of a strong genetic relationship between OCD and generalized anxiety disorder (GAD).
While identifying that OCD and GAD are genetically linked likely won’t change clinical care, “I think it at least allows clinicians to know when we see that comorbidity that it may be much more genetically linked in the case of GAD,” Dr. Grant said.
The study was funded by the Swedish Research Council, as well as Avtal om Läkarutbildning och Forskning funding from Region Skåne. Dr. Kendler and Dr. Grant reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
No spike in overdose deaths from relaxed buprenorphine regulations
Researchers say the data add weight to the argument for permanently adopting the pandemic-era prescribing regulations for buprenorphine, a treatment for opioid use disorder.
“We saw no evidence that increased availability of buprenorphine through the loosening of rules around prescribing and dispensing of buprenorphine during the pandemic increased overdose deaths,” investigator Wilson Compton, MD, deputy director of the National Institute on Drug Abuse, told this news organization.
“This is reassuring that, even when we opened up the doors to easier access to buprenorphine, we didn’t see that most serious consequence,” Dr. Compton said.
The findings were published online in JAMA Network Open .
Cause and effect
Federal agencies relaxed prescribing regulations for buprenorphine in March 2020 to make it easier for clinicians to prescribe the drug via telemedicine and for patients to take the medication at home.
The number of buprenorphine prescriptions has increased since that change, with more than 1 million people receiving the medication in 2021 from retail pharmacies in the United States.
However, questions remained about whether increased access would lead to an increase in buprenorphine-involved overdose.
Researchers with NIDA and the Centers for Disease Control and Prevention analyzed data from the State Unintentional Drug Overdose Reporting System, a CDC database that combines medical examiner and coroner reports and postmortem toxicology testing.
The study included information about overdose deaths from July 2019 to June 2021 in 46 states and the District of Columbia.
Between July 2019 and June 2021, there were 1,955 buprenorphine-involved overdose deaths, which accounted for 2.2% of all drug overdose deaths and 2.6% of opioid-involved overdose deaths.
However, researchers went beyond overall numbers and evaluated details from coroner’s and medical examiner reports, something they had not done before.
“For the first time we looked at the characteristics of decedents from buprenorphine because this has not been studied in this type of detail with a near-national sample,” Dr. Compton said.
“That allowed us to look at patterns of use of other substances as well as the circumstances that are recorded at the death scene that are in the data set,” he added.
Important insights
Reports from nearly all buprenorphine-involved deaths included the presence of at least one other drug, compared with opioid overdose deaths that typically involved only one drug.
“This is consistent with the pharmacology of buprenorphine being a partial agonist, so it may not be as fatal all by itself as some of the other opioids,” Dr. Compton said.
Deaths involving buprenorphine were less likely to include illicitly manufactured fentanyls, and other prescription medications were more often found on the scene, such as antidepressants.
Compared with opioid decedents, buprenorphine decedents were more likely to be women, age 35-44, White, and receiving treatment for mental health conditions, including for substance use disorder (SUD).
These kinds of characteristics provide important insights about potential ways to improve safety and clinical outcomes, Dr. Compton noted.
“When we see things like a little higher rate of SUD treatment and this evidence of other prescription drugs on the scene, and some higher rates of antidepressants in these decedents than I might have expected, I’m very curious about their use of other medical services outside of substance use treatment, because that might be a place where some interventions could be implemented,” he said.
A similar study showed pandemic-era policy changes that allowed methadone to be taken at home was followed by a decrease in methadone-related overdose deaths.
The new findings are consistent with those results, Dr. Compton said.
‘Chipping away’ at stigma
Commenting on the study, O. Trent Hall, DO, assistant professor of addiction medicine, Department of Psychiatry and Behavioral Health, Ohio State University Wexner Medical Center, Columbus, said that, although he welcomed the findings, they aren’t unexpected.
“Buprenorphine is well established as a safe and effective medication for opioid use disorder and as a physician who routinely cares for patients in the hospital after opioid overdose, I am not at all surprised by these results,” said Dr. Hall, who was not involved with the research.
“When my patients leave the hospital with a buprenorphine prescription, they are much less likely to return with another overdose or serious opioid-related medical problem,” he added.
U.S. drug overdose deaths topped 100,000 for the first time in 2021, and most were opioid-related. Although the latest data from the CDC shows drug overdose deaths have been declining slowly since early 2022, the numbers remain high.
Buprenorphine is one of only two drugs known to reduce the risk of opioid overdose. While prescriptions have increased since 2020, the medication remains underutilized, despite its known effectiveness in treating opioid use disorder.
Dr. Hall noted that research such as the new study could help increase buprenorphine’s use.
“Studies like this one chip away at the stigma that has been misapplied to buprenorphine,” he said. “I hope this article will encourage more providers to offer buprenorphine to patients with opioid use disorder.”
The study was funded internally by NIDA and the CDC. Dr. Compton reported owning stock in General Electric, 3M, and Pfizer outside the submitted work. Dr. Hall has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Researchers say the data add weight to the argument for permanently adopting the pandemic-era prescribing regulations for buprenorphine, a treatment for opioid use disorder.
“We saw no evidence that increased availability of buprenorphine through the loosening of rules around prescribing and dispensing of buprenorphine during the pandemic increased overdose deaths,” investigator Wilson Compton, MD, deputy director of the National Institute on Drug Abuse, told this news organization.
“This is reassuring that, even when we opened up the doors to easier access to buprenorphine, we didn’t see that most serious consequence,” Dr. Compton said.
The findings were published online in JAMA Network Open .
Cause and effect
Federal agencies relaxed prescribing regulations for buprenorphine in March 2020 to make it easier for clinicians to prescribe the drug via telemedicine and for patients to take the medication at home.
The number of buprenorphine prescriptions has increased since that change, with more than 1 million people receiving the medication in 2021 from retail pharmacies in the United States.
However, questions remained about whether increased access would lead to an increase in buprenorphine-involved overdose.
Researchers with NIDA and the Centers for Disease Control and Prevention analyzed data from the State Unintentional Drug Overdose Reporting System, a CDC database that combines medical examiner and coroner reports and postmortem toxicology testing.
The study included information about overdose deaths from July 2019 to June 2021 in 46 states and the District of Columbia.
Between July 2019 and June 2021, there were 1,955 buprenorphine-involved overdose deaths, which accounted for 2.2% of all drug overdose deaths and 2.6% of opioid-involved overdose deaths.
However, researchers went beyond overall numbers and evaluated details from coroner’s and medical examiner reports, something they had not done before.
“For the first time we looked at the characteristics of decedents from buprenorphine because this has not been studied in this type of detail with a near-national sample,” Dr. Compton said.
“That allowed us to look at patterns of use of other substances as well as the circumstances that are recorded at the death scene that are in the data set,” he added.
Important insights
Reports from nearly all buprenorphine-involved deaths included the presence of at least one other drug, compared with opioid overdose deaths that typically involved only one drug.
“This is consistent with the pharmacology of buprenorphine being a partial agonist, so it may not be as fatal all by itself as some of the other opioids,” Dr. Compton said.
Deaths involving buprenorphine were less likely to include illicitly manufactured fentanyls, and other prescription medications were more often found on the scene, such as antidepressants.
Compared with opioid decedents, buprenorphine decedents were more likely to be women, age 35-44, White, and receiving treatment for mental health conditions, including for substance use disorder (SUD).
These kinds of characteristics provide important insights about potential ways to improve safety and clinical outcomes, Dr. Compton noted.
“When we see things like a little higher rate of SUD treatment and this evidence of other prescription drugs on the scene, and some higher rates of antidepressants in these decedents than I might have expected, I’m very curious about their use of other medical services outside of substance use treatment, because that might be a place where some interventions could be implemented,” he said.
A similar study showed pandemic-era policy changes that allowed methadone to be taken at home was followed by a decrease in methadone-related overdose deaths.
The new findings are consistent with those results, Dr. Compton said.
‘Chipping away’ at stigma
Commenting on the study, O. Trent Hall, DO, assistant professor of addiction medicine, Department of Psychiatry and Behavioral Health, Ohio State University Wexner Medical Center, Columbus, said that, although he welcomed the findings, they aren’t unexpected.
“Buprenorphine is well established as a safe and effective medication for opioid use disorder and as a physician who routinely cares for patients in the hospital after opioid overdose, I am not at all surprised by these results,” said Dr. Hall, who was not involved with the research.
“When my patients leave the hospital with a buprenorphine prescription, they are much less likely to return with another overdose or serious opioid-related medical problem,” he added.
U.S. drug overdose deaths topped 100,000 for the first time in 2021, and most were opioid-related. Although the latest data from the CDC shows drug overdose deaths have been declining slowly since early 2022, the numbers remain high.
Buprenorphine is one of only two drugs known to reduce the risk of opioid overdose. While prescriptions have increased since 2020, the medication remains underutilized, despite its known effectiveness in treating opioid use disorder.
Dr. Hall noted that research such as the new study could help increase buprenorphine’s use.
“Studies like this one chip away at the stigma that has been misapplied to buprenorphine,” he said. “I hope this article will encourage more providers to offer buprenorphine to patients with opioid use disorder.”
The study was funded internally by NIDA and the CDC. Dr. Compton reported owning stock in General Electric, 3M, and Pfizer outside the submitted work. Dr. Hall has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Researchers say the data add weight to the argument for permanently adopting the pandemic-era prescribing regulations for buprenorphine, a treatment for opioid use disorder.
“We saw no evidence that increased availability of buprenorphine through the loosening of rules around prescribing and dispensing of buprenorphine during the pandemic increased overdose deaths,” investigator Wilson Compton, MD, deputy director of the National Institute on Drug Abuse, told this news organization.
“This is reassuring that, even when we opened up the doors to easier access to buprenorphine, we didn’t see that most serious consequence,” Dr. Compton said.
The findings were published online in JAMA Network Open .
Cause and effect
Federal agencies relaxed prescribing regulations for buprenorphine in March 2020 to make it easier for clinicians to prescribe the drug via telemedicine and for patients to take the medication at home.
The number of buprenorphine prescriptions has increased since that change, with more than 1 million people receiving the medication in 2021 from retail pharmacies in the United States.
However, questions remained about whether increased access would lead to an increase in buprenorphine-involved overdose.
Researchers with NIDA and the Centers for Disease Control and Prevention analyzed data from the State Unintentional Drug Overdose Reporting System, a CDC database that combines medical examiner and coroner reports and postmortem toxicology testing.
The study included information about overdose deaths from July 2019 to June 2021 in 46 states and the District of Columbia.
Between July 2019 and June 2021, there were 1,955 buprenorphine-involved overdose deaths, which accounted for 2.2% of all drug overdose deaths and 2.6% of opioid-involved overdose deaths.
However, researchers went beyond overall numbers and evaluated details from coroner’s and medical examiner reports, something they had not done before.
“For the first time we looked at the characteristics of decedents from buprenorphine because this has not been studied in this type of detail with a near-national sample,” Dr. Compton said.
“That allowed us to look at patterns of use of other substances as well as the circumstances that are recorded at the death scene that are in the data set,” he added.
Important insights
Reports from nearly all buprenorphine-involved deaths included the presence of at least one other drug, compared with opioid overdose deaths that typically involved only one drug.
“This is consistent with the pharmacology of buprenorphine being a partial agonist, so it may not be as fatal all by itself as some of the other opioids,” Dr. Compton said.
Deaths involving buprenorphine were less likely to include illicitly manufactured fentanyls, and other prescription medications were more often found on the scene, such as antidepressants.
Compared with opioid decedents, buprenorphine decedents were more likely to be women, age 35-44, White, and receiving treatment for mental health conditions, including for substance use disorder (SUD).
These kinds of characteristics provide important insights about potential ways to improve safety and clinical outcomes, Dr. Compton noted.
“When we see things like a little higher rate of SUD treatment and this evidence of other prescription drugs on the scene, and some higher rates of antidepressants in these decedents than I might have expected, I’m very curious about their use of other medical services outside of substance use treatment, because that might be a place where some interventions could be implemented,” he said.
A similar study showed pandemic-era policy changes that allowed methadone to be taken at home was followed by a decrease in methadone-related overdose deaths.
The new findings are consistent with those results, Dr. Compton said.
‘Chipping away’ at stigma
Commenting on the study, O. Trent Hall, DO, assistant professor of addiction medicine, Department of Psychiatry and Behavioral Health, Ohio State University Wexner Medical Center, Columbus, said that, although he welcomed the findings, they aren’t unexpected.
“Buprenorphine is well established as a safe and effective medication for opioid use disorder and as a physician who routinely cares for patients in the hospital after opioid overdose, I am not at all surprised by these results,” said Dr. Hall, who was not involved with the research.
“When my patients leave the hospital with a buprenorphine prescription, they are much less likely to return with another overdose or serious opioid-related medical problem,” he added.
U.S. drug overdose deaths topped 100,000 for the first time in 2021, and most were opioid-related. Although the latest data from the CDC shows drug overdose deaths have been declining slowly since early 2022, the numbers remain high.
Buprenorphine is one of only two drugs known to reduce the risk of opioid overdose. While prescriptions have increased since 2020, the medication remains underutilized, despite its known effectiveness in treating opioid use disorder.
Dr. Hall noted that research such as the new study could help increase buprenorphine’s use.
“Studies like this one chip away at the stigma that has been misapplied to buprenorphine,” he said. “I hope this article will encourage more providers to offer buprenorphine to patients with opioid use disorder.”
The study was funded internally by NIDA and the CDC. Dr. Compton reported owning stock in General Electric, 3M, and Pfizer outside the submitted work. Dr. Hall has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Positive top-line results for novel psychedelic in major depression
Top-line results from a phase 2a study of SPL026 (intravenous N,N-Dimethyltryptamine [DMT]) showed a 57% remission rate 3 months after participants received a single dose of the drug, the developer reports.
Small Pharma noted in a press release that this is the first placebo-controlled efficacy trial of a short-duration psychedelic for depression completed to date.
Investigators reported significant improvement in depression symptoms 2 weeks after dosing, which was the primary endpoint, and the improvement persisted at week 12.
“We now have the first evidence that SPL026 DMT, combined with supportive therapy, may be effective for people suffering from MDD,” chief investigator David Erritzoe, MD, PhD, clinical psychiatrist at Imperial College London, said in a statement.
“For patients who are unfortunate to experience little benefit from existing antidepressants, the potential for rapid and durable relief from a single treatment, as shown in this trial, is very promising,” Dr. Erritzoe added.
Randomized trial results
The blinded, randomized, placebo-controlled, two-staged phase 2a study included 34 patients with moderate to severe MDD. Those who were taking pharmacological antidepressant medication at baseline stopped taking the medication prior to dosing with SPL026.
Patients received a placebo (n = 17) or active treatment (n = 17). The latter consisted of a short IV infusion of 21.5 mg of SPL026, resulting in a 20- to 30-minute psychedelic experience, and supportive therapy.
The dose was selected based on data analysis from the company’s phase 1 study in healthy volunteers.
Efficacy was assessed using the Montgomery-Asberg Depression Rating Scale (MADRS) to measure changes in MDD symptoms.
Two weeks after dosing, those receiving the novel therapy showed a significant reduction in depressive symptoms, demonstrating a –7.4-point difference versus the placebo group in MADRS score (P = .02).
Analysis of key secondary endpoints showed a rapid onset of antidepressant effect 1 week post-dose, with a statistically significant difference in MADRS score between the active and placebo groups of –10.8 points (P = .002).
Next steps?
All participants were subsequently enrolled into an open-label phase of the trial where they received a single dose of SPL026 with supportive therapy. They were then followed for a further 12 weeks.
In the open-label phase, patients who received at least one active dose of SPL026 with supportive therapy reported a durable improvement in depression symptoms.
No apparent difference in antidepressant effect was observed between a one- or two-dose regimen of SPL026.
“SPL026 with supportive therapy was shown to have a significant antidepressant effect that was rapid and durable,” Carol Routledge, PhD, chief medical and scientific officer at Small Pharma, said in the statement.
“The results are clinically meaningful and enable us to progress into an international multisite phase 2b study where we seek to further explore the efficacy and safety profile of SPL026 in a larger MDD patient population,” Dr. Routledge added.
A version of this article first appeared on Medscape.com.
Top-line results from a phase 2a study of SPL026 (intravenous N,N-Dimethyltryptamine [DMT]) showed a 57% remission rate 3 months after participants received a single dose of the drug, the developer reports.
Small Pharma noted in a press release that this is the first placebo-controlled efficacy trial of a short-duration psychedelic for depression completed to date.
Investigators reported significant improvement in depression symptoms 2 weeks after dosing, which was the primary endpoint, and the improvement persisted at week 12.
“We now have the first evidence that SPL026 DMT, combined with supportive therapy, may be effective for people suffering from MDD,” chief investigator David Erritzoe, MD, PhD, clinical psychiatrist at Imperial College London, said in a statement.
“For patients who are unfortunate to experience little benefit from existing antidepressants, the potential for rapid and durable relief from a single treatment, as shown in this trial, is very promising,” Dr. Erritzoe added.
Randomized trial results
The blinded, randomized, placebo-controlled, two-staged phase 2a study included 34 patients with moderate to severe MDD. Those who were taking pharmacological antidepressant medication at baseline stopped taking the medication prior to dosing with SPL026.
Patients received a placebo (n = 17) or active treatment (n = 17). The latter consisted of a short IV infusion of 21.5 mg of SPL026, resulting in a 20- to 30-minute psychedelic experience, and supportive therapy.
The dose was selected based on data analysis from the company’s phase 1 study in healthy volunteers.
Efficacy was assessed using the Montgomery-Asberg Depression Rating Scale (MADRS) to measure changes in MDD symptoms.
Two weeks after dosing, those receiving the novel therapy showed a significant reduction in depressive symptoms, demonstrating a –7.4-point difference versus the placebo group in MADRS score (P = .02).
Analysis of key secondary endpoints showed a rapid onset of antidepressant effect 1 week post-dose, with a statistically significant difference in MADRS score between the active and placebo groups of –10.8 points (P = .002).
Next steps?
All participants were subsequently enrolled into an open-label phase of the trial where they received a single dose of SPL026 with supportive therapy. They were then followed for a further 12 weeks.
In the open-label phase, patients who received at least one active dose of SPL026 with supportive therapy reported a durable improvement in depression symptoms.
No apparent difference in antidepressant effect was observed between a one- or two-dose regimen of SPL026.
“SPL026 with supportive therapy was shown to have a significant antidepressant effect that was rapid and durable,” Carol Routledge, PhD, chief medical and scientific officer at Small Pharma, said in the statement.
“The results are clinically meaningful and enable us to progress into an international multisite phase 2b study where we seek to further explore the efficacy and safety profile of SPL026 in a larger MDD patient population,” Dr. Routledge added.
A version of this article first appeared on Medscape.com.
Top-line results from a phase 2a study of SPL026 (intravenous N,N-Dimethyltryptamine [DMT]) showed a 57% remission rate 3 months after participants received a single dose of the drug, the developer reports.
Small Pharma noted in a press release that this is the first placebo-controlled efficacy trial of a short-duration psychedelic for depression completed to date.
Investigators reported significant improvement in depression symptoms 2 weeks after dosing, which was the primary endpoint, and the improvement persisted at week 12.
“We now have the first evidence that SPL026 DMT, combined with supportive therapy, may be effective for people suffering from MDD,” chief investigator David Erritzoe, MD, PhD, clinical psychiatrist at Imperial College London, said in a statement.
“For patients who are unfortunate to experience little benefit from existing antidepressants, the potential for rapid and durable relief from a single treatment, as shown in this trial, is very promising,” Dr. Erritzoe added.
Randomized trial results
The blinded, randomized, placebo-controlled, two-staged phase 2a study included 34 patients with moderate to severe MDD. Those who were taking pharmacological antidepressant medication at baseline stopped taking the medication prior to dosing with SPL026.
Patients received a placebo (n = 17) or active treatment (n = 17). The latter consisted of a short IV infusion of 21.5 mg of SPL026, resulting in a 20- to 30-minute psychedelic experience, and supportive therapy.
The dose was selected based on data analysis from the company’s phase 1 study in healthy volunteers.
Efficacy was assessed using the Montgomery-Asberg Depression Rating Scale (MADRS) to measure changes in MDD symptoms.
Two weeks after dosing, those receiving the novel therapy showed a significant reduction in depressive symptoms, demonstrating a –7.4-point difference versus the placebo group in MADRS score (P = .02).
Analysis of key secondary endpoints showed a rapid onset of antidepressant effect 1 week post-dose, with a statistically significant difference in MADRS score between the active and placebo groups of –10.8 points (P = .002).
Next steps?
All participants were subsequently enrolled into an open-label phase of the trial where they received a single dose of SPL026 with supportive therapy. They were then followed for a further 12 weeks.
In the open-label phase, patients who received at least one active dose of SPL026 with supportive therapy reported a durable improvement in depression symptoms.
No apparent difference in antidepressant effect was observed between a one- or two-dose regimen of SPL026.
“SPL026 with supportive therapy was shown to have a significant antidepressant effect that was rapid and durable,” Carol Routledge, PhD, chief medical and scientific officer at Small Pharma, said in the statement.
“The results are clinically meaningful and enable us to progress into an international multisite phase 2b study where we seek to further explore the efficacy and safety profile of SPL026 in a larger MDD patient population,” Dr. Routledge added.
A version of this article first appeared on Medscape.com.
Lipid signature may flag schizophrenia
Although such a test remains a long way off, investigators said, the identification of the unique lipid signature is a critical first step. However, one expert noted that the lipid signature not accurately differentiating patients with schizophrenia from those with bipolar disorder (BD) and major depressive disorder (MDD) limits the findings’ applicability.
The profile includes 77 lipids identified from a large analysis of many different classes of lipid species. Lipids such as cholesterol and triglycerides made up only a small fraction of the classes assessed.
The investigators noted that some of the lipids in the profile associated with schizophrenia are involved in determining cell membrane structure and fluidity or cell-to-cell messaging, which could be important to synaptic function.
“These 77 lipids jointly constitute a lipidomic profile that discriminated between individuals with schizophrenia and individuals without a mental health diagnosis with very high accuracy,” investigator Eva C. Schulte, MD, PhD, of the Institute of Psychiatric Phenomics and Genomics (IPPG) and the department of psychiatry and psychotherapy at University Hospital of Ludwig-Maximilians-University, Munich, told this news organization.
“Of note, we did not see large profile differences between patients with a first psychotic episode who had only been treated for a few days and individuals on long-term antipsychotic therapy,” Dr. Schulte said.
The findings were published online in JAMA Psychiatry.
Detailed analysis
Lipid profiles in patients with psychiatric diagnoses have been reported previously, but those studies were small and did not identify a reliable signature independent of demographic and environmental factors.
For the current study, researchers analyzed blood plasma lipid levels from 980 individuals with severe psychiatric illness and 572 people without mental illness from three cohorts in China, Germany, Austria, and Russia.
The study sample included patients with schizophrenia (n = 478), BD (n = 184), and MDD (n = 256), as well as 104 patients with a first psychotic episode who had no long-term psychopharmacology use.
Results showed 77 lipids in 14 classes were significantly altered between participants with schizophrenia and the healthy control in all three cohorts.
The most prominent alterations at the lipid class level included increases in ceramide, triacylglyceride, and phosphatidylcholine and decreases in acylcarnitine and phosphatidylcholine plasmalogen (P < .05 for each cohort).
Schizophrenia-associated lipid differences were similar between patients with high and low symptom severity (P < .001), suggesting that the lipid alterations might represent a trait of the psychiatric disorder.
No medication effect
Most patients in the study received long-term antipsychotic medication, which has been shown previously to affect some plasma lipid compounds.
So, to assess a possible effect of medication, the investigators evaluated 13 patients with schizophrenia who were not medicated for at least 6 months prior to blood sample collection and the cohort of patients with a first psychotic episode who had been medicated for less than 1 week.
Comparison of the lipid intensity differences between the healthy controls group and either participants receiving medication or those who were not medicated revealed highly correlated alterations in both patient groups (P < .001).
“Taken together, these results indicate that the identified schizophrenia-associated alterations cannot be attributed to medication effects,” the investigators wrote.
Lipidome alterations in BPD and MDD, assessed in 184 and 256 individuals, respectively, were similar to those of schizophrenia but not identical.
Researchers isolated 97 lipids altered in the MDD cohorts and 47 in the BPD cohorts – with 30 and 28, respectively, overlapping with the schizophrenia-associated features and seven of the lipids found among all three disorders.
Although this was significantly more than expected by chance (P < .001), it was not strong enough to demonstrate a clear association, the investigators wrote.
“The profiles were very successful at differentiating individuals with severe mental health conditions from individuals without a diagnosed mental health condition, but much less so at differentiating between the different diagnostic entities,” coinvestigator Thomas G. Schulze, MD, director of IPPG, said in an interview.
“An important caveat, however, is that the available sample sizes for bipolar disorder and major depressive disorder were smaller than those for schizophrenia, which makes a direct comparison between these difficult,” added Dr. Schulze, clinical professor in psychiatry and behavioral sciences at State University of New York, Syracuse.
More work remains
Although the study is thought to be the largest to date to examine lipid profiles associated with serious psychiatric illness, much work remains, Dr. Schulze noted.
“At this time, based on these first results, no clinical diagnostic test can be derived from these results,” he said.
He added that the development of reliable biomarkers based on lipidomic profiles would require large prospective randomized trials, complemented by observational studies assessing full lipidomic profiles across the lifespan.
Researchers also need to better understand the exact mechanism by which lipid alterations are associated with schizophrenia and other illnesses.
Physiologically, the investigated lipids have many additional functions, such as determining cell membrane structure and fluidity or cell-to-cell messaging.
Dr. Schulte noted that several lipid species may be involved in determining mechanisms important to synaptic function, such as cell membrane fluidity and vesicle release.
“As is commonly known, alterations in synaptic function underly many severe psychiatric disorders,” she said. “Changes in lipid species could theoretically be related to these synaptic alterations.”
A better marker needed
In a comment, Stephen Strakowski, MD, professor and vice chair of research in the department of psychiatry, Indiana University, Indianapolis and Evansville, noted that while the findings are interesting, they don’t really offer the kind of information clinicians who treat patients with serious mental illness need most.
“Do we need a marker to tell us if someone’s got a major mental illness compared to a healthy person?” asked Dr. Strakowski, who was not part of the study. “The answer to that is no. We already know how to do that.”
A truly useful marker would help clinicians differentiate between schizophrenia, bipolar disorder, major depression, or another serious mental illness, he said.
“That’s the marker that would be most helpful,” he added. “This can’t address that, but perhaps it could be a step to start designing a test for that.”
Dr. Strakowksi noted that the findings do not clarify whether the lipid profile found in patients with schizophrenia predates diagnosis or whether it is a result of the mental illness, an unrelated illness, or another factor that could be critical in treating patients.
However, he was quick to point out the limitations don’t diminish the importance of the study.
“It’s a large dataset that’s cross-national, cross-diagnostic that says there appears to be a signal here that there’s something about lipid profiles that may be independent of treatment that could be worth understanding,” Dr. Strakowksi said.
“It allows us to think about developing different models based on lipid profiles, and that’s important,” he added.
The study was funded by the National Key R&D Program of China, National One Thousand Foreign Experts Plan, Moscow Center for Innovative Technologies in Healthcare, European Union’s Horizon 2020 Research and Innovation Programme, NARSAD Young Investigator Grant, German Research Foundation, German Ministry for Education and Research, the Dr. Lisa Oehler Foundation, and the Munich Clinician Scientist Program. Dr. Schulze and Dr. Schulte reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Although such a test remains a long way off, investigators said, the identification of the unique lipid signature is a critical first step. However, one expert noted that the lipid signature not accurately differentiating patients with schizophrenia from those with bipolar disorder (BD) and major depressive disorder (MDD) limits the findings’ applicability.
The profile includes 77 lipids identified from a large analysis of many different classes of lipid species. Lipids such as cholesterol and triglycerides made up only a small fraction of the classes assessed.
The investigators noted that some of the lipids in the profile associated with schizophrenia are involved in determining cell membrane structure and fluidity or cell-to-cell messaging, which could be important to synaptic function.
“These 77 lipids jointly constitute a lipidomic profile that discriminated between individuals with schizophrenia and individuals without a mental health diagnosis with very high accuracy,” investigator Eva C. Schulte, MD, PhD, of the Institute of Psychiatric Phenomics and Genomics (IPPG) and the department of psychiatry and psychotherapy at University Hospital of Ludwig-Maximilians-University, Munich, told this news organization.
“Of note, we did not see large profile differences between patients with a first psychotic episode who had only been treated for a few days and individuals on long-term antipsychotic therapy,” Dr. Schulte said.
The findings were published online in JAMA Psychiatry.
Detailed analysis
Lipid profiles in patients with psychiatric diagnoses have been reported previously, but those studies were small and did not identify a reliable signature independent of demographic and environmental factors.
For the current study, researchers analyzed blood plasma lipid levels from 980 individuals with severe psychiatric illness and 572 people without mental illness from three cohorts in China, Germany, Austria, and Russia.
The study sample included patients with schizophrenia (n = 478), BD (n = 184), and MDD (n = 256), as well as 104 patients with a first psychotic episode who had no long-term psychopharmacology use.
Results showed 77 lipids in 14 classes were significantly altered between participants with schizophrenia and the healthy control in all three cohorts.
The most prominent alterations at the lipid class level included increases in ceramide, triacylglyceride, and phosphatidylcholine and decreases in acylcarnitine and phosphatidylcholine plasmalogen (P < .05 for each cohort).
Schizophrenia-associated lipid differences were similar between patients with high and low symptom severity (P < .001), suggesting that the lipid alterations might represent a trait of the psychiatric disorder.
No medication effect
Most patients in the study received long-term antipsychotic medication, which has been shown previously to affect some plasma lipid compounds.
So, to assess a possible effect of medication, the investigators evaluated 13 patients with schizophrenia who were not medicated for at least 6 months prior to blood sample collection and the cohort of patients with a first psychotic episode who had been medicated for less than 1 week.
Comparison of the lipid intensity differences between the healthy controls group and either participants receiving medication or those who were not medicated revealed highly correlated alterations in both patient groups (P < .001).
“Taken together, these results indicate that the identified schizophrenia-associated alterations cannot be attributed to medication effects,” the investigators wrote.
Lipidome alterations in BPD and MDD, assessed in 184 and 256 individuals, respectively, were similar to those of schizophrenia but not identical.
Researchers isolated 97 lipids altered in the MDD cohorts and 47 in the BPD cohorts – with 30 and 28, respectively, overlapping with the schizophrenia-associated features and seven of the lipids found among all three disorders.
Although this was significantly more than expected by chance (P < .001), it was not strong enough to demonstrate a clear association, the investigators wrote.
“The profiles were very successful at differentiating individuals with severe mental health conditions from individuals without a diagnosed mental health condition, but much less so at differentiating between the different diagnostic entities,” coinvestigator Thomas G. Schulze, MD, director of IPPG, said in an interview.
“An important caveat, however, is that the available sample sizes for bipolar disorder and major depressive disorder were smaller than those for schizophrenia, which makes a direct comparison between these difficult,” added Dr. Schulze, clinical professor in psychiatry and behavioral sciences at State University of New York, Syracuse.
More work remains
Although the study is thought to be the largest to date to examine lipid profiles associated with serious psychiatric illness, much work remains, Dr. Schulze noted.
“At this time, based on these first results, no clinical diagnostic test can be derived from these results,” he said.
He added that the development of reliable biomarkers based on lipidomic profiles would require large prospective randomized trials, complemented by observational studies assessing full lipidomic profiles across the lifespan.
Researchers also need to better understand the exact mechanism by which lipid alterations are associated with schizophrenia and other illnesses.
Physiologically, the investigated lipids have many additional functions, such as determining cell membrane structure and fluidity or cell-to-cell messaging.
Dr. Schulte noted that several lipid species may be involved in determining mechanisms important to synaptic function, such as cell membrane fluidity and vesicle release.
“As is commonly known, alterations in synaptic function underly many severe psychiatric disorders,” she said. “Changes in lipid species could theoretically be related to these synaptic alterations.”
A better marker needed
In a comment, Stephen Strakowski, MD, professor and vice chair of research in the department of psychiatry, Indiana University, Indianapolis and Evansville, noted that while the findings are interesting, they don’t really offer the kind of information clinicians who treat patients with serious mental illness need most.
“Do we need a marker to tell us if someone’s got a major mental illness compared to a healthy person?” asked Dr. Strakowski, who was not part of the study. “The answer to that is no. We already know how to do that.”
A truly useful marker would help clinicians differentiate between schizophrenia, bipolar disorder, major depression, or another serious mental illness, he said.
“That’s the marker that would be most helpful,” he added. “This can’t address that, but perhaps it could be a step to start designing a test for that.”
Dr. Strakowksi noted that the findings do not clarify whether the lipid profile found in patients with schizophrenia predates diagnosis or whether it is a result of the mental illness, an unrelated illness, or another factor that could be critical in treating patients.
However, he was quick to point out the limitations don’t diminish the importance of the study.
“It’s a large dataset that’s cross-national, cross-diagnostic that says there appears to be a signal here that there’s something about lipid profiles that may be independent of treatment that could be worth understanding,” Dr. Strakowksi said.
“It allows us to think about developing different models based on lipid profiles, and that’s important,” he added.
The study was funded by the National Key R&D Program of China, National One Thousand Foreign Experts Plan, Moscow Center for Innovative Technologies in Healthcare, European Union’s Horizon 2020 Research and Innovation Programme, NARSAD Young Investigator Grant, German Research Foundation, German Ministry for Education and Research, the Dr. Lisa Oehler Foundation, and the Munich Clinician Scientist Program. Dr. Schulze and Dr. Schulte reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Although such a test remains a long way off, investigators said, the identification of the unique lipid signature is a critical first step. However, one expert noted that the lipid signature not accurately differentiating patients with schizophrenia from those with bipolar disorder (BD) and major depressive disorder (MDD) limits the findings’ applicability.
The profile includes 77 lipids identified from a large analysis of many different classes of lipid species. Lipids such as cholesterol and triglycerides made up only a small fraction of the classes assessed.
The investigators noted that some of the lipids in the profile associated with schizophrenia are involved in determining cell membrane structure and fluidity or cell-to-cell messaging, which could be important to synaptic function.
“These 77 lipids jointly constitute a lipidomic profile that discriminated between individuals with schizophrenia and individuals without a mental health diagnosis with very high accuracy,” investigator Eva C. Schulte, MD, PhD, of the Institute of Psychiatric Phenomics and Genomics (IPPG) and the department of psychiatry and psychotherapy at University Hospital of Ludwig-Maximilians-University, Munich, told this news organization.
“Of note, we did not see large profile differences between patients with a first psychotic episode who had only been treated for a few days and individuals on long-term antipsychotic therapy,” Dr. Schulte said.
The findings were published online in JAMA Psychiatry.
Detailed analysis
Lipid profiles in patients with psychiatric diagnoses have been reported previously, but those studies were small and did not identify a reliable signature independent of demographic and environmental factors.
For the current study, researchers analyzed blood plasma lipid levels from 980 individuals with severe psychiatric illness and 572 people without mental illness from three cohorts in China, Germany, Austria, and Russia.
The study sample included patients with schizophrenia (n = 478), BD (n = 184), and MDD (n = 256), as well as 104 patients with a first psychotic episode who had no long-term psychopharmacology use.
Results showed 77 lipids in 14 classes were significantly altered between participants with schizophrenia and the healthy control in all three cohorts.
The most prominent alterations at the lipid class level included increases in ceramide, triacylglyceride, and phosphatidylcholine and decreases in acylcarnitine and phosphatidylcholine plasmalogen (P < .05 for each cohort).
Schizophrenia-associated lipid differences were similar between patients with high and low symptom severity (P < .001), suggesting that the lipid alterations might represent a trait of the psychiatric disorder.
No medication effect
Most patients in the study received long-term antipsychotic medication, which has been shown previously to affect some plasma lipid compounds.
So, to assess a possible effect of medication, the investigators evaluated 13 patients with schizophrenia who were not medicated for at least 6 months prior to blood sample collection and the cohort of patients with a first psychotic episode who had been medicated for less than 1 week.
Comparison of the lipid intensity differences between the healthy controls group and either participants receiving medication or those who were not medicated revealed highly correlated alterations in both patient groups (P < .001).
“Taken together, these results indicate that the identified schizophrenia-associated alterations cannot be attributed to medication effects,” the investigators wrote.
Lipidome alterations in BPD and MDD, assessed in 184 and 256 individuals, respectively, were similar to those of schizophrenia but not identical.
Researchers isolated 97 lipids altered in the MDD cohorts and 47 in the BPD cohorts – with 30 and 28, respectively, overlapping with the schizophrenia-associated features and seven of the lipids found among all three disorders.
Although this was significantly more than expected by chance (P < .001), it was not strong enough to demonstrate a clear association, the investigators wrote.
“The profiles were very successful at differentiating individuals with severe mental health conditions from individuals without a diagnosed mental health condition, but much less so at differentiating between the different diagnostic entities,” coinvestigator Thomas G. Schulze, MD, director of IPPG, said in an interview.
“An important caveat, however, is that the available sample sizes for bipolar disorder and major depressive disorder were smaller than those for schizophrenia, which makes a direct comparison between these difficult,” added Dr. Schulze, clinical professor in psychiatry and behavioral sciences at State University of New York, Syracuse.
More work remains
Although the study is thought to be the largest to date to examine lipid profiles associated with serious psychiatric illness, much work remains, Dr. Schulze noted.
“At this time, based on these first results, no clinical diagnostic test can be derived from these results,” he said.
He added that the development of reliable biomarkers based on lipidomic profiles would require large prospective randomized trials, complemented by observational studies assessing full lipidomic profiles across the lifespan.
Researchers also need to better understand the exact mechanism by which lipid alterations are associated with schizophrenia and other illnesses.
Physiologically, the investigated lipids have many additional functions, such as determining cell membrane structure and fluidity or cell-to-cell messaging.
Dr. Schulte noted that several lipid species may be involved in determining mechanisms important to synaptic function, such as cell membrane fluidity and vesicle release.
“As is commonly known, alterations in synaptic function underly many severe psychiatric disorders,” she said. “Changes in lipid species could theoretically be related to these synaptic alterations.”
A better marker needed
In a comment, Stephen Strakowski, MD, professor and vice chair of research in the department of psychiatry, Indiana University, Indianapolis and Evansville, noted that while the findings are interesting, they don’t really offer the kind of information clinicians who treat patients with serious mental illness need most.
“Do we need a marker to tell us if someone’s got a major mental illness compared to a healthy person?” asked Dr. Strakowski, who was not part of the study. “The answer to that is no. We already know how to do that.”
A truly useful marker would help clinicians differentiate between schizophrenia, bipolar disorder, major depression, or another serious mental illness, he said.
“That’s the marker that would be most helpful,” he added. “This can’t address that, but perhaps it could be a step to start designing a test for that.”
Dr. Strakowksi noted that the findings do not clarify whether the lipid profile found in patients with schizophrenia predates diagnosis or whether it is a result of the mental illness, an unrelated illness, or another factor that could be critical in treating patients.
However, he was quick to point out the limitations don’t diminish the importance of the study.
“It’s a large dataset that’s cross-national, cross-diagnostic that says there appears to be a signal here that there’s something about lipid profiles that may be independent of treatment that could be worth understanding,” Dr. Strakowksi said.
“It allows us to think about developing different models based on lipid profiles, and that’s important,” he added.
The study was funded by the National Key R&D Program of China, National One Thousand Foreign Experts Plan, Moscow Center for Innovative Technologies in Healthcare, European Union’s Horizon 2020 Research and Innovation Programme, NARSAD Young Investigator Grant, German Research Foundation, German Ministry for Education and Research, the Dr. Lisa Oehler Foundation, and the Munich Clinician Scientist Program. Dr. Schulze and Dr. Schulte reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
Poor sleep quality as a teen may up MS risk in adulthood
Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.
In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.
On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.
While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.
“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.
“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.
The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
Strong association
Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.
Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.
The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.
Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).
Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).
The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
Long sleep ‘apparently good’
The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.
“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.
The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.
“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.
“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.
The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
Underestimated problem?
Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.
“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.
“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.
That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.
Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.
“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.
The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.
In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.
On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.
While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.
“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.
“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.
The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
Strong association
Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.
Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.
The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.
Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).
Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).
The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
Long sleep ‘apparently good’
The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.
“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.
The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.
“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.
“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.
The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
Underestimated problem?
Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.
“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.
“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.
That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.
Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.
“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.
The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.
In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.
On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.
While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.
“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.
“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.
The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
Strong association
Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.
Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.
The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.
Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).
Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).
The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
Long sleep ‘apparently good’
The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.
“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.
The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.
“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.
“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.
The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
Underestimated problem?
Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.
“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.
“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.
That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.
Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.
“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.
The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Minorities with epilepsy blocked from receiving ‘highest quality of care’
, new research shows.
Even after controlling for epilepsy severity, comorbid conditions, and other factors that might affect medication choice, researchers found that newer medication use was 29% less likely in Black patients, 23% less likely in Native Hawaiian and other Pacific Islander patients, and 7% less likely in Hispanic patients, compared with White individuals.
“I hope that clinicians will see from our findings that minoritized patients with epilepsy face a myriad of barriers in receiving the highest quality of care, including ASM use,” said lead investigator Wyatt P. Bensken, PhD, adjunct assistant professor of Population and Quantitative Health Sciences at Case Western Reserve University, Cleveland. “Considering your patients’ barriers, and how that influences their care – including ASM selection – will be critical to helping reduce these population-level inequities.”
The study was published online in Neurology Clinical Practice.
A prompt for practice change
For the study, researchers used Medicaid claims for more than 78,000 people who had filled at least two prescriptions for an ASM between 2010 and 2014.
Most patients were White (53.4%); 22.6% were Black; 11.9% were Hispanic; 1.6% were Asian; 1.5% were Native Hawaiian or other Pacific Islander; 0.6% American Indian or Alaskan Native; and 8.3% were classified as “other.”
One-quarter of participants were taking an older ASM, such as carbamazepine, phenytoin, and valproate. About 65% were taking second-generation ASMs, including gabapentin, levetiracetam, and zonisamide. A little less than 10% were taking lacosamide, perampenel, or another third-generation ASM.
Compared with White patients, newer medication prescriptions were significantly less likely in Black individuals (adjusted odds ratio, 0.71; 95% confidence interval, 0.68-0.75), Native Hawaiian or other Pacific Islanders (aOR, 0.77; 95% CI, 0.67-0.88), and Hispanic patients (aOR, 0.93; 95% CI, 0.88-0.99).
Third-generation ASMs were used by 10.7% of White patients versus 6% of Black individuals and 5.1% of American Indian or Alaskan Native patients.
Researchers also found that taking a second-generation ASM was associated with better treatment adherence (aOR, 1.17; 95% CI, 1.11-1.23) and that patients on newer ASMs were more than three times as likely to be under the care of a neurologist (aOR, 3.26; 95% CI, 3.13-3.41).
The findings draw attention to racial inequities surrounding access to medication and specialists and subspecialists, Dr. Bensken said. Identifying specific barriers and developing solutions is the long-range goal, he added.
“In the interim, increasing the attention to these inequities will, we hope, prompt changes across practices,” Dr. Bensken said.
A ‘wake-up call’
Commenting on the findings, Joseph Sirven, MD, professor of neurology at the Mayo Clinic Florida, Jacksonville, said the results were “striking” because newer ASMs are generally the go-to for most physicians who treat epilepsy.
“Use of first-generation ASMs is typically reserved [for] if one runs out of options,” Dr. Sirven said.
This study and others like it should serve as a “wake-up call” for clinicians, Dr. Sirven added.
“This study is important because it shows that whether we realize it or not, race and ethnicities are playing a role in ASM, and this is related to financial access to newer-generation drugs,” he said. “Similar findings are seen in impoverished countries where first-generation ASM drugs are routinely used because of drug pricing.”
More to explore
Also commenting on the study, Scott Mintzer, MD, a professor and director of the Epilepsy Monitoring Unit at Thomas Jefferson University, Philadelphia, said using first-generation ASMs as a proxy for quality of care is “a very innovative concept.”
“From that perspective, the finding that racial minority patients are more likely to be on a first-generation drug is not surprising. But after that it gets far more complicated to interpret,” he added.
Neither adherence nor care by a neurologist was different in a consistent direction within the various minority populations, Dr. Mintzer noted. In addition, Black patients were as likely to see a neurologist as White patients but still more likely to be on a first-generation drug.
There are also a few caveats to the findings that should be considered, Dr. Mintzer added. First, the sample included only Medicaid recipients, nearly 35% of whom had a comorbid psychosis. Those and other characteristics of the study pool suggest participants aren’t representative of the United States population as a whole. Second, significant shifts in ASM use have occurred since the study data cutoff in 2014, none of which are reflected in these findings.
“So, I don’t think we can really say how to address this yet,” Dr. Mintzer said. “There’s a lot to explore about whether this is still occurring, how generalizable these findings are, and what they might be due to, as there are a host of potential explanations, which the authors themselves acknowledge.”
The study was funded by the U.S. Centers for Disease Control and Prevention and the National Institute on Minority Health and Health Disparities. Dr. Bensken has received support for this work from NIMHD and serves on the Editorial Board of the journal Neurology. Dr. Sirven and Mintzer report no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
, new research shows.
Even after controlling for epilepsy severity, comorbid conditions, and other factors that might affect medication choice, researchers found that newer medication use was 29% less likely in Black patients, 23% less likely in Native Hawaiian and other Pacific Islander patients, and 7% less likely in Hispanic patients, compared with White individuals.
“I hope that clinicians will see from our findings that minoritized patients with epilepsy face a myriad of barriers in receiving the highest quality of care, including ASM use,” said lead investigator Wyatt P. Bensken, PhD, adjunct assistant professor of Population and Quantitative Health Sciences at Case Western Reserve University, Cleveland. “Considering your patients’ barriers, and how that influences their care – including ASM selection – will be critical to helping reduce these population-level inequities.”
The study was published online in Neurology Clinical Practice.
A prompt for practice change
For the study, researchers used Medicaid claims for more than 78,000 people who had filled at least two prescriptions for an ASM between 2010 and 2014.
Most patients were White (53.4%); 22.6% were Black; 11.9% were Hispanic; 1.6% were Asian; 1.5% were Native Hawaiian or other Pacific Islander; 0.6% American Indian or Alaskan Native; and 8.3% were classified as “other.”
One-quarter of participants were taking an older ASM, such as carbamazepine, phenytoin, and valproate. About 65% were taking second-generation ASMs, including gabapentin, levetiracetam, and zonisamide. A little less than 10% were taking lacosamide, perampenel, or another third-generation ASM.
Compared with White patients, newer medication prescriptions were significantly less likely in Black individuals (adjusted odds ratio, 0.71; 95% confidence interval, 0.68-0.75), Native Hawaiian or other Pacific Islanders (aOR, 0.77; 95% CI, 0.67-0.88), and Hispanic patients (aOR, 0.93; 95% CI, 0.88-0.99).
Third-generation ASMs were used by 10.7% of White patients versus 6% of Black individuals and 5.1% of American Indian or Alaskan Native patients.
Researchers also found that taking a second-generation ASM was associated with better treatment adherence (aOR, 1.17; 95% CI, 1.11-1.23) and that patients on newer ASMs were more than three times as likely to be under the care of a neurologist (aOR, 3.26; 95% CI, 3.13-3.41).
The findings draw attention to racial inequities surrounding access to medication and specialists and subspecialists, Dr. Bensken said. Identifying specific barriers and developing solutions is the long-range goal, he added.
“In the interim, increasing the attention to these inequities will, we hope, prompt changes across practices,” Dr. Bensken said.
A ‘wake-up call’
Commenting on the findings, Joseph Sirven, MD, professor of neurology at the Mayo Clinic Florida, Jacksonville, said the results were “striking” because newer ASMs are generally the go-to for most physicians who treat epilepsy.
“Use of first-generation ASMs is typically reserved [for] if one runs out of options,” Dr. Sirven said.
This study and others like it should serve as a “wake-up call” for clinicians, Dr. Sirven added.
“This study is important because it shows that whether we realize it or not, race and ethnicities are playing a role in ASM, and this is related to financial access to newer-generation drugs,” he said. “Similar findings are seen in impoverished countries where first-generation ASM drugs are routinely used because of drug pricing.”
More to explore
Also commenting on the study, Scott Mintzer, MD, a professor and director of the Epilepsy Monitoring Unit at Thomas Jefferson University, Philadelphia, said using first-generation ASMs as a proxy for quality of care is “a very innovative concept.”
“From that perspective, the finding that racial minority patients are more likely to be on a first-generation drug is not surprising. But after that it gets far more complicated to interpret,” he added.
Neither adherence nor care by a neurologist was different in a consistent direction within the various minority populations, Dr. Mintzer noted. In addition, Black patients were as likely to see a neurologist as White patients but still more likely to be on a first-generation drug.
There are also a few caveats to the findings that should be considered, Dr. Mintzer added. First, the sample included only Medicaid recipients, nearly 35% of whom had a comorbid psychosis. Those and other characteristics of the study pool suggest participants aren’t representative of the United States population as a whole. Second, significant shifts in ASM use have occurred since the study data cutoff in 2014, none of which are reflected in these findings.
“So, I don’t think we can really say how to address this yet,” Dr. Mintzer said. “There’s a lot to explore about whether this is still occurring, how generalizable these findings are, and what they might be due to, as there are a host of potential explanations, which the authors themselves acknowledge.”
The study was funded by the U.S. Centers for Disease Control and Prevention and the National Institute on Minority Health and Health Disparities. Dr. Bensken has received support for this work from NIMHD and serves on the Editorial Board of the journal Neurology. Dr. Sirven and Mintzer report no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
, new research shows.
Even after controlling for epilepsy severity, comorbid conditions, and other factors that might affect medication choice, researchers found that newer medication use was 29% less likely in Black patients, 23% less likely in Native Hawaiian and other Pacific Islander patients, and 7% less likely in Hispanic patients, compared with White individuals.
“I hope that clinicians will see from our findings that minoritized patients with epilepsy face a myriad of barriers in receiving the highest quality of care, including ASM use,” said lead investigator Wyatt P. Bensken, PhD, adjunct assistant professor of Population and Quantitative Health Sciences at Case Western Reserve University, Cleveland. “Considering your patients’ barriers, and how that influences their care – including ASM selection – will be critical to helping reduce these population-level inequities.”
The study was published online in Neurology Clinical Practice.
A prompt for practice change
For the study, researchers used Medicaid claims for more than 78,000 people who had filled at least two prescriptions for an ASM between 2010 and 2014.
Most patients were White (53.4%); 22.6% were Black; 11.9% were Hispanic; 1.6% were Asian; 1.5% were Native Hawaiian or other Pacific Islander; 0.6% American Indian or Alaskan Native; and 8.3% were classified as “other.”
One-quarter of participants were taking an older ASM, such as carbamazepine, phenytoin, and valproate. About 65% were taking second-generation ASMs, including gabapentin, levetiracetam, and zonisamide. A little less than 10% were taking lacosamide, perampenel, or another third-generation ASM.
Compared with White patients, newer medication prescriptions were significantly less likely in Black individuals (adjusted odds ratio, 0.71; 95% confidence interval, 0.68-0.75), Native Hawaiian or other Pacific Islanders (aOR, 0.77; 95% CI, 0.67-0.88), and Hispanic patients (aOR, 0.93; 95% CI, 0.88-0.99).
Third-generation ASMs were used by 10.7% of White patients versus 6% of Black individuals and 5.1% of American Indian or Alaskan Native patients.
Researchers also found that taking a second-generation ASM was associated with better treatment adherence (aOR, 1.17; 95% CI, 1.11-1.23) and that patients on newer ASMs were more than three times as likely to be under the care of a neurologist (aOR, 3.26; 95% CI, 3.13-3.41).
The findings draw attention to racial inequities surrounding access to medication and specialists and subspecialists, Dr. Bensken said. Identifying specific barriers and developing solutions is the long-range goal, he added.
“In the interim, increasing the attention to these inequities will, we hope, prompt changes across practices,” Dr. Bensken said.
A ‘wake-up call’
Commenting on the findings, Joseph Sirven, MD, professor of neurology at the Mayo Clinic Florida, Jacksonville, said the results were “striking” because newer ASMs are generally the go-to for most physicians who treat epilepsy.
“Use of first-generation ASMs is typically reserved [for] if one runs out of options,” Dr. Sirven said.
This study and others like it should serve as a “wake-up call” for clinicians, Dr. Sirven added.
“This study is important because it shows that whether we realize it or not, race and ethnicities are playing a role in ASM, and this is related to financial access to newer-generation drugs,” he said. “Similar findings are seen in impoverished countries where first-generation ASM drugs are routinely used because of drug pricing.”
More to explore
Also commenting on the study, Scott Mintzer, MD, a professor and director of the Epilepsy Monitoring Unit at Thomas Jefferson University, Philadelphia, said using first-generation ASMs as a proxy for quality of care is “a very innovative concept.”
“From that perspective, the finding that racial minority patients are more likely to be on a first-generation drug is not surprising. But after that it gets far more complicated to interpret,” he added.
Neither adherence nor care by a neurologist was different in a consistent direction within the various minority populations, Dr. Mintzer noted. In addition, Black patients were as likely to see a neurologist as White patients but still more likely to be on a first-generation drug.
There are also a few caveats to the findings that should be considered, Dr. Mintzer added. First, the sample included only Medicaid recipients, nearly 35% of whom had a comorbid psychosis. Those and other characteristics of the study pool suggest participants aren’t representative of the United States population as a whole. Second, significant shifts in ASM use have occurred since the study data cutoff in 2014, none of which are reflected in these findings.
“So, I don’t think we can really say how to address this yet,” Dr. Mintzer said. “There’s a lot to explore about whether this is still occurring, how generalizable these findings are, and what they might be due to, as there are a host of potential explanations, which the authors themselves acknowledge.”
The study was funded by the U.S. Centers for Disease Control and Prevention and the National Institute on Minority Health and Health Disparities. Dr. Bensken has received support for this work from NIMHD and serves on the Editorial Board of the journal Neurology. Dr. Sirven and Mintzer report no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM NEUROLOGY CLINICAL PRACTICE
U.S. ketamine poisonings up 81%
Although the overall ketamine exposures were low, researchers say the findings add to a growing body of research that suggests recreational ketamine use may be on the rise.
“Ketamine is by no means the most dangerous drug, but it could be dangerous if combined with drugs such as alcohol or if used in potentially hazardous situations – physically hazardous or socially hazardous,” lead author Joseph Palamar, PhD, associate professor and epidemiologist at New York University Langone Health, New York, told this news organization.
“People who decide to use ketamine recreationally need to be educated about potential risks,” Dr. Palamar said.
The findings were recently published online in the Journal of Psychopharmacology.
More widespread use
Researchers noted that ketamine use has become more widespread in the United States due in part to increasing availability of ketamine in both clinical and nonclinical settings.
Previous work by Dr. Palamar documented an increase in recreational use of ketamine at dance clubs and an increase in ketamine seizures by the Drug Enforcement Administration.
In the current study, investigators analyzed data from the National Poison Control database and included cases reported by 51 of the 55 poison control centers in the United States.
They identified 758 cases involving ketamine exposure between the first quarter of 2019 and the last quarter of 2021 in individuals aged 13 and older, more than half of whom were men.
The number of ketamine exposures increased 81.1% during the study period, rising from 37 to 67 (P = .018).
Nearly 40% of callers reported intentional misuse or abuse of ketamine, while 19.7% involved a suspected suicide or suicide attempt. The ketamine exposure was unintended in 18.9% of cases, and 10.6% of calls involved an adverse drug reaction.
Onep-third of cases involved co-use of other substances, most commonly benzodiazepines, opioids, or alcohol.
The route of administration was ingestion for 44.3%, injection for 18.8%, and inhalation for 17.6%. Another 19.3% involved another route or a combination of routes.
Nearly 20% of cases reported a major adverse effect or death, 42.8% reported a moderate effect, 25.8% a minor effect, and 11.8% no effect. There were seven deaths reported in ketamine-related calls, although Dr. Palamar noted it is unlikely those deaths were due solely to ketamine use.
Researchers didn’t analyze specific harms reported in the calls, but chronic and heavy ketamine use has been previously associated with cognitive impairment, urinary cystitis and other urinary tract issues, and upper gastrointestinal problems.
In addition, using ketamine with gamma-hydroxybutyrate (GHB) or opioids was associated with a significantly higher risk for major adverse effects (P < .001 for both). Injecting ketamine was also linked to a higher prevalence of major adverse effects, although the association did not quite reach significance (P < .05).
Cause for concern
Commenting on the findings, Timothy Wiegand, MD, director of Addiction Toxicology and Toxicology Consult Service and associate professor of emergency medicine at the University of Rochester Medical Center and Strong Memorial Hospital, New York, noted the data on co-use of ketamine with other drugs were cause for concern.
“I think the co-occurring behaviors are critical here with concomitant use of opioids and GHB, intravenous drug use, or that it is used in an attempt to harm one’s self because it allows for identification of these behaviors or use patterns,” said Dr. Wiegand, who was not involved with the research.
He added that it is important for “addiction providers and others in medicine or in the addiction field to be aware of trends” associated with ketamine.
“At the same time, a focus on general prevention, and access to care and treatment, and understanding how to implement harm reduction strategies remain high priorities,” Dr. Wiegand said.
The study was funded by the National Institute on Drug Abuse. Dr. Palamar has reported consulting for Alkermes. Dr. Wiegand has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Although the overall ketamine exposures were low, researchers say the findings add to a growing body of research that suggests recreational ketamine use may be on the rise.
“Ketamine is by no means the most dangerous drug, but it could be dangerous if combined with drugs such as alcohol or if used in potentially hazardous situations – physically hazardous or socially hazardous,” lead author Joseph Palamar, PhD, associate professor and epidemiologist at New York University Langone Health, New York, told this news organization.
“People who decide to use ketamine recreationally need to be educated about potential risks,” Dr. Palamar said.
The findings were recently published online in the Journal of Psychopharmacology.
More widespread use
Researchers noted that ketamine use has become more widespread in the United States due in part to increasing availability of ketamine in both clinical and nonclinical settings.
Previous work by Dr. Palamar documented an increase in recreational use of ketamine at dance clubs and an increase in ketamine seizures by the Drug Enforcement Administration.
In the current study, investigators analyzed data from the National Poison Control database and included cases reported by 51 of the 55 poison control centers in the United States.
They identified 758 cases involving ketamine exposure between the first quarter of 2019 and the last quarter of 2021 in individuals aged 13 and older, more than half of whom were men.
The number of ketamine exposures increased 81.1% during the study period, rising from 37 to 67 (P = .018).
Nearly 40% of callers reported intentional misuse or abuse of ketamine, while 19.7% involved a suspected suicide or suicide attempt. The ketamine exposure was unintended in 18.9% of cases, and 10.6% of calls involved an adverse drug reaction.
Onep-third of cases involved co-use of other substances, most commonly benzodiazepines, opioids, or alcohol.
The route of administration was ingestion for 44.3%, injection for 18.8%, and inhalation for 17.6%. Another 19.3% involved another route or a combination of routes.
Nearly 20% of cases reported a major adverse effect or death, 42.8% reported a moderate effect, 25.8% a minor effect, and 11.8% no effect. There were seven deaths reported in ketamine-related calls, although Dr. Palamar noted it is unlikely those deaths were due solely to ketamine use.
Researchers didn’t analyze specific harms reported in the calls, but chronic and heavy ketamine use has been previously associated with cognitive impairment, urinary cystitis and other urinary tract issues, and upper gastrointestinal problems.
In addition, using ketamine with gamma-hydroxybutyrate (GHB) or opioids was associated with a significantly higher risk for major adverse effects (P < .001 for both). Injecting ketamine was also linked to a higher prevalence of major adverse effects, although the association did not quite reach significance (P < .05).
Cause for concern
Commenting on the findings, Timothy Wiegand, MD, director of Addiction Toxicology and Toxicology Consult Service and associate professor of emergency medicine at the University of Rochester Medical Center and Strong Memorial Hospital, New York, noted the data on co-use of ketamine with other drugs were cause for concern.
“I think the co-occurring behaviors are critical here with concomitant use of opioids and GHB, intravenous drug use, or that it is used in an attempt to harm one’s self because it allows for identification of these behaviors or use patterns,” said Dr. Wiegand, who was not involved with the research.
He added that it is important for “addiction providers and others in medicine or in the addiction field to be aware of trends” associated with ketamine.
“At the same time, a focus on general prevention, and access to care and treatment, and understanding how to implement harm reduction strategies remain high priorities,” Dr. Wiegand said.
The study was funded by the National Institute on Drug Abuse. Dr. Palamar has reported consulting for Alkermes. Dr. Wiegand has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Although the overall ketamine exposures were low, researchers say the findings add to a growing body of research that suggests recreational ketamine use may be on the rise.
“Ketamine is by no means the most dangerous drug, but it could be dangerous if combined with drugs such as alcohol or if used in potentially hazardous situations – physically hazardous or socially hazardous,” lead author Joseph Palamar, PhD, associate professor and epidemiologist at New York University Langone Health, New York, told this news organization.
“People who decide to use ketamine recreationally need to be educated about potential risks,” Dr. Palamar said.
The findings were recently published online in the Journal of Psychopharmacology.
More widespread use
Researchers noted that ketamine use has become more widespread in the United States due in part to increasing availability of ketamine in both clinical and nonclinical settings.
Previous work by Dr. Palamar documented an increase in recreational use of ketamine at dance clubs and an increase in ketamine seizures by the Drug Enforcement Administration.
In the current study, investigators analyzed data from the National Poison Control database and included cases reported by 51 of the 55 poison control centers in the United States.
They identified 758 cases involving ketamine exposure between the first quarter of 2019 and the last quarter of 2021 in individuals aged 13 and older, more than half of whom were men.
The number of ketamine exposures increased 81.1% during the study period, rising from 37 to 67 (P = .018).
Nearly 40% of callers reported intentional misuse or abuse of ketamine, while 19.7% involved a suspected suicide or suicide attempt. The ketamine exposure was unintended in 18.9% of cases, and 10.6% of calls involved an adverse drug reaction.
Onep-third of cases involved co-use of other substances, most commonly benzodiazepines, opioids, or alcohol.
The route of administration was ingestion for 44.3%, injection for 18.8%, and inhalation for 17.6%. Another 19.3% involved another route or a combination of routes.
Nearly 20% of cases reported a major adverse effect or death, 42.8% reported a moderate effect, 25.8% a minor effect, and 11.8% no effect. There were seven deaths reported in ketamine-related calls, although Dr. Palamar noted it is unlikely those deaths were due solely to ketamine use.
Researchers didn’t analyze specific harms reported in the calls, but chronic and heavy ketamine use has been previously associated with cognitive impairment, urinary cystitis and other urinary tract issues, and upper gastrointestinal problems.
In addition, using ketamine with gamma-hydroxybutyrate (GHB) or opioids was associated with a significantly higher risk for major adverse effects (P < .001 for both). Injecting ketamine was also linked to a higher prevalence of major adverse effects, although the association did not quite reach significance (P < .05).
Cause for concern
Commenting on the findings, Timothy Wiegand, MD, director of Addiction Toxicology and Toxicology Consult Service and associate professor of emergency medicine at the University of Rochester Medical Center and Strong Memorial Hospital, New York, noted the data on co-use of ketamine with other drugs were cause for concern.
“I think the co-occurring behaviors are critical here with concomitant use of opioids and GHB, intravenous drug use, or that it is used in an attempt to harm one’s self because it allows for identification of these behaviors or use patterns,” said Dr. Wiegand, who was not involved with the research.
He added that it is important for “addiction providers and others in medicine or in the addiction field to be aware of trends” associated with ketamine.
“At the same time, a focus on general prevention, and access to care and treatment, and understanding how to implement harm reduction strategies remain high priorities,” Dr. Wiegand said.
The study was funded by the National Institute on Drug Abuse. Dr. Palamar has reported consulting for Alkermes. Dr. Wiegand has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF PSYCHOPHARMACOLOGY
Hearing loss strongly tied to increased dementia risk
, new national data show. Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.
“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” said lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore.
The findings were published online in JAMA.
Dose dependent effect
For their study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.
Data from the study was collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.
“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.
Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.
Those with moderate to severe hearing loss were 61% more likely to have dementia than were those with normal hearing (prevalence ratio, 1.61; 95% confidence interval [CI], 1.09-2.38).
Dementia prevalence increased with increasing severity of hearing loss: Normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate to severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).
Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).
Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assisted devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). Similar data were published in JAMA Neurology, suggesting that hearing aids reduce dementia risk.
“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
Robust association
Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.
“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”
Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.
“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.
“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.
The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships. Full disclosures for study authors are included in the original article.
A version of this article first appeared on Medscape.com.
, new national data show. Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.
“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” said lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore.
The findings were published online in JAMA.
Dose dependent effect
For their study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.
Data from the study was collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.
“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.
Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.
Those with moderate to severe hearing loss were 61% more likely to have dementia than were those with normal hearing (prevalence ratio, 1.61; 95% confidence interval [CI], 1.09-2.38).
Dementia prevalence increased with increasing severity of hearing loss: Normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate to severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).
Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).
Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assisted devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). Similar data were published in JAMA Neurology, suggesting that hearing aids reduce dementia risk.
“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
Robust association
Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.
“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”
Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.
“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.
“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.
The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships. Full disclosures for study authors are included in the original article.
A version of this article first appeared on Medscape.com.
, new national data show. Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.
“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” said lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore.
The findings were published online in JAMA.
Dose dependent effect
For their study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.
Data from the study was collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.
“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.
Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.
Those with moderate to severe hearing loss were 61% more likely to have dementia than were those with normal hearing (prevalence ratio, 1.61; 95% confidence interval [CI], 1.09-2.38).
Dementia prevalence increased with increasing severity of hearing loss: Normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate to severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).
Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).
Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assisted devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). Similar data were published in JAMA Neurology, suggesting that hearing aids reduce dementia risk.
“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
Robust association
Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.
“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”
Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.
“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.
“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.
The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships. Full disclosures for study authors are included in the original article.
A version of this article first appeared on Medscape.com.
Hearing loss strongly tied to increased dementia risk
Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.
“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore, Md., told this news organization.
The findings were published online in JAMA.
Dose-dependent effect
For the study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.
Data from the study were collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.
“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.
Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.
Those with moderate to severe hearing loss were 61% more likely to have dementia than those with normal hearing (prevalence ratio, 1.61; 95% confidence interval, 1.09-2.38).
Dementia prevalence increased with increasing severity of hearing loss: normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate/severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).
Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).
Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assistive devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). This news organization last month reported on similar data published in JAMA Neurology suggesting that hearing aids reduce dementia risk.
“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
Robust association
Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.
“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”
Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.
“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.
“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.
The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.
“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore, Md., told this news organization.
The findings were published online in JAMA.
Dose-dependent effect
For the study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.
Data from the study were collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.
“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.
Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.
Those with moderate to severe hearing loss were 61% more likely to have dementia than those with normal hearing (prevalence ratio, 1.61; 95% confidence interval, 1.09-2.38).
Dementia prevalence increased with increasing severity of hearing loss: normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate/severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).
Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).
Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assistive devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). This news organization last month reported on similar data published in JAMA Neurology suggesting that hearing aids reduce dementia risk.
“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
Robust association
Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.
“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”
Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.
“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.
“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.
The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.
“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore, Md., told this news organization.
The findings were published online in JAMA.
Dose-dependent effect
For the study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.
Data from the study were collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.
“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.
Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.
Those with moderate to severe hearing loss were 61% more likely to have dementia than those with normal hearing (prevalence ratio, 1.61; 95% confidence interval, 1.09-2.38).
Dementia prevalence increased with increasing severity of hearing loss: normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate/severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).
Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).
Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assistive devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). This news organization last month reported on similar data published in JAMA Neurology suggesting that hearing aids reduce dementia risk.
“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
Robust association
Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.
“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”
Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.
“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.
“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.
The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA