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Chronic opioid use linked to low testosterone levels
NEW ORLEANS – About two thirds of men who chronically use opioids have low testosterone levels, based on a literature search of more than 50 randomized and observational studies that examined endocrine function in patients on chronic opioid therapy.
Hypocortisolism, seen in about 20% of the men in these studies, was among the other potentially significant deficiencies in endocrine function, Amir H. Zamanipoor Najafabadi, PhD, reported at the annual meeting of the Endocrine Society.
Dr. Najafabadi of Leiden University in the Netherlands, and Friso de Vries, PhD, analyzed the link between opioid use and changes in the gonadal axis. Most of the subjects in their study were men (J Endocr Soc. 2019. doi. 10.1210/js.2019-SUN-489).
While the data do not support firm conclusions on the health consequences of these endocrine observations, Dr. Najafabadi said that a prospective trial is needed to determine whether there is a potential benefit from screening patients on chronic opioids for potentially treatable endocrine deficiencies.
NEW ORLEANS – About two thirds of men who chronically use opioids have low testosterone levels, based on a literature search of more than 50 randomized and observational studies that examined endocrine function in patients on chronic opioid therapy.
Hypocortisolism, seen in about 20% of the men in these studies, was among the other potentially significant deficiencies in endocrine function, Amir H. Zamanipoor Najafabadi, PhD, reported at the annual meeting of the Endocrine Society.
Dr. Najafabadi of Leiden University in the Netherlands, and Friso de Vries, PhD, analyzed the link between opioid use and changes in the gonadal axis. Most of the subjects in their study were men (J Endocr Soc. 2019. doi. 10.1210/js.2019-SUN-489).
While the data do not support firm conclusions on the health consequences of these endocrine observations, Dr. Najafabadi said that a prospective trial is needed to determine whether there is a potential benefit from screening patients on chronic opioids for potentially treatable endocrine deficiencies.
NEW ORLEANS – About two thirds of men who chronically use opioids have low testosterone levels, based on a literature search of more than 50 randomized and observational studies that examined endocrine function in patients on chronic opioid therapy.
Hypocortisolism, seen in about 20% of the men in these studies, was among the other potentially significant deficiencies in endocrine function, Amir H. Zamanipoor Najafabadi, PhD, reported at the annual meeting of the Endocrine Society.
Dr. Najafabadi of Leiden University in the Netherlands, and Friso de Vries, PhD, analyzed the link between opioid use and changes in the gonadal axis. Most of the subjects in their study were men (J Endocr Soc. 2019. doi. 10.1210/js.2019-SUN-489).
While the data do not support firm conclusions on the health consequences of these endocrine observations, Dr. Najafabadi said that a prospective trial is needed to determine whether there is a potential benefit from screening patients on chronic opioids for potentially treatable endocrine deficiencies.
REPORTING FROM ENDO 2019
Smoking rates remain steady among the poor
While an increasing number of U.S. citizens are saying no to cigarettes, a recent study shows.
The odds of current smoking, versus never smoking, declined significantly during 2008-2017 for individuals with none of six disadvantages tied to cigarette use, including disability, unemployment, poverty, low education, psychological distress, and heavy alcohol intake, according to researchers.
Individuals with one or two of those disadvantages have also been cutting back, the data suggest. But, by contrast, odds of current versus never smoking did not significantly change for those with three or more disadvantages, according to Adam M. Leventhal, PhD, of the University of Southern California, Los Angeles, and coinvestigators.
“How this pattern can inform a cohesive policy agenda is unknown, but it is clear from these findings that the crux of the recently expanding tobacco-related health disparity problem in the United States is not tied to groups facing merely a single form of disadvantage,” Dr. Leventhal and coauthors wrote in a report on the study in JAMA Internal Medicine.
The cross-sectional analysis by Dr. Leventhal and colleagues was based on National Health Interview Survey (NHIS) data from 2008-2017 including more than 278,000 respondents aged 25 years or older.
A snapshot of that 10-year period showed that current smoking prevalence was successively higher depending on the number of socioeconomic or health-related disadvantages.
The mean prevalence of current smoking over that entire time period was just 13.8% for people with zero of the six disadvantages, 21.4% for those with one disadvantage, and so on, up to 58.2% for those with all six disadvantages, according to data in the published report.
Encouragingly, overall smoking prevalence fell from 20.8% in 2008-2009 to 15.8% in 2016-2017, the researchers found. However, the decreasing trend was not apparent for individuals with many disadvantages.
The odds ratio for change in odds of smoking per year was 0.951 (95% confidence interval, 0.944-0.958) for those with zero disadvantages, 0.96 (95% CI, 0.95-0.97) for one disadvantage, and 0.98 (95% CI, 0.97-0.99) for two, all representing significant annual reductions in current versus never smoking, investigators said. By contrast, no such significant changes were apparent for those with three, four, five, or six such disadvantages.
Tobacco control or regulatory policies that consider these disadvantages separately may be overlooking a “broader pattern” showing that the cumulative number of disadvantages correlates with the magnitude of disparity, wrote Dr. Leventhal and colleagues in their report.
“Successful prevention of smoking initiation and promotion of smoking cessation in multi-disadvantaged populations would substantially reduce the smoking-related public health burden in the United States,” they concluded.
Dr. Leventhal and colleagues reported no conflicts related to their research, which was supported in part by a Tobacco Centers of Regulatory Science award from the National Cancer Institute and the Food and Drug Administration, among other sources.
SOURCE: Leventhal AM et al. JAMA Intern Med. 2019 Apr 22. doi: 10.1001/jamainternmed.2019.0192.
While an increasing number of U.S. citizens are saying no to cigarettes, a recent study shows.
The odds of current smoking, versus never smoking, declined significantly during 2008-2017 for individuals with none of six disadvantages tied to cigarette use, including disability, unemployment, poverty, low education, psychological distress, and heavy alcohol intake, according to researchers.
Individuals with one or two of those disadvantages have also been cutting back, the data suggest. But, by contrast, odds of current versus never smoking did not significantly change for those with three or more disadvantages, according to Adam M. Leventhal, PhD, of the University of Southern California, Los Angeles, and coinvestigators.
“How this pattern can inform a cohesive policy agenda is unknown, but it is clear from these findings that the crux of the recently expanding tobacco-related health disparity problem in the United States is not tied to groups facing merely a single form of disadvantage,” Dr. Leventhal and coauthors wrote in a report on the study in JAMA Internal Medicine.
The cross-sectional analysis by Dr. Leventhal and colleagues was based on National Health Interview Survey (NHIS) data from 2008-2017 including more than 278,000 respondents aged 25 years or older.
A snapshot of that 10-year period showed that current smoking prevalence was successively higher depending on the number of socioeconomic or health-related disadvantages.
The mean prevalence of current smoking over that entire time period was just 13.8% for people with zero of the six disadvantages, 21.4% for those with one disadvantage, and so on, up to 58.2% for those with all six disadvantages, according to data in the published report.
Encouragingly, overall smoking prevalence fell from 20.8% in 2008-2009 to 15.8% in 2016-2017, the researchers found. However, the decreasing trend was not apparent for individuals with many disadvantages.
The odds ratio for change in odds of smoking per year was 0.951 (95% confidence interval, 0.944-0.958) for those with zero disadvantages, 0.96 (95% CI, 0.95-0.97) for one disadvantage, and 0.98 (95% CI, 0.97-0.99) for two, all representing significant annual reductions in current versus never smoking, investigators said. By contrast, no such significant changes were apparent for those with three, four, five, or six such disadvantages.
Tobacco control or regulatory policies that consider these disadvantages separately may be overlooking a “broader pattern” showing that the cumulative number of disadvantages correlates with the magnitude of disparity, wrote Dr. Leventhal and colleagues in their report.
“Successful prevention of smoking initiation and promotion of smoking cessation in multi-disadvantaged populations would substantially reduce the smoking-related public health burden in the United States,” they concluded.
Dr. Leventhal and colleagues reported no conflicts related to their research, which was supported in part by a Tobacco Centers of Regulatory Science award from the National Cancer Institute and the Food and Drug Administration, among other sources.
SOURCE: Leventhal AM et al. JAMA Intern Med. 2019 Apr 22. doi: 10.1001/jamainternmed.2019.0192.
While an increasing number of U.S. citizens are saying no to cigarettes, a recent study shows.
The odds of current smoking, versus never smoking, declined significantly during 2008-2017 for individuals with none of six disadvantages tied to cigarette use, including disability, unemployment, poverty, low education, psychological distress, and heavy alcohol intake, according to researchers.
Individuals with one or two of those disadvantages have also been cutting back, the data suggest. But, by contrast, odds of current versus never smoking did not significantly change for those with three or more disadvantages, according to Adam M. Leventhal, PhD, of the University of Southern California, Los Angeles, and coinvestigators.
“How this pattern can inform a cohesive policy agenda is unknown, but it is clear from these findings that the crux of the recently expanding tobacco-related health disparity problem in the United States is not tied to groups facing merely a single form of disadvantage,” Dr. Leventhal and coauthors wrote in a report on the study in JAMA Internal Medicine.
The cross-sectional analysis by Dr. Leventhal and colleagues was based on National Health Interview Survey (NHIS) data from 2008-2017 including more than 278,000 respondents aged 25 years or older.
A snapshot of that 10-year period showed that current smoking prevalence was successively higher depending on the number of socioeconomic or health-related disadvantages.
The mean prevalence of current smoking over that entire time period was just 13.8% for people with zero of the six disadvantages, 21.4% for those with one disadvantage, and so on, up to 58.2% for those with all six disadvantages, according to data in the published report.
Encouragingly, overall smoking prevalence fell from 20.8% in 2008-2009 to 15.8% in 2016-2017, the researchers found. However, the decreasing trend was not apparent for individuals with many disadvantages.
The odds ratio for change in odds of smoking per year was 0.951 (95% confidence interval, 0.944-0.958) for those with zero disadvantages, 0.96 (95% CI, 0.95-0.97) for one disadvantage, and 0.98 (95% CI, 0.97-0.99) for two, all representing significant annual reductions in current versus never smoking, investigators said. By contrast, no such significant changes were apparent for those with three, four, five, or six such disadvantages.
Tobacco control or regulatory policies that consider these disadvantages separately may be overlooking a “broader pattern” showing that the cumulative number of disadvantages correlates with the magnitude of disparity, wrote Dr. Leventhal and colleagues in their report.
“Successful prevention of smoking initiation and promotion of smoking cessation in multi-disadvantaged populations would substantially reduce the smoking-related public health burden in the United States,” they concluded.
Dr. Leventhal and colleagues reported no conflicts related to their research, which was supported in part by a Tobacco Centers of Regulatory Science award from the National Cancer Institute and the Food and Drug Administration, among other sources.
SOURCE: Leventhal AM et al. JAMA Intern Med. 2019 Apr 22. doi: 10.1001/jamainternmed.2019.0192.
FROM JAMA INTERNAL MEDICINE
Key clinical point: Current U.S. smoking rates have not declined among individuals with multiple socioeconomic or health-related disadvantages.
Major finding: The odds ratio for change in odds of smoking per year was 0.951 for individuals with zero disadvantages, 0.96 for one disadvantage, and 0.97-0.99 for two, with no significant annual reductions in those with three or more disadvantages.
Study details: Cross-sectional analysis of 278,048 respondents aged 25 years or older in the National Health Interview Survey during 2008-2017.
Disclosures: Authors reported no conflicts of interest related to the study, which was supported in part by a Tobacco Centers of Regulatory Science award from the National Cancer Institute and the Food and Drug Administration, among other sources.
Source: Leventhal AM et al. JAMA Intern Med. 2019 Apr 22. doi: 10.1001/jamainternmed.2019.0192.
More than 40% of U.K. physicians report binge drinking
Many doctors say they cope with job-related stress by drinking alcohol or taking drugs
Occupational distress among physicians is tied to increased odds of substance use, sleep disturbance, binge eating, and poor health in general, a cross-sectional study of 417 U.K. doctors shows.
Burned-out or depressed doctors had higher risks of those health problems regardless of whether or not they worked in a hospital setting, according to Asta Medisauskaite, PhD, of University College London and Caroline Kamau, PhD, of the University of London. The study was published in BMJ Open.
The investigators asked the participants to answer a battery of validated questionnaires online, including the Alcohol Use Disorders Identification Test, the Eating Disorder Diagnostic Scale, and the Insomnia Severity Index.
The odds of many health problems were increased among the physicians with emotional exhaustion, as indicated by the Maslach Burnout Inventory, as was also the case with psychiatric disorders, according to the General Health Questionnaire-12, which investigators noted has been used extensively to examine medical doctors and other working populations.
Sleep disturbances were, for example, more likely in physicians with burnout or psychiatric morbidity, with odds ratios ranging from 1.344 to 3.826, the investigators reported. Likewise, these indicators of occupational distress increased the risk of suffering from frequent poor health, with odds ratios from 1.050 to 3.544, and of binge eating, with odds ratios from 1.311 to 1.841, Dr. Medisauskaite and Dr. Kamau reported.
Distressed doctors more often used alcohol, according to the researchers, who said that they found a higher risk of alcohol dependence (odds ratio, 6.165) among physicians reporting that they used substances to feel better or cope with stress. Those doctors also had higher risk of binge drinking, drinking larger quantities, and using alcohol more often, the data show. In fact, 44% of the physicians reported binge drinking, and 5% met the criteria for alcohol dependence, Dr. Medisauskaite and Dr. Kamau wrote. Binge drinking was defined as consuming more than six drinks on a single occasion.
Previous studies have indicated that occupational distress among physicians has negative effects on quality of care and patient safety, the authors noted. This latest cross-sectional study builds on those findings by showing that occupational distress increases risk of health problems among doctors. “The impact of occupational distress or ill health could increase levels of sickness-absence among doctors, thus reducing patient safety because of understaffing,” Dr. Medisauskaite and Dr. Kamau wrote.
Similarly, physicians with sleep problems or substance use related to occupational distress could perform poorly on the job because of being groggy, intoxicated, or hung over, they said.
“We recommend that doctors’ mentors, supervisors, peers, and occupational health support services recognize and act on (1) the prevalence of occupational distress and health problems among doctors; (2) the possibility that occupational distress raises the risk of several health problems; and (3) the need to provide early interventions,” Dr. Medisauskaite and Dr. Kamau wrote. Such interventions could help prevent physicians who are experiencing occupational distress from suffering the long-term health effects from sleep disturbances, binge drinking and binge eating, and ill health, they suggested.
One limitation cited was the study’s cross-sectional design, which makes it impossible to draw conclusions about causation. The researchers also conceded that some participants might not have been comfortable answering questions about illicit use of drugs or alcohol. Nevertheless, they said,
Dr. Medisauskaite and Dr. Kamau declared no competing interests related to the study.
SOURCE: Medisauskaite A, Kamau C. BMJ Open. 2019 May 15. doi: 10.1136/bmjopen-2018-027362.
Many doctors say they cope with job-related stress by drinking alcohol or taking drugs
Many doctors say they cope with job-related stress by drinking alcohol or taking drugs
Occupational distress among physicians is tied to increased odds of substance use, sleep disturbance, binge eating, and poor health in general, a cross-sectional study of 417 U.K. doctors shows.
Burned-out or depressed doctors had higher risks of those health problems regardless of whether or not they worked in a hospital setting, according to Asta Medisauskaite, PhD, of University College London and Caroline Kamau, PhD, of the University of London. The study was published in BMJ Open.
The investigators asked the participants to answer a battery of validated questionnaires online, including the Alcohol Use Disorders Identification Test, the Eating Disorder Diagnostic Scale, and the Insomnia Severity Index.
The odds of many health problems were increased among the physicians with emotional exhaustion, as indicated by the Maslach Burnout Inventory, as was also the case with psychiatric disorders, according to the General Health Questionnaire-12, which investigators noted has been used extensively to examine medical doctors and other working populations.
Sleep disturbances were, for example, more likely in physicians with burnout or psychiatric morbidity, with odds ratios ranging from 1.344 to 3.826, the investigators reported. Likewise, these indicators of occupational distress increased the risk of suffering from frequent poor health, with odds ratios from 1.050 to 3.544, and of binge eating, with odds ratios from 1.311 to 1.841, Dr. Medisauskaite and Dr. Kamau reported.
Distressed doctors more often used alcohol, according to the researchers, who said that they found a higher risk of alcohol dependence (odds ratio, 6.165) among physicians reporting that they used substances to feel better or cope with stress. Those doctors also had higher risk of binge drinking, drinking larger quantities, and using alcohol more often, the data show. In fact, 44% of the physicians reported binge drinking, and 5% met the criteria for alcohol dependence, Dr. Medisauskaite and Dr. Kamau wrote. Binge drinking was defined as consuming more than six drinks on a single occasion.
Previous studies have indicated that occupational distress among physicians has negative effects on quality of care and patient safety, the authors noted. This latest cross-sectional study builds on those findings by showing that occupational distress increases risk of health problems among doctors. “The impact of occupational distress or ill health could increase levels of sickness-absence among doctors, thus reducing patient safety because of understaffing,” Dr. Medisauskaite and Dr. Kamau wrote.
Similarly, physicians with sleep problems or substance use related to occupational distress could perform poorly on the job because of being groggy, intoxicated, or hung over, they said.
“We recommend that doctors’ mentors, supervisors, peers, and occupational health support services recognize and act on (1) the prevalence of occupational distress and health problems among doctors; (2) the possibility that occupational distress raises the risk of several health problems; and (3) the need to provide early interventions,” Dr. Medisauskaite and Dr. Kamau wrote. Such interventions could help prevent physicians who are experiencing occupational distress from suffering the long-term health effects from sleep disturbances, binge drinking and binge eating, and ill health, they suggested.
One limitation cited was the study’s cross-sectional design, which makes it impossible to draw conclusions about causation. The researchers also conceded that some participants might not have been comfortable answering questions about illicit use of drugs or alcohol. Nevertheless, they said,
Dr. Medisauskaite and Dr. Kamau declared no competing interests related to the study.
SOURCE: Medisauskaite A, Kamau C. BMJ Open. 2019 May 15. doi: 10.1136/bmjopen-2018-027362.
Occupational distress among physicians is tied to increased odds of substance use, sleep disturbance, binge eating, and poor health in general, a cross-sectional study of 417 U.K. doctors shows.
Burned-out or depressed doctors had higher risks of those health problems regardless of whether or not they worked in a hospital setting, according to Asta Medisauskaite, PhD, of University College London and Caroline Kamau, PhD, of the University of London. The study was published in BMJ Open.
The investigators asked the participants to answer a battery of validated questionnaires online, including the Alcohol Use Disorders Identification Test, the Eating Disorder Diagnostic Scale, and the Insomnia Severity Index.
The odds of many health problems were increased among the physicians with emotional exhaustion, as indicated by the Maslach Burnout Inventory, as was also the case with psychiatric disorders, according to the General Health Questionnaire-12, which investigators noted has been used extensively to examine medical doctors and other working populations.
Sleep disturbances were, for example, more likely in physicians with burnout or psychiatric morbidity, with odds ratios ranging from 1.344 to 3.826, the investigators reported. Likewise, these indicators of occupational distress increased the risk of suffering from frequent poor health, with odds ratios from 1.050 to 3.544, and of binge eating, with odds ratios from 1.311 to 1.841, Dr. Medisauskaite and Dr. Kamau reported.
Distressed doctors more often used alcohol, according to the researchers, who said that they found a higher risk of alcohol dependence (odds ratio, 6.165) among physicians reporting that they used substances to feel better or cope with stress. Those doctors also had higher risk of binge drinking, drinking larger quantities, and using alcohol more often, the data show. In fact, 44% of the physicians reported binge drinking, and 5% met the criteria for alcohol dependence, Dr. Medisauskaite and Dr. Kamau wrote. Binge drinking was defined as consuming more than six drinks on a single occasion.
Previous studies have indicated that occupational distress among physicians has negative effects on quality of care and patient safety, the authors noted. This latest cross-sectional study builds on those findings by showing that occupational distress increases risk of health problems among doctors. “The impact of occupational distress or ill health could increase levels of sickness-absence among doctors, thus reducing patient safety because of understaffing,” Dr. Medisauskaite and Dr. Kamau wrote.
Similarly, physicians with sleep problems or substance use related to occupational distress could perform poorly on the job because of being groggy, intoxicated, or hung over, they said.
“We recommend that doctors’ mentors, supervisors, peers, and occupational health support services recognize and act on (1) the prevalence of occupational distress and health problems among doctors; (2) the possibility that occupational distress raises the risk of several health problems; and (3) the need to provide early interventions,” Dr. Medisauskaite and Dr. Kamau wrote. Such interventions could help prevent physicians who are experiencing occupational distress from suffering the long-term health effects from sleep disturbances, binge drinking and binge eating, and ill health, they suggested.
One limitation cited was the study’s cross-sectional design, which makes it impossible to draw conclusions about causation. The researchers also conceded that some participants might not have been comfortable answering questions about illicit use of drugs or alcohol. Nevertheless, they said,
Dr. Medisauskaite and Dr. Kamau declared no competing interests related to the study.
SOURCE: Medisauskaite A, Kamau C. BMJ Open. 2019 May 15. doi: 10.1136/bmjopen-2018-027362.
FROM BMJ OPEN
Key clinical point: Occupational distress increased the odds of substance use, sleep disturbance, binge eating, and poor health among medical doctors in the United Kingdom.
Major finding: Distressed medical doctors had a higher risk of binge drinking. In fact, 44% reported binge drinking, defined as consuming more than six drinks on a single occasion.
Study details: A U.K. cross-sectional study of 417 doctors who answered a series of validated health-related questionnaires online.
Disclosures: The authors declared no competing interests related to the study.
Source: Medisauskaite A, Kamau C. BMJ Open. 2019 May 15. doi: 10.1136/bmjopen-2018-027362.
Racial, economic disparities found in buprenorphine prescriptions
Buprenorphine for opioid use disorder is much less likely to be prescribed to patients who are black or who do not have health insurance, an analysis of two national surveys shows.
Researchers analyzed data from the National Ambulatory Medical Care Survey and the National Hospital Ambulatory Medical Care Survey from 2004 to 2015, including 13.4 million visits in which buprenorphine was prescribed. The analysis was published as a research letter in JAMA Psychiatry.
From 2012 to 2015, the number of ambulatory visits involving buprenorphine rose from 0.04% to 0.36%. Black patients were 77% less likely to receive a prescription for buprenorphine at their visit – even after adjustment for payment method, sex, and age – while the number of prescription received by white patients was considerably higher than for patients of any other ethnicity, wrote Pooja A. Lagisetty, MD, and coauthors.
, and the age group with the highest incidence of buprenorphine prescriptions was 30-50 years.
Self-pay and private health insurance were the most common payment methods, but the number of self-paying patients receiving buprenorphine prescriptions dramatically increased from 585,568 in 2004-2007 to 5.3 million in 2012-2015.
“This finding in nationally representative data builds on a previous study that reported buprenorphine treatment disparities on the basis of race/ethnicity and income in New York City,” said Dr. Lagisetty of the department of medicine at the University of Michigan, Ann Arbor, and coauthors.
However, they acknowledged that it was unclear whether the treatment disparity might in fact reflect a difference in the prevalence of opioid use disorder across ethnicities.
Commenting on the differences in payment methods, the authors noted that, despite the enactment of mental health parity legislation and the expansion of Medicaid, the proportion of self-pay visits remained relatively unchanged across the study period.
“A recent study demonstrated that half of the physicians prescribing buprenorphine in Ohio accepted cash alone, and our findings suggest that this practice may be widespread and may be associated with additional financial barriers for low-income populations,” the researchers wrote. “With rising rates of opioid overdoses, it is imperative that policy and research efforts specifically address racial/ethnic and economic differences in treatment access and engagement.”
No conflicts of interest were declared.
SOURCE: Lagisetty P et al. JAMA Psychiatry. 2019 May 8. doi: 10.1001/jamapsychiatry.2019.0876.
Buprenorphine for opioid use disorder is much less likely to be prescribed to patients who are black or who do not have health insurance, an analysis of two national surveys shows.
Researchers analyzed data from the National Ambulatory Medical Care Survey and the National Hospital Ambulatory Medical Care Survey from 2004 to 2015, including 13.4 million visits in which buprenorphine was prescribed. The analysis was published as a research letter in JAMA Psychiatry.
From 2012 to 2015, the number of ambulatory visits involving buprenorphine rose from 0.04% to 0.36%. Black patients were 77% less likely to receive a prescription for buprenorphine at their visit – even after adjustment for payment method, sex, and age – while the number of prescription received by white patients was considerably higher than for patients of any other ethnicity, wrote Pooja A. Lagisetty, MD, and coauthors.
, and the age group with the highest incidence of buprenorphine prescriptions was 30-50 years.
Self-pay and private health insurance were the most common payment methods, but the number of self-paying patients receiving buprenorphine prescriptions dramatically increased from 585,568 in 2004-2007 to 5.3 million in 2012-2015.
“This finding in nationally representative data builds on a previous study that reported buprenorphine treatment disparities on the basis of race/ethnicity and income in New York City,” said Dr. Lagisetty of the department of medicine at the University of Michigan, Ann Arbor, and coauthors.
However, they acknowledged that it was unclear whether the treatment disparity might in fact reflect a difference in the prevalence of opioid use disorder across ethnicities.
Commenting on the differences in payment methods, the authors noted that, despite the enactment of mental health parity legislation and the expansion of Medicaid, the proportion of self-pay visits remained relatively unchanged across the study period.
“A recent study demonstrated that half of the physicians prescribing buprenorphine in Ohio accepted cash alone, and our findings suggest that this practice may be widespread and may be associated with additional financial barriers for low-income populations,” the researchers wrote. “With rising rates of opioid overdoses, it is imperative that policy and research efforts specifically address racial/ethnic and economic differences in treatment access and engagement.”
No conflicts of interest were declared.
SOURCE: Lagisetty P et al. JAMA Psychiatry. 2019 May 8. doi: 10.1001/jamapsychiatry.2019.0876.
Buprenorphine for opioid use disorder is much less likely to be prescribed to patients who are black or who do not have health insurance, an analysis of two national surveys shows.
Researchers analyzed data from the National Ambulatory Medical Care Survey and the National Hospital Ambulatory Medical Care Survey from 2004 to 2015, including 13.4 million visits in which buprenorphine was prescribed. The analysis was published as a research letter in JAMA Psychiatry.
From 2012 to 2015, the number of ambulatory visits involving buprenorphine rose from 0.04% to 0.36%. Black patients were 77% less likely to receive a prescription for buprenorphine at their visit – even after adjustment for payment method, sex, and age – while the number of prescription received by white patients was considerably higher than for patients of any other ethnicity, wrote Pooja A. Lagisetty, MD, and coauthors.
, and the age group with the highest incidence of buprenorphine prescriptions was 30-50 years.
Self-pay and private health insurance were the most common payment methods, but the number of self-paying patients receiving buprenorphine prescriptions dramatically increased from 585,568 in 2004-2007 to 5.3 million in 2012-2015.
“This finding in nationally representative data builds on a previous study that reported buprenorphine treatment disparities on the basis of race/ethnicity and income in New York City,” said Dr. Lagisetty of the department of medicine at the University of Michigan, Ann Arbor, and coauthors.
However, they acknowledged that it was unclear whether the treatment disparity might in fact reflect a difference in the prevalence of opioid use disorder across ethnicities.
Commenting on the differences in payment methods, the authors noted that, despite the enactment of mental health parity legislation and the expansion of Medicaid, the proportion of self-pay visits remained relatively unchanged across the study period.
“A recent study demonstrated that half of the physicians prescribing buprenorphine in Ohio accepted cash alone, and our findings suggest that this practice may be widespread and may be associated with additional financial barriers for low-income populations,” the researchers wrote. “With rising rates of opioid overdoses, it is imperative that policy and research efforts specifically address racial/ethnic and economic differences in treatment access and engagement.”
No conflicts of interest were declared.
SOURCE: Lagisetty P et al. JAMA Psychiatry. 2019 May 8. doi: 10.1001/jamapsychiatry.2019.0876.
FROM JAMA PSYCHIATRY
Overdoses are driving down life expectancy
The average life expectancy in the United States declined from 78.9 years in 2014 to 78.6 years in 2017.1 The 2017 figure—78.6 years—means life expectancy is shorter in the United States than in other countries.1 The decline is due, in part, to the drug overdose epidemic in the United States.2 In 2017, 70,237 people died by drug overdose2—with prescription drugs, heroin, and opioids (especially fentanyl) being the major threats.3 From 2016 to 2017, overdoses from synthetic opioids, such as fentanyl, fentanyl analogs, and tramadol, increased from 6.2 to 9 per 100,000 people.2
These statistics should motivate all health care professionals to improve the general public’s health metrics, especially when treating patients with substance use disorders. But to best do so, we need a collaborative effort across many professions—not just health care providers, but also public health officials, elected government leaders, and law enforcement. To better define what this would entail, we suggest ways in which these groups could expand their roles to help reduce overdose deaths.
Health care professionals:
- implement safer opioid prescribing for patients who have chronic pain;
- educate patients about the risks of opioid use;
- consider alternative therapies for pain management; and
- utilize electronic databases to monitor controlled substance prescribing.
Public health officials:
- expand naloxone distribution; and
- enhance harm reduction (eg, syringe exchange programs, substance abuse treatment options).
Government leaders:
- draft legislation that allows the use of better interventions for treating individuals with drug dependence or those who overdose; and
- improve criminal justice approaches so that laws are less punitive and more therapeutic for individuals who suffer from drug dependence.
Law enforcement:
- supply naltrexone kits to first responders and provide appropriate training.
Kuldeep Ghosh, MD, MS
Rajashekhar Yeruva, MD
Steven Lippmann, MD
Louisville, Ky
1. National Center for Health Statistics. Table 15. Life expectancy at birth, at age 65, and at age 75, by sex, race, and Hispanic origin: United States, selected years 1900-2015. Centers for Disease Control and Prevention. https://www.cdc.gov/nchs/data/hus/2016/015.pdf. Published 2016. Accessed April 24, 2019.
2. Hedegaard H, Miniño AM, Warner M. Drug overdose deaths in the United States, 1999-2017. NCHS Data Brief No 329. National Center for Health Statistics. https://www.cdc.gov/nchs/products/databriefs/db294.htm. Published November 2019. Accessed April 24, 2019.
3. United States Drug Enforcement Administration. DEA releases 2018 National Drug Threat Assessment. https://www.dea.gov/press-releases/2018/11/02/dea-releases-2018-national-drug-threat-assessment-0. Published November 2, 2018. Accessed April 24, 2019.
The average life expectancy in the United States declined from 78.9 years in 2014 to 78.6 years in 2017.1 The 2017 figure—78.6 years—means life expectancy is shorter in the United States than in other countries.1 The decline is due, in part, to the drug overdose epidemic in the United States.2 In 2017, 70,237 people died by drug overdose2—with prescription drugs, heroin, and opioids (especially fentanyl) being the major threats.3 From 2016 to 2017, overdoses from synthetic opioids, such as fentanyl, fentanyl analogs, and tramadol, increased from 6.2 to 9 per 100,000 people.2
These statistics should motivate all health care professionals to improve the general public’s health metrics, especially when treating patients with substance use disorders. But to best do so, we need a collaborative effort across many professions—not just health care providers, but also public health officials, elected government leaders, and law enforcement. To better define what this would entail, we suggest ways in which these groups could expand their roles to help reduce overdose deaths.
Health care professionals:
- implement safer opioid prescribing for patients who have chronic pain;
- educate patients about the risks of opioid use;
- consider alternative therapies for pain management; and
- utilize electronic databases to monitor controlled substance prescribing.
Public health officials:
- expand naloxone distribution; and
- enhance harm reduction (eg, syringe exchange programs, substance abuse treatment options).
Government leaders:
- draft legislation that allows the use of better interventions for treating individuals with drug dependence or those who overdose; and
- improve criminal justice approaches so that laws are less punitive and more therapeutic for individuals who suffer from drug dependence.
Law enforcement:
- supply naltrexone kits to first responders and provide appropriate training.
Kuldeep Ghosh, MD, MS
Rajashekhar Yeruva, MD
Steven Lippmann, MD
Louisville, Ky
The average life expectancy in the United States declined from 78.9 years in 2014 to 78.6 years in 2017.1 The 2017 figure—78.6 years—means life expectancy is shorter in the United States than in other countries.1 The decline is due, in part, to the drug overdose epidemic in the United States.2 In 2017, 70,237 people died by drug overdose2—with prescription drugs, heroin, and opioids (especially fentanyl) being the major threats.3 From 2016 to 2017, overdoses from synthetic opioids, such as fentanyl, fentanyl analogs, and tramadol, increased from 6.2 to 9 per 100,000 people.2
These statistics should motivate all health care professionals to improve the general public’s health metrics, especially when treating patients with substance use disorders. But to best do so, we need a collaborative effort across many professions—not just health care providers, but also public health officials, elected government leaders, and law enforcement. To better define what this would entail, we suggest ways in which these groups could expand their roles to help reduce overdose deaths.
Health care professionals:
- implement safer opioid prescribing for patients who have chronic pain;
- educate patients about the risks of opioid use;
- consider alternative therapies for pain management; and
- utilize electronic databases to monitor controlled substance prescribing.
Public health officials:
- expand naloxone distribution; and
- enhance harm reduction (eg, syringe exchange programs, substance abuse treatment options).
Government leaders:
- draft legislation that allows the use of better interventions for treating individuals with drug dependence or those who overdose; and
- improve criminal justice approaches so that laws are less punitive and more therapeutic for individuals who suffer from drug dependence.
Law enforcement:
- supply naltrexone kits to first responders and provide appropriate training.
Kuldeep Ghosh, MD, MS
Rajashekhar Yeruva, MD
Steven Lippmann, MD
Louisville, Ky
1. National Center for Health Statistics. Table 15. Life expectancy at birth, at age 65, and at age 75, by sex, race, and Hispanic origin: United States, selected years 1900-2015. Centers for Disease Control and Prevention. https://www.cdc.gov/nchs/data/hus/2016/015.pdf. Published 2016. Accessed April 24, 2019.
2. Hedegaard H, Miniño AM, Warner M. Drug overdose deaths in the United States, 1999-2017. NCHS Data Brief No 329. National Center for Health Statistics. https://www.cdc.gov/nchs/products/databriefs/db294.htm. Published November 2019. Accessed April 24, 2019.
3. United States Drug Enforcement Administration. DEA releases 2018 National Drug Threat Assessment. https://www.dea.gov/press-releases/2018/11/02/dea-releases-2018-national-drug-threat-assessment-0. Published November 2, 2018. Accessed April 24, 2019.
1. National Center for Health Statistics. Table 15. Life expectancy at birth, at age 65, and at age 75, by sex, race, and Hispanic origin: United States, selected years 1900-2015. Centers for Disease Control and Prevention. https://www.cdc.gov/nchs/data/hus/2016/015.pdf. Published 2016. Accessed April 24, 2019.
2. Hedegaard H, Miniño AM, Warner M. Drug overdose deaths in the United States, 1999-2017. NCHS Data Brief No 329. National Center for Health Statistics. https://www.cdc.gov/nchs/products/databriefs/db294.htm. Published November 2019. Accessed April 24, 2019.
3. United States Drug Enforcement Administration. DEA releases 2018 National Drug Threat Assessment. https://www.dea.gov/press-releases/2018/11/02/dea-releases-2018-national-drug-threat-assessment-0. Published November 2, 2018. Accessed April 24, 2019.
Direct pharmacy dispensing of naloxone linked to drop in fatal overdoses
investigators reported.
By contrast, state laws that stopped short of allowing pharmacists to directly dispense the opioid antagonist did not appear to impact mortality, according to the report, which appears in JAMA Internal Medicine (2019 May 6. doi: 10.1001/jamainternmed.2019.0272).
The report, based on state-level trends tracked from 2005 to 2016, indicates that fatal opioid overdoses fell by nearly one-third in states that adopted direct dispensing laws as compared with states that adopted other naloxone laws.
That finding suggests that the policy type determines whether a naloxone law is useful in combating fatal opioid overdoses, said Rahi Abouk, PhD, of William Paterson University, Wayne, N.J. and co-authors of the paper.
“Enabling distribution through various sources, or requiring gatekeepers, will not be as beneficial,” Dr. Abouk and co-authors said in their report.
The current rate of deaths from fentanyl, heroin, and prescription analgesic overdose has outpaced all previous drug epidemics on record, and even surpasses the number of deaths in the peak year of the HIV epidemic of the 1980s, Dr. Abouk and colleagues wrote in their paper.
The number of states with naloxone access laws grew from just 2 in 2005 to 47 by 2016, including 9 states that granted direct authority to pharmacists and 38 that granted indirect authority, according to the researchers.
The analysis of overdose trends from 2005 to 2016 was based on naloxone distribution data from state Medicaid agencies and opioid-related mortality data from a national statistics system. Forty percent of nonelderly adults with an opioid addiction are covered by Medicaid, the researchers said.
They found that naloxone laws granting pharmacists direct dispensing authority were linked to a drop in opioid deaths that increased in magnitude over time, according to researchers. The mean number of opioid deaths dropped by 27% in the second year after adoption of direct authority laws, relative to opioid deaths in states with indirect access laws, while in subsequent years, deaths dropped by 34%.
Emergency department visits related to opioids increased by 15% in direct authority states 3 or more years after adoption, as compared to states that did not adopt direct authority laws. According to investigators, that translated into 15 additional opioid-related emergency department visits each month.
That increase suggests that, alongside direct dispensing laws, “useful interventions” and connections to treatment are needed for the emergency department, according to Dr. Abouk and colleagues.
“This is the location where such programs may be the most effective,” they said in their report.
Future research should be done to determine whether removing gatekeepers increases the value of naloxone distribution policies, they concluded in the report.
Dr. Abouk had no disclosures. Co-authors on the study reported funding and conflict of interest disclosures related to the National Institute on Drug Abuse and the Centers for Disease Control and Prevention.
SOURCE: Abouk R, et al. JAMA Intern Med. 2019 May 6. doi:10.1001/jamainternmed.2019.0272.
investigators reported.
By contrast, state laws that stopped short of allowing pharmacists to directly dispense the opioid antagonist did not appear to impact mortality, according to the report, which appears in JAMA Internal Medicine (2019 May 6. doi: 10.1001/jamainternmed.2019.0272).
The report, based on state-level trends tracked from 2005 to 2016, indicates that fatal opioid overdoses fell by nearly one-third in states that adopted direct dispensing laws as compared with states that adopted other naloxone laws.
That finding suggests that the policy type determines whether a naloxone law is useful in combating fatal opioid overdoses, said Rahi Abouk, PhD, of William Paterson University, Wayne, N.J. and co-authors of the paper.
“Enabling distribution through various sources, or requiring gatekeepers, will not be as beneficial,” Dr. Abouk and co-authors said in their report.
The current rate of deaths from fentanyl, heroin, and prescription analgesic overdose has outpaced all previous drug epidemics on record, and even surpasses the number of deaths in the peak year of the HIV epidemic of the 1980s, Dr. Abouk and colleagues wrote in their paper.
The number of states with naloxone access laws grew from just 2 in 2005 to 47 by 2016, including 9 states that granted direct authority to pharmacists and 38 that granted indirect authority, according to the researchers.
The analysis of overdose trends from 2005 to 2016 was based on naloxone distribution data from state Medicaid agencies and opioid-related mortality data from a national statistics system. Forty percent of nonelderly adults with an opioid addiction are covered by Medicaid, the researchers said.
They found that naloxone laws granting pharmacists direct dispensing authority were linked to a drop in opioid deaths that increased in magnitude over time, according to researchers. The mean number of opioid deaths dropped by 27% in the second year after adoption of direct authority laws, relative to opioid deaths in states with indirect access laws, while in subsequent years, deaths dropped by 34%.
Emergency department visits related to opioids increased by 15% in direct authority states 3 or more years after adoption, as compared to states that did not adopt direct authority laws. According to investigators, that translated into 15 additional opioid-related emergency department visits each month.
That increase suggests that, alongside direct dispensing laws, “useful interventions” and connections to treatment are needed for the emergency department, according to Dr. Abouk and colleagues.
“This is the location where such programs may be the most effective,” they said in their report.
Future research should be done to determine whether removing gatekeepers increases the value of naloxone distribution policies, they concluded in the report.
Dr. Abouk had no disclosures. Co-authors on the study reported funding and conflict of interest disclosures related to the National Institute on Drug Abuse and the Centers for Disease Control and Prevention.
SOURCE: Abouk R, et al. JAMA Intern Med. 2019 May 6. doi:10.1001/jamainternmed.2019.0272.
investigators reported.
By contrast, state laws that stopped short of allowing pharmacists to directly dispense the opioid antagonist did not appear to impact mortality, according to the report, which appears in JAMA Internal Medicine (2019 May 6. doi: 10.1001/jamainternmed.2019.0272).
The report, based on state-level trends tracked from 2005 to 2016, indicates that fatal opioid overdoses fell by nearly one-third in states that adopted direct dispensing laws as compared with states that adopted other naloxone laws.
That finding suggests that the policy type determines whether a naloxone law is useful in combating fatal opioid overdoses, said Rahi Abouk, PhD, of William Paterson University, Wayne, N.J. and co-authors of the paper.
“Enabling distribution through various sources, or requiring gatekeepers, will not be as beneficial,” Dr. Abouk and co-authors said in their report.
The current rate of deaths from fentanyl, heroin, and prescription analgesic overdose has outpaced all previous drug epidemics on record, and even surpasses the number of deaths in the peak year of the HIV epidemic of the 1980s, Dr. Abouk and colleagues wrote in their paper.
The number of states with naloxone access laws grew from just 2 in 2005 to 47 by 2016, including 9 states that granted direct authority to pharmacists and 38 that granted indirect authority, according to the researchers.
The analysis of overdose trends from 2005 to 2016 was based on naloxone distribution data from state Medicaid agencies and opioid-related mortality data from a national statistics system. Forty percent of nonelderly adults with an opioid addiction are covered by Medicaid, the researchers said.
They found that naloxone laws granting pharmacists direct dispensing authority were linked to a drop in opioid deaths that increased in magnitude over time, according to researchers. The mean number of opioid deaths dropped by 27% in the second year after adoption of direct authority laws, relative to opioid deaths in states with indirect access laws, while in subsequent years, deaths dropped by 34%.
Emergency department visits related to opioids increased by 15% in direct authority states 3 or more years after adoption, as compared to states that did not adopt direct authority laws. According to investigators, that translated into 15 additional opioid-related emergency department visits each month.
That increase suggests that, alongside direct dispensing laws, “useful interventions” and connections to treatment are needed for the emergency department, according to Dr. Abouk and colleagues.
“This is the location where such programs may be the most effective,” they said in their report.
Future research should be done to determine whether removing gatekeepers increases the value of naloxone distribution policies, they concluded in the report.
Dr. Abouk had no disclosures. Co-authors on the study reported funding and conflict of interest disclosures related to the National Institute on Drug Abuse and the Centers for Disease Control and Prevention.
SOURCE: Abouk R, et al. JAMA Intern Med. 2019 May 6. doi:10.1001/jamainternmed.2019.0272.
FROM JAMA Internal Medicine
Key clinical point: State laws granting pharmacists direct authority to dispense naloxone were linked to significant drops in opioid-related fatal overdoses.
Major finding: The mean number of opioid deaths dropped by 27% in the second year after adoption of direct authority laws relative to opioid deaths in states with indirect access laws, while in subsequent years, deaths dropped by 34%.
Study details: Analysis of naloxone distribution data and opioid-related mortality data from 2005 to 2016 for all 50 states and the District of Columbia.
Disclosures: Study authors reported funding and conflict of interest disclosures related to the National Institute on Drug Abuse and the Centers for Disease Control and Prevention.
Source: Abouk R, et al. JAMA Intern Med. 2019 May 6.
Only 1.5% of individuals at high risk of opioid overdose receive naloxone
The vast majority of individuals at high risk for opioid overdose do not receive naloxone, despite numerous opportunities, according to Sarah Follman and associates from the University of Chicago.
In a retrospective study published in JAMA Network Open, the study authors analyzed data from individuals in the Truven Health MarketScan Research Database who had ICD-10 codes related to opioid use, misuse, dependence, and overdose. Data from Oct. 1, 2015, through Dec. 31, 2016, were included; a total of 138,108 high-risk individuals were identified as interacting with the health care system nearly 1.2 million times (88,618 hospitalizations, 229,680 ED visits, 298,058 internal medicine visits, and 568,448 family practice visits).
Of the 138,108 individuals in the study, only 2,135 (1.5%) were prescribed naloxone during the study period. Patients who had prior diagnoses of both opioid misuse/dependence and overdose were significantly more likely to receive naloxone than were those who only had a history of opioid dependence (odds ratio, 2.32; 95% confidence interval, 1.98-2.72; P less than .001). In addition, having a history of overdose alone was associated with a decreased chance of receiving naloxone, compared with those with a history of opioid misuse alone (OR, 0.73; 95% CI, 0.57-0.94; P = .01).
Other factors that significantly reduced the odds of receiving naloxone included being aged 30-44 years and being from the Midwest or West. Factors that reduced the odds include having received treatment for opioid use disorder, visiting a detoxification facility, receiving other substance use disorder treatment; and having received outpatient care from a pain specialist, psychologist, or surgeon.
“Most individuals at high risk of opioid overdose do not receive naloxone through direct prescribing,” Ms. Follman and associates wrote. “Clinicians can address this gap by regularly prescribing naloxone to eligible patients. To address barriers to prescribing, hospital systems and medical schools can support clinicians by improving education on screening and treating substance use disorders, clarifying legal concerns, and developing policies and protocols to guide implementation of increased prescribing.
No conflicts of interest were reported; one coauthor reported receiving a grant from the National Institutes of Health.
SOURCE: Follman S et al. JAMA Netw Open. 2019 May 3. doi: 10.1001/jamanetworkopen.2019.3209.
The vast majority of individuals at high risk for opioid overdose do not receive naloxone, despite numerous opportunities, according to Sarah Follman and associates from the University of Chicago.
In a retrospective study published in JAMA Network Open, the study authors analyzed data from individuals in the Truven Health MarketScan Research Database who had ICD-10 codes related to opioid use, misuse, dependence, and overdose. Data from Oct. 1, 2015, through Dec. 31, 2016, were included; a total of 138,108 high-risk individuals were identified as interacting with the health care system nearly 1.2 million times (88,618 hospitalizations, 229,680 ED visits, 298,058 internal medicine visits, and 568,448 family practice visits).
Of the 138,108 individuals in the study, only 2,135 (1.5%) were prescribed naloxone during the study period. Patients who had prior diagnoses of both opioid misuse/dependence and overdose were significantly more likely to receive naloxone than were those who only had a history of opioid dependence (odds ratio, 2.32; 95% confidence interval, 1.98-2.72; P less than .001). In addition, having a history of overdose alone was associated with a decreased chance of receiving naloxone, compared with those with a history of opioid misuse alone (OR, 0.73; 95% CI, 0.57-0.94; P = .01).
Other factors that significantly reduced the odds of receiving naloxone included being aged 30-44 years and being from the Midwest or West. Factors that reduced the odds include having received treatment for opioid use disorder, visiting a detoxification facility, receiving other substance use disorder treatment; and having received outpatient care from a pain specialist, psychologist, or surgeon.
“Most individuals at high risk of opioid overdose do not receive naloxone through direct prescribing,” Ms. Follman and associates wrote. “Clinicians can address this gap by regularly prescribing naloxone to eligible patients. To address barriers to prescribing, hospital systems and medical schools can support clinicians by improving education on screening and treating substance use disorders, clarifying legal concerns, and developing policies and protocols to guide implementation of increased prescribing.
No conflicts of interest were reported; one coauthor reported receiving a grant from the National Institutes of Health.
SOURCE: Follman S et al. JAMA Netw Open. 2019 May 3. doi: 10.1001/jamanetworkopen.2019.3209.
The vast majority of individuals at high risk for opioid overdose do not receive naloxone, despite numerous opportunities, according to Sarah Follman and associates from the University of Chicago.
In a retrospective study published in JAMA Network Open, the study authors analyzed data from individuals in the Truven Health MarketScan Research Database who had ICD-10 codes related to opioid use, misuse, dependence, and overdose. Data from Oct. 1, 2015, through Dec. 31, 2016, were included; a total of 138,108 high-risk individuals were identified as interacting with the health care system nearly 1.2 million times (88,618 hospitalizations, 229,680 ED visits, 298,058 internal medicine visits, and 568,448 family practice visits).
Of the 138,108 individuals in the study, only 2,135 (1.5%) were prescribed naloxone during the study period. Patients who had prior diagnoses of both opioid misuse/dependence and overdose were significantly more likely to receive naloxone than were those who only had a history of opioid dependence (odds ratio, 2.32; 95% confidence interval, 1.98-2.72; P less than .001). In addition, having a history of overdose alone was associated with a decreased chance of receiving naloxone, compared with those with a history of opioid misuse alone (OR, 0.73; 95% CI, 0.57-0.94; P = .01).
Other factors that significantly reduced the odds of receiving naloxone included being aged 30-44 years and being from the Midwest or West. Factors that reduced the odds include having received treatment for opioid use disorder, visiting a detoxification facility, receiving other substance use disorder treatment; and having received outpatient care from a pain specialist, psychologist, or surgeon.
“Most individuals at high risk of opioid overdose do not receive naloxone through direct prescribing,” Ms. Follman and associates wrote. “Clinicians can address this gap by regularly prescribing naloxone to eligible patients. To address barriers to prescribing, hospital systems and medical schools can support clinicians by improving education on screening and treating substance use disorders, clarifying legal concerns, and developing policies and protocols to guide implementation of increased prescribing.
No conflicts of interest were reported; one coauthor reported receiving a grant from the National Institutes of Health.
SOURCE: Follman S et al. JAMA Netw Open. 2019 May 3. doi: 10.1001/jamanetworkopen.2019.3209.
FROM JAMA NETWORK OPEN
Outpatient program successfully tackles substance use and chronic pain
MILWAUKEE – An interdisciplinary intensive outpatient treatment program addressing chronic pain and substance use disorder effectively addressed both diagnoses in a military population.
Intensive outpatient programs (IOPs) frequently address these conditions within a biopsychosocial format, but it’s not common for IOPs to have this dual focus on chronic pain and substance use disorder (SUD), said Michael Stockin, MD, speaking in an interview at the scientific meeting of the American Pain Society.
Dr. Stockin said he and his collaborators recognized that, especially among a military population, the two conditions have considerable overlap, so it made sense to integrate behavioral treatment for both conditions in an intensive outpatient program. “Our hypothesis was that if you can use an intensive outpatient program to address substance use disorder, maybe you can actually add a chronic pain curriculum – like a functional restoration program to it.
“As a result of our study, we did find that there were significant differences in worst pain scores as a result of the program. In the people who took both the substance use disorder and chronic pain curriculum, we found significant reductions in total impairment, worst pain, and they also had less … substance use as well,” said Dr. Stockin.
In a quality improvement project, Dr. Stockin and collaborators compared short-term outcomes for patients who received IOP treatment addressing both chronic pain and SUD with those receiving SUD-only IOP.
For those participating in the joint IOP, scores indicating worst pain on the 0-10 numeric rating scale were reduced significantly, from 7.55 to 6.23 (P = .013). Scores on a functional measure of impairment, the Pain Outcomes Questionnaire Short Form (POQ-SF) also dropped significantly, from 84.92 to 63.50 (P = .034). The vitality domain of the POQ-SF also showed that patients had less impairment after participation in the joint IOP, with scores in that domain dropping from 20.17 to 17.25 (P = .024).
Looking at the total cohort, patient scores on the Brief Addiction Monitor (BAM) dropped significantly from baseline to the end of the intervention, indicating reduced substance use (P = .041). Mean scores for participants in the joint IOP were higher at baseline than for those in the SUD-only IOP (1.000 vs. 0.565). However, those participating in the joint IOP had lower mean postintervention BAM scores than the SUD-only cohort (0.071 vs. 0.174).
American veterans experience more severe pain and have a higher prevalence of chronic pain than nonveterans. Similarly, wrote Dr. Stockin, a chronic pain fellow in pain management at Walter Reed National Military Medical Center, Bethesda, Md., and colleagues in the poster presentation.
The project enrolled a total of 66 patients (10 female and 56 male). Of these, 18 participated in the joint SUD–chronic pain program, and 48 received usual treatment of the SUD-only IOP treatment. The mean overall age was 33.2 years, and 71.2% of participants were white.
Overall, 51 patients (77.3%) of participants had alcohol use disorder. Participants included active duty service members, veterans, and their dependents. Opioid and cannabis use disorders were experienced by a total of eight patients, and seven more patients had diagnoses of alcohol use disorder along with other substance use disorders.
All patients completed the BAM and received urine toxicology and alcohol breath testing at enrollment; drug and alcohol screening was completed at other points during the IOP treatment for both groups as well.
The joint IOP ran 3 full days a week, with a substance use curriculum in the morning and a pain management program in the afternoon; the SUD-only participants had three morning sessions weekly. Both interventions lasted 6 weeks, and Dr. Stockin said he and his colleagues would like to acquire longitudinal data to assess the durability of gains seen from the joint IOP.
The multidisciplinary team running the joint IOP was made up of an addiction/pain medicine physician, a clinical health psychologist, a physical therapist, social workers, and a nurse.
“This project is the first of its kind to find a significant reduction in pain burden while concurrently treating addiction and pain in an outpatient military health care setting,” Dr. Stockin and colleagues wrote in the poster accompanying the presentation.
“We had outcomes in both substance use and chronic pain that were positive, so it suggests that in the military health system, people may actually benefit from treating both chronic pain and substance use disorder concurrently. If you could harmonize those programs, you might be able to get good outcomes for soldiers and their families,” Dr. Stockin said.
Dr. Stockin reported no conflicts of interest. The project was funded by the Defense Health Agency.
MILWAUKEE – An interdisciplinary intensive outpatient treatment program addressing chronic pain and substance use disorder effectively addressed both diagnoses in a military population.
Intensive outpatient programs (IOPs) frequently address these conditions within a biopsychosocial format, but it’s not common for IOPs to have this dual focus on chronic pain and substance use disorder (SUD), said Michael Stockin, MD, speaking in an interview at the scientific meeting of the American Pain Society.
Dr. Stockin said he and his collaborators recognized that, especially among a military population, the two conditions have considerable overlap, so it made sense to integrate behavioral treatment for both conditions in an intensive outpatient program. “Our hypothesis was that if you can use an intensive outpatient program to address substance use disorder, maybe you can actually add a chronic pain curriculum – like a functional restoration program to it.
“As a result of our study, we did find that there were significant differences in worst pain scores as a result of the program. In the people who took both the substance use disorder and chronic pain curriculum, we found significant reductions in total impairment, worst pain, and they also had less … substance use as well,” said Dr. Stockin.
In a quality improvement project, Dr. Stockin and collaborators compared short-term outcomes for patients who received IOP treatment addressing both chronic pain and SUD with those receiving SUD-only IOP.
For those participating in the joint IOP, scores indicating worst pain on the 0-10 numeric rating scale were reduced significantly, from 7.55 to 6.23 (P = .013). Scores on a functional measure of impairment, the Pain Outcomes Questionnaire Short Form (POQ-SF) also dropped significantly, from 84.92 to 63.50 (P = .034). The vitality domain of the POQ-SF also showed that patients had less impairment after participation in the joint IOP, with scores in that domain dropping from 20.17 to 17.25 (P = .024).
Looking at the total cohort, patient scores on the Brief Addiction Monitor (BAM) dropped significantly from baseline to the end of the intervention, indicating reduced substance use (P = .041). Mean scores for participants in the joint IOP were higher at baseline than for those in the SUD-only IOP (1.000 vs. 0.565). However, those participating in the joint IOP had lower mean postintervention BAM scores than the SUD-only cohort (0.071 vs. 0.174).
American veterans experience more severe pain and have a higher prevalence of chronic pain than nonveterans. Similarly, wrote Dr. Stockin, a chronic pain fellow in pain management at Walter Reed National Military Medical Center, Bethesda, Md., and colleagues in the poster presentation.
The project enrolled a total of 66 patients (10 female and 56 male). Of these, 18 participated in the joint SUD–chronic pain program, and 48 received usual treatment of the SUD-only IOP treatment. The mean overall age was 33.2 years, and 71.2% of participants were white.
Overall, 51 patients (77.3%) of participants had alcohol use disorder. Participants included active duty service members, veterans, and their dependents. Opioid and cannabis use disorders were experienced by a total of eight patients, and seven more patients had diagnoses of alcohol use disorder along with other substance use disorders.
All patients completed the BAM and received urine toxicology and alcohol breath testing at enrollment; drug and alcohol screening was completed at other points during the IOP treatment for both groups as well.
The joint IOP ran 3 full days a week, with a substance use curriculum in the morning and a pain management program in the afternoon; the SUD-only participants had three morning sessions weekly. Both interventions lasted 6 weeks, and Dr. Stockin said he and his colleagues would like to acquire longitudinal data to assess the durability of gains seen from the joint IOP.
The multidisciplinary team running the joint IOP was made up of an addiction/pain medicine physician, a clinical health psychologist, a physical therapist, social workers, and a nurse.
“This project is the first of its kind to find a significant reduction in pain burden while concurrently treating addiction and pain in an outpatient military health care setting,” Dr. Stockin and colleagues wrote in the poster accompanying the presentation.
“We had outcomes in both substance use and chronic pain that were positive, so it suggests that in the military health system, people may actually benefit from treating both chronic pain and substance use disorder concurrently. If you could harmonize those programs, you might be able to get good outcomes for soldiers and their families,” Dr. Stockin said.
Dr. Stockin reported no conflicts of interest. The project was funded by the Defense Health Agency.
MILWAUKEE – An interdisciplinary intensive outpatient treatment program addressing chronic pain and substance use disorder effectively addressed both diagnoses in a military population.
Intensive outpatient programs (IOPs) frequently address these conditions within a biopsychosocial format, but it’s not common for IOPs to have this dual focus on chronic pain and substance use disorder (SUD), said Michael Stockin, MD, speaking in an interview at the scientific meeting of the American Pain Society.
Dr. Stockin said he and his collaborators recognized that, especially among a military population, the two conditions have considerable overlap, so it made sense to integrate behavioral treatment for both conditions in an intensive outpatient program. “Our hypothesis was that if you can use an intensive outpatient program to address substance use disorder, maybe you can actually add a chronic pain curriculum – like a functional restoration program to it.
“As a result of our study, we did find that there were significant differences in worst pain scores as a result of the program. In the people who took both the substance use disorder and chronic pain curriculum, we found significant reductions in total impairment, worst pain, and they also had less … substance use as well,” said Dr. Stockin.
In a quality improvement project, Dr. Stockin and collaborators compared short-term outcomes for patients who received IOP treatment addressing both chronic pain and SUD with those receiving SUD-only IOP.
For those participating in the joint IOP, scores indicating worst pain on the 0-10 numeric rating scale were reduced significantly, from 7.55 to 6.23 (P = .013). Scores on a functional measure of impairment, the Pain Outcomes Questionnaire Short Form (POQ-SF) also dropped significantly, from 84.92 to 63.50 (P = .034). The vitality domain of the POQ-SF also showed that patients had less impairment after participation in the joint IOP, with scores in that domain dropping from 20.17 to 17.25 (P = .024).
Looking at the total cohort, patient scores on the Brief Addiction Monitor (BAM) dropped significantly from baseline to the end of the intervention, indicating reduced substance use (P = .041). Mean scores for participants in the joint IOP were higher at baseline than for those in the SUD-only IOP (1.000 vs. 0.565). However, those participating in the joint IOP had lower mean postintervention BAM scores than the SUD-only cohort (0.071 vs. 0.174).
American veterans experience more severe pain and have a higher prevalence of chronic pain than nonveterans. Similarly, wrote Dr. Stockin, a chronic pain fellow in pain management at Walter Reed National Military Medical Center, Bethesda, Md., and colleagues in the poster presentation.
The project enrolled a total of 66 patients (10 female and 56 male). Of these, 18 participated in the joint SUD–chronic pain program, and 48 received usual treatment of the SUD-only IOP treatment. The mean overall age was 33.2 years, and 71.2% of participants were white.
Overall, 51 patients (77.3%) of participants had alcohol use disorder. Participants included active duty service members, veterans, and their dependents. Opioid and cannabis use disorders were experienced by a total of eight patients, and seven more patients had diagnoses of alcohol use disorder along with other substance use disorders.
All patients completed the BAM and received urine toxicology and alcohol breath testing at enrollment; drug and alcohol screening was completed at other points during the IOP treatment for both groups as well.
The joint IOP ran 3 full days a week, with a substance use curriculum in the morning and a pain management program in the afternoon; the SUD-only participants had three morning sessions weekly. Both interventions lasted 6 weeks, and Dr. Stockin said he and his colleagues would like to acquire longitudinal data to assess the durability of gains seen from the joint IOP.
The multidisciplinary team running the joint IOP was made up of an addiction/pain medicine physician, a clinical health psychologist, a physical therapist, social workers, and a nurse.
“This project is the first of its kind to find a significant reduction in pain burden while concurrently treating addiction and pain in an outpatient military health care setting,” Dr. Stockin and colleagues wrote in the poster accompanying the presentation.
“We had outcomes in both substance use and chronic pain that were positive, so it suggests that in the military health system, people may actually benefit from treating both chronic pain and substance use disorder concurrently. If you could harmonize those programs, you might be able to get good outcomes for soldiers and their families,” Dr. Stockin said.
Dr. Stockin reported no conflicts of interest. The project was funded by the Defense Health Agency.
REPORTING FROM APS 2019
Key clinical point: An intensive, 6-week joint substance use disorder and chronic pain intensive outpatient program significantly reduced both substance use and pain.
Major finding: Patients had less pain and reduced substance use after completing the program, compared with baseline (P = .013 and .041, respectively).
Study details: A quality improvement project including 66 patients at a military health facility.
Disclosures: The study was sponsored by the Defense Health Agency. Dr. Stockin reported no conflicts of interest.
Cannabidiol (CBD) for schizophrenia: Promise or pipe dream?
Over the past few decades, it has become increasingly clear that cannabis use can increase the risk of developing a psychotic disorder and worsen the course of existing schizophrenia in a dose-dependent fashion.1-3 Beyond psychosis, although many patients with mental illness use cannabis for recreational purposes or as purported “self-medication,” currently available evidence suggests that marijuana is more likely to represent a harm than a benefit for psychiatric disorders4 (Box4-8). Our current state of knowledge therefore suggests that psychiatrists should caution their patients against using cannabis and prioritize interventions to reduce or discontinue use, especially among those with psychotic disorders.
Box
Data from California in 2006—a decade after the state’s legalization of “medical marijuana”—revealed that 23% of patients in a sample enrolled in medical marijuana clinics were receiving cannabis to treat a mental disorder.5 That was a striking statistic given the dearth of evidence to support a benefit of cannabis for psychiatric conditions at the time, leaving clinicians who provided the necessary recommendations to obtain medical marijuana largely unable to give informed consent about the risks and benefits, much less recommendations about specific products, routes of administration, or dosing. In 2019, we know considerably more about the interaction between cannabinoids and mental health, but research findings thus far warrant more caution than enthusiasm, with one recent review concluding that “whenever an association is observed between cannabis use and psychiatric disorders, the relationship is generally an adverse one.”4
Some critics have argued that the medical marijuana industry represents little more than a front for recreational use. In California and other states that have legalized recreational use, that claim has been rendered all but moot, although the public remains curious about the potential health benefits of cannabinoids and will likely continue to look to clinicians for advice. For those seeking guidance from evidence-based research, the existing state of knowledge can seem like a “Wild West” of anecdotal subjective reports, biased opinions, and uncontrolled clinical studies. Cannabis remains a Schedule I drug at the federal level, and quality clinical research has been limited to a relatively modest number of randomized controlled trials (RCTs), mostly involving FDA-approved cannabinoids rather than smoked cannabis. Randomized controlled trials that have involved smoked marijuana have generally involved low-potency delta-9-tetrahydrocannabinol (THC) cannabis that may not reflect the same therapeutic and adverse effects of the increasingly high potency cannabis now available on the street and in dispensaries.
In psychiatry, a few RCTs are underway exploring cannabis as a viable treatment for mental disorders (eg, posttraumatic stress disorder), but none have yet been completed or published. At best, retrospective studies to date have failed to support a consistent benefit of cannabis for any psychiatric disorder and at worst increasingly suggest a negative impact on psychotic, mood, and anxiety disorders.4,6 Meanwhile, synthetic cannabinoid receptor agonists (eg, “Spice” products) have come to represent a clear public health risk, with both medical and psychiatric toxicity.7
A more cautiously optimistic case for the therapeutic potential of cannabinoids in psychiatry could be made for cannabidiol (CBD), which may possess anxiolytic, antipsychotic, and neuroprotective properties.8 Based on its purported health benefits, it is possible that CBD may even gain widespread popularity as a food supplement. Because a pharmaceutically-manufactured form of CBD was recently FDA-approved for the treatment of seizures associated with Lennox-Gastaut syndrome and Dravet syndrome, off-label prescribing of CBD for psychiatric disorders can be anticipated. While there is not yet sufficient evidence about risks and benefits to justify CBD being recommended broadly in psychiatry, that same informational vacuum has not stopped eager patients from seeking approval for cannabis, and some physicians from providing it.
Despite that conclusion, because cannabis is classified as a Schedule I drug by the US Drug Enforcement Agency, clinical research investigating the risks and benefits of cannabis has been limited. It therefore remains possible that cannabis, or individual cannabinoids such as cannabidiol (CBD), may yet find a therapeutic niche in psychiatry. This article reviews evidence on CBD for the treatment of schizophrenia.
Cannabinergic drugs as potential antipsychotics
Although the bulk of evidence indicates a harmful effect of cannabis in individuals with or at risk for psychosis, there have been a few published cases of schizophrenia improving with dronabinol, an FDA-approved, synthetic form of delta-9-tetrahydrocannabinol (THC).9,10 THC is the constituent of cannabis that produces euphoric effects. These provocative findings have not been replicated in controlled clinical trials, but suggest at least the theoretical possibility of idiosyncratic benefits from THC for some individuals within the psychotic spectrum.
Still, given that most available evidence supports that THC has a harmful effect on psychosis and psychosis risk, researchers have instead performed randomized controlled trials (RCTs) to investigate a possible therapeutic role for medications that oppose the agonist effects of THC at cannabinoid type 1 (CB1) receptors. To date, 2 RCTs comparing rimonabant, a CB1 inverse agonist, with placebo (PLB) in patients with schizophrenia have failed to demonstrate any benefit for psychotic symptoms or cognitive deficits.11,12 A third trial examining rimonabant for people diagnosed with schizophrenia who were overweight found significant benefits for anxiety and depressive symptoms, but none for positive symptoms or the primary outcome of weight loss.13 While these results are discouraging, the role of THC in precipitating psychosis suggests that novel agents opposing the actions of THC on the cannabinoid system could have antipsychotic properties.14
Cannabidiol: An antipsychotic medication?
In contrast to THC, CBD has minimal euphorigenic properties and has recently been heralded in the popular press as a “miracle drug” with benefits for medical and psychiatric disorders alike.15 It has even been speculated that it could become a popular food supplement.16 In 2018, the FDA gave full approval to a pharmaceutically manufactured form of CBD (brand name: Epidiolex) as a novel treatment for 2 rare and severe forms of pediatric epilepsy, Lennox-Gastaut syndrome and Dravet syndrome,17 based on RCTs supporting its efficacy for these often refractory and life-threatening conditions.18-20
In psychiatry, there have not yet been enough robust clinical studies to support broad therapeutic claims for CBD as a treatment for any mental disorder.21 However, there is growing evidence that CBD has potential as an antipsychotic medication. In 1995, the first case report was published describing the efficacy of CBD, 1,500 mg/d, as standalone therapy in a single individual with schizophrenia.22 In 2006, the same research group followed up with a case series in which only 1 out of 3 patients with treatment-refractory schizophrenia improved with flexible dosing of CBD to a maximum dose of 1,280 mg/d.23
There have been 3 published RCTs exploring the efficacy of CBD in schizophrenia (Table24-26). The first study, published in 2012, included 39 adults with schizophrenia who were randomized to 800 mg/d of CBD or amisulpride (AMS), a second-generation antipsychotic that is popular in Europe but is not available in the United States.24 Over 4 weeks of randomized treatment, CBD resulted in as much improvement in overall symptoms and positive symptoms as AMS, and improvement of negative symptoms was significantly greater with CBD. Compared with patients treated with antipsychotic medication, patients who were treated with CBD had fewer extrapyramidal symptoms, less weight gain, and less prolactin elevation. This initial trial suggests that CBD might be as efficacious in schizophrenia as antipsychotic medication, without its burdensome adverse effects. However, this is the only RCT of CBD monotherapy published to date.
Continue to: Two other recently published RCTs...
Two other recently published RCTs compared CBD with PLB as add-on therapy to antipsychotics. McGuire et al25 compared CBD, 1,000 mg/d, to PLB over 6 weeks in 88 patients with schizophrenia. Positive symptom improvement was statistically greater with CBD than with PLB, although the magnitude of clinical change was modest (using the Positive and Negative Syndrome Scale [PANSS] positive symptom subscale: −3.2 points for CBD vs −1.7 points for PLB). Changes in PANSS total score and subscales for general and negative symptoms were not significantly different between treatment groups. There was also no significant difference in overall change in neurocognitive symptoms, although post-hoc analysis revealed significantly greater improvement in motor speed for patients treated with CBD. More than twice the number of patients treated with CBD were rated as “much improved” by the Clinical Global Impressions scale compared with patients treated with PLB, but this was not a statistically significant finding, and most patients experienced only “minimal” or “no improvement.” In terms of adverse events, there were no significant differences between patients in the CBD and PLB groups. Although this study is technically “positive” for CBD and suggests minimal adverse effects, it is not clear whether the statistically significant positive symptom improvements (+1.5 PANSS points for CBD over PLB) were clinically significant.
The most recently published placebo-controlled RCT of CBD as add-on therapy to antipsychotic medication included 36 patients with schizophrenia treated over 6 weeks.26 In this study, there was no benefit of CBD, 600 mg/d, on any PANSS score outcome (total, general, positive, or negative symptoms). For the primary outcome of the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery, there were no significant drug × time effects, and post-hoc analyses showed that only patients treated with PLB improved with time. Sedation was more common among patients treated with CBD compared with PLB.
Making sense of the data
There have been mixed results from the few case reports and 3 RCTs of patients with schizophrenia who were treated with CBD. How can we resolve these disparate findings? A few possible interpretations of the data that warrant clarification through additional research include:
Dosing. In the first case report with positive results, CBD was dosed at 1,500 mg/d,22 whereas in the subsequent case series with mixed results, the maximum allowable dose of CBD was 1,280 mg/d.23 Likewise, in the RCTs, positive results were found when CBD was dosed at 800 to 1,000 mg/d,24,25 but not at 600 mg/d.26 The efficacy of CBD for schizophrenia might depend on higher doses.
Treatment resistance. In the second case series in which only 1 out of 3 patients responded to treatment with CBD,23 the patients had demonstrated previous nonresponse to at least 2 first-generation antipsychotics (FGAs) and risperidone, 6 mg/d. In the RCTs, all patients were antipsychotic-responsive.24-26 Cannabidiol may not be as effective for patients with treatment-refractory schizophrenia as it is for patients with schizophrenia who respond to antipsychotics.
Continue to: Clinical stability
Clinical stability. Within the RCTs, the greatest response was observed in the study that enrolled patients who were hospitalized with acute symptoms of schizophrenia.23 In the 2 studies that found either modest or no benefit with CBD, the patients had been stabilized on antipsychotic medications prior to randomization. Cannabidiol may offer limited benefit as add-on therapy to patients who have already responded to antipsychotic treatment, where there is “less room” for additional improvement.
Monotherapy. Both the case reports22,23 and the RCT with the most robust positive findings24 involved treatment with CBD as monotherapy. For some patients with schizophrenia, CBD might be effective as standalone therapy as an alternative to antipsychotics that is better tolerated. Adding CBD to antipsychotic therapy might be redundant and therefore less effective.
Answering questions about CBD
Cannabidiol is becoming increasingly popular for its purported health benefits. The mixed results of the few studies published on CBD for schizophrenia place clinicians in a difficult position when attempting to answer questions about how cannabinoids might fit into treatment of patients with psychosis. Consider the following:
Is cannabis helpful for patients with schizophrenia? No. Aside from the few case reports suggesting that FDA-approved THC (dronabinol) can improve symptoms in some patients,9,10 most of the evidence from anecdotal reports and both experimental and observational studies indicate that cannabis, THC, and synthetic cannabinoids have a harmful effect in patients with or at risk for psychosis.1-3
If you are considering recommending some form of cannabis to patients with schizophrenia, what kind should you recommend? Recommending or encouraging cannabis use for patients with psychosis is ill-advised. Although certain types of cannabis might contain more THC (eg, Cannabis indica vs Cannabis sativa) or variable amounts of CBD, in general the amount of CBD in whole leaf cannabis is minimal, with the ratio of THC to CBD increasingly significantly over the past decade.3,27 Most forms of cannabis should therefore be avoided by individuals with or at risk for psychotic disorders.
Continue to: What about CBD oil and other CBD products sold in dispensaries?
What about CBD oil and other CBD products sold in dispensaries? Cannabidiol is increasingly available in various forms based on its ability to be designated as a legal hemp product (containing <0.3% THC) at the federal level or as a cannabinoid in states where cannabis is legal. However, several studies have now shown that cannabis products sold online or in dispensaries are often labeled inaccurately, with both under- and over-reporting of THC and CBD content.28-30 Some CBD products have been found to have almost no CBD at all.29,30 The unreliability of product labeling makes it difficult to predict the effects of CBD products that are not subject to FDA purity standards for medications or dietary supplements. It also raises questions about the sources of CBD and the reliability of dosing in the studies discussed above.
Why might CBD work as an antipsychotic? Although CBD has minimal affinity for cannabinoid receptors, it appears to act as a partial agonist of dopamine D2 receptors and an agonist at 5-HT1A receptors, with overall effects that decrease mesolimbic dopamine activity.31,32 In addition, CBD increases the availability of the endogenous cannabinoid anandamide, which may have antipsychotic properties.14,33
Now that the FDA has approved CBD manufactured by a pharmaceutical company, should it be prescribed “off-label” for patients with schizophrenia? This is the “million dollar question,” with insufficient evidence to provide a clear answer. It should now be possible to prescribe FDA-approved CBD for off-label purposes, including the treatment of schizophrenia and other psychiatric disorders. No doubt, some clinicians are already doing so. This will predictably yield more anecdotal evidence about efficacy and adverse effects in the future, but there is not yet adequate evidence to support an FDA indication for CBD in schizophrenia. Additional studies of CBD for schizophrenia are ongoing.
Bottom Line
Cannabidiol (CBD) is becoming increasingly popular based on its purported health benefits, but the evidence supporting a therapeutic role in psychiatry is preliminary at best. Although CBD is now available by prescription as an FDA-approved drug for the treatment of 2 rare forms of epilepsy, its benefits in patients with schizophrenia are uncertain based on mixed results in clinical trials.
Related Resources
- Clinicaltrials.gov. Studies of “cannabidiol” and “schizophrenia.” U.S. National Library of Medicine. https://clinicaltrials.gov/ct2/results?cond=Schizophrenia&term=cannabidiol.
- Grinspoon P. Cannabidiol (CBD) – what we know and what we don’t. Harvard Health Blog. https://www.health.harvard.edu/blog/cannabidiol-cbd-what-we-know-and-what-wedont-2018082414476. Published August 24, 2018.
Drug Brand Names
Cannabidiol • Epidiolex
Dronabinol • Marinol
Risperidone • Risperdal
1. Pierre JM. Cannabis, synthetic cannabinoids, and psychosis risk: what the evidence says. Current Psychiatry. 2011;10(9):49-58.
2. Radhakrishan R, Wilkinson ST, D’Souza DC. Gone to pot – a review of the association between cannabis and psychosis. Front Psychiatry. 2014;5:54.
3. Pierre JM. Risks of increasingly potent cannabis: joint effects of potency and frequency. Current Psychiatry. 2016;16(2):14-20.
4. Hanna RC, Perez JM, Ghose S. Cannabis and development of dual diagnoses: a literature review. Am J Drug Alcohol Abuse. 2017;43(4):442-255.
5. Nunberg H, Kilmer B, Pacula RL, et al. An analysis of applicants presenting to a medical marijuana specialty practice in California. J Drug Policy Anal. 2011;4(1):1.
6. Wilkinson ST, Radhakrishnan, D’Souza DC. A systematic review of the evidence for medical marijuana in psychiatric indications. J Clin Psychiatry. 2016;77(8):1050-1064.
7. Tournebize J, Gibaja V, Kahn JP. Acute effects of synthetic cannabinoids: Update 2015. Subst Abus. 2016;38(3):344-366.
8. Crippa JA, Guimarães FS, Campos A, et al. Translational investigation of the therapeutic potential of cannabidiol (CBD): toward a new age. Front Immunol. 2018;9:2009.
9. Schwarz G, Karajgi B. Improvement in refractory psychosis with dronabinol: four case reports. J Clin Psychiatry. 2010;71(11):1552-1553.
10. Schwarz G, Karajgi B, McCarthy R. Synthetic delta-9-tetrahydrocannabinol (dronabinol) can improve the symptoms of schizophrenia. J Clin Psychopharmacol. 2009;29(3):255-258.
11. Meltzer HY, Arvanitis L, Bauer D, et al. Placebo-controlled evaluation of four novel compounds for the treatment of schizophrenia and schizoaffective disorder. Am J Psychiatry. 2004;161(6):975-984.
12. Boggs DL, Kelly DL, McMahon RP, et al. Rimonabant for neurocognition in schizophrenia: a 16-week double blind placebo controlled trial. Schizophr Res. 2012;134(2-3):207-210.
13. Kelly DL, Gorelick DA, Conley RR, et al. Effects of cannabinoid-1 receptor antagonist rimonabant on psychiatric symptoms in overweight people with schizophrenia: a randomized, double-blind, pilot study. J Clin Psychopharmacol. 2011;31(1):86-91.
14. Leweke FM, Mueller JK, Lange B, et al. Therapeutic potential of cannabinoids in psychosis. Biol Psychiatry. 2016;79(7):604-612.
15. Halperin A. What is CBD? The ‘miracle’ cannabis compound that doesn’t get you high. The Guardian. https://www.theguardian.com/society/2018/may/28/what-is-cbd-cannabidiol-cannabis-medical-uses. Published May 28, 2018. Accessed April 3, 2019.
16. Pierre J. Coca, cola, and cannabis: psychoactive drugs as beverages. Psychology Today (blog) Psych Unseen. https://www.psychologytoday.com/us/blog/psych-unseen/201810/coca-cola-and-cannabis-psychoactive-drugs-beverages. Published October 1, 2018. Accessed April 3, 2019.
17. U.S. Food and Drug Administration. FDA approves first drug comprised of an active ingredient derived from marijuana to treat rare, severe forms of epilepsy. FDA News Release. https://www.fda.gov/newsevents/newsroom/pressannouncements/ucm611046.htm. Published June 25, 2018. Accessed April 3, 2019.
18. Devinsky O, Cross JH, Laux L, et al. Trial of cannabidiol for drug-resistant seizures in the Dravet syndrome. N Engl J Med. 2017;376:2011-2020.
19. Thiele EA, March ED, French JA, et al. Cannabidiol in patients with seizures associated with Lennox-Gastaut syndrome (GWPCARE4): a randomised, double-blind, placebo-controlled phase 3 trial. Lancet. 2018;391(10125):1085-1096.
20. Devinsky O, Patel AD, Cross JH, et al. Effect of cannabidiol on drop seizures in the Lennox-Gastaut syndrome. N Engl J Med. 2018;378:1888-1897.
21. Khoury JM, Neves MCLD, Rogue MAV, et al. Is there a role of cannabidiol in psychiatry? World J Biol Psychiatry. 2017:1-16.
22. Zuardi AW, Morais SL, Guimares FS, et al. Antipsychotic effect of cannabidiol. J Clin Psychiatry. 1995;56(10):485-486.
23. Zuardi AW, Hallak JEC, Dursun SM. Cannabidiol monotherapy for treatment-resistant schizophrenia. J Psychopharmacol. 2006;20(5):683-686.
24. Leweke FM, Piomelli D, Pahlisch F, et al. Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Transl Psychiatry. 2012;2:e94. doi: 10.1038/tp.2012.15.
25. McGuire P, Robson P, Cubala WJ, et al. Cannabidiol (CBD) as an adjunctive therapy in schizophrenia: a multicenter randomized controlled trial. Am J Psychiatry. 2018;175(3):225-231.
26. Boggs DL, Surti I, Gupta A, et al. The effects of cannabidiol (CBD) on cognition and symptoms in outpatients with chronic schizophrenia a randomized placebo controlled trial. Psychopharmacol. 2018;235(7):1923-1932.
27. ElSohly MA, Mehmedic Z, Foster S, et al. Changes in cannabis potency over the last 2 decades (1995-2014): analysis of current data in the United States. Biol Psychiatry. 2016; 79(7):613-619.
28. Vandrey R, Raber JC, Raber ME, et al. Cannabinoid dose and label accuracy in edible medical cannabis products. JAMA. 2015;313(24):2491-2492.
29. Ruth AC, Gryniewicz-Ruzicka CM, Trehy ML, et al. Consistency of label claims of internet-purchased hemp oil and cannabis products as determined using IMS and LC-MS: a marketplace study. J Reg Sci. 2016;3:1-6.
30. Bonn-Miller MO, Loflin MJE, Thomas BF, et al. Labeling accuracy of cannabidiol extracts sold online. JAMA. 2017;318(17):1708-1709.
31. Seeman P. Cannabidiol is a partial agonist at dopamine D2High receptors, predicting its antipsychotic clinical dose. Transl Psychiatry. 2016;6(10):e920. doi: 10.1038/tp.2016.195.
32. Renard J, Norris C, Rushlow W, et al. Neuronal and molecular effects of cannabidiol on the mesolimbic dopamine system: implications for novel schizophrenia treatments. Neurosci Biobehav Rev. 2017;157-165.
33. Gururajan A, Malone DT. Does cannabidiol have a role in the treatment of schizophrenia? Schizophr Res. 2016;176(2-3):281-290.
Over the past few decades, it has become increasingly clear that cannabis use can increase the risk of developing a psychotic disorder and worsen the course of existing schizophrenia in a dose-dependent fashion.1-3 Beyond psychosis, although many patients with mental illness use cannabis for recreational purposes or as purported “self-medication,” currently available evidence suggests that marijuana is more likely to represent a harm than a benefit for psychiatric disorders4 (Box4-8). Our current state of knowledge therefore suggests that psychiatrists should caution their patients against using cannabis and prioritize interventions to reduce or discontinue use, especially among those with psychotic disorders.
Box
Data from California in 2006—a decade after the state’s legalization of “medical marijuana”—revealed that 23% of patients in a sample enrolled in medical marijuana clinics were receiving cannabis to treat a mental disorder.5 That was a striking statistic given the dearth of evidence to support a benefit of cannabis for psychiatric conditions at the time, leaving clinicians who provided the necessary recommendations to obtain medical marijuana largely unable to give informed consent about the risks and benefits, much less recommendations about specific products, routes of administration, or dosing. In 2019, we know considerably more about the interaction between cannabinoids and mental health, but research findings thus far warrant more caution than enthusiasm, with one recent review concluding that “whenever an association is observed between cannabis use and psychiatric disorders, the relationship is generally an adverse one.”4
Some critics have argued that the medical marijuana industry represents little more than a front for recreational use. In California and other states that have legalized recreational use, that claim has been rendered all but moot, although the public remains curious about the potential health benefits of cannabinoids and will likely continue to look to clinicians for advice. For those seeking guidance from evidence-based research, the existing state of knowledge can seem like a “Wild West” of anecdotal subjective reports, biased opinions, and uncontrolled clinical studies. Cannabis remains a Schedule I drug at the federal level, and quality clinical research has been limited to a relatively modest number of randomized controlled trials (RCTs), mostly involving FDA-approved cannabinoids rather than smoked cannabis. Randomized controlled trials that have involved smoked marijuana have generally involved low-potency delta-9-tetrahydrocannabinol (THC) cannabis that may not reflect the same therapeutic and adverse effects of the increasingly high potency cannabis now available on the street and in dispensaries.
In psychiatry, a few RCTs are underway exploring cannabis as a viable treatment for mental disorders (eg, posttraumatic stress disorder), but none have yet been completed or published. At best, retrospective studies to date have failed to support a consistent benefit of cannabis for any psychiatric disorder and at worst increasingly suggest a negative impact on psychotic, mood, and anxiety disorders.4,6 Meanwhile, synthetic cannabinoid receptor agonists (eg, “Spice” products) have come to represent a clear public health risk, with both medical and psychiatric toxicity.7
A more cautiously optimistic case for the therapeutic potential of cannabinoids in psychiatry could be made for cannabidiol (CBD), which may possess anxiolytic, antipsychotic, and neuroprotective properties.8 Based on its purported health benefits, it is possible that CBD may even gain widespread popularity as a food supplement. Because a pharmaceutically-manufactured form of CBD was recently FDA-approved for the treatment of seizures associated with Lennox-Gastaut syndrome and Dravet syndrome, off-label prescribing of CBD for psychiatric disorders can be anticipated. While there is not yet sufficient evidence about risks and benefits to justify CBD being recommended broadly in psychiatry, that same informational vacuum has not stopped eager patients from seeking approval for cannabis, and some physicians from providing it.
Despite that conclusion, because cannabis is classified as a Schedule I drug by the US Drug Enforcement Agency, clinical research investigating the risks and benefits of cannabis has been limited. It therefore remains possible that cannabis, or individual cannabinoids such as cannabidiol (CBD), may yet find a therapeutic niche in psychiatry. This article reviews evidence on CBD for the treatment of schizophrenia.
Cannabinergic drugs as potential antipsychotics
Although the bulk of evidence indicates a harmful effect of cannabis in individuals with or at risk for psychosis, there have been a few published cases of schizophrenia improving with dronabinol, an FDA-approved, synthetic form of delta-9-tetrahydrocannabinol (THC).9,10 THC is the constituent of cannabis that produces euphoric effects. These provocative findings have not been replicated in controlled clinical trials, but suggest at least the theoretical possibility of idiosyncratic benefits from THC for some individuals within the psychotic spectrum.
Still, given that most available evidence supports that THC has a harmful effect on psychosis and psychosis risk, researchers have instead performed randomized controlled trials (RCTs) to investigate a possible therapeutic role for medications that oppose the agonist effects of THC at cannabinoid type 1 (CB1) receptors. To date, 2 RCTs comparing rimonabant, a CB1 inverse agonist, with placebo (PLB) in patients with schizophrenia have failed to demonstrate any benefit for psychotic symptoms or cognitive deficits.11,12 A third trial examining rimonabant for people diagnosed with schizophrenia who were overweight found significant benefits for anxiety and depressive symptoms, but none for positive symptoms or the primary outcome of weight loss.13 While these results are discouraging, the role of THC in precipitating psychosis suggests that novel agents opposing the actions of THC on the cannabinoid system could have antipsychotic properties.14
Cannabidiol: An antipsychotic medication?
In contrast to THC, CBD has minimal euphorigenic properties and has recently been heralded in the popular press as a “miracle drug” with benefits for medical and psychiatric disorders alike.15 It has even been speculated that it could become a popular food supplement.16 In 2018, the FDA gave full approval to a pharmaceutically manufactured form of CBD (brand name: Epidiolex) as a novel treatment for 2 rare and severe forms of pediatric epilepsy, Lennox-Gastaut syndrome and Dravet syndrome,17 based on RCTs supporting its efficacy for these often refractory and life-threatening conditions.18-20
In psychiatry, there have not yet been enough robust clinical studies to support broad therapeutic claims for CBD as a treatment for any mental disorder.21 However, there is growing evidence that CBD has potential as an antipsychotic medication. In 1995, the first case report was published describing the efficacy of CBD, 1,500 mg/d, as standalone therapy in a single individual with schizophrenia.22 In 2006, the same research group followed up with a case series in which only 1 out of 3 patients with treatment-refractory schizophrenia improved with flexible dosing of CBD to a maximum dose of 1,280 mg/d.23
There have been 3 published RCTs exploring the efficacy of CBD in schizophrenia (Table24-26). The first study, published in 2012, included 39 adults with schizophrenia who were randomized to 800 mg/d of CBD or amisulpride (AMS), a second-generation antipsychotic that is popular in Europe but is not available in the United States.24 Over 4 weeks of randomized treatment, CBD resulted in as much improvement in overall symptoms and positive symptoms as AMS, and improvement of negative symptoms was significantly greater with CBD. Compared with patients treated with antipsychotic medication, patients who were treated with CBD had fewer extrapyramidal symptoms, less weight gain, and less prolactin elevation. This initial trial suggests that CBD might be as efficacious in schizophrenia as antipsychotic medication, without its burdensome adverse effects. However, this is the only RCT of CBD monotherapy published to date.
Continue to: Two other recently published RCTs...
Two other recently published RCTs compared CBD with PLB as add-on therapy to antipsychotics. McGuire et al25 compared CBD, 1,000 mg/d, to PLB over 6 weeks in 88 patients with schizophrenia. Positive symptom improvement was statistically greater with CBD than with PLB, although the magnitude of clinical change was modest (using the Positive and Negative Syndrome Scale [PANSS] positive symptom subscale: −3.2 points for CBD vs −1.7 points for PLB). Changes in PANSS total score and subscales for general and negative symptoms were not significantly different between treatment groups. There was also no significant difference in overall change in neurocognitive symptoms, although post-hoc analysis revealed significantly greater improvement in motor speed for patients treated with CBD. More than twice the number of patients treated with CBD were rated as “much improved” by the Clinical Global Impressions scale compared with patients treated with PLB, but this was not a statistically significant finding, and most patients experienced only “minimal” or “no improvement.” In terms of adverse events, there were no significant differences between patients in the CBD and PLB groups. Although this study is technically “positive” for CBD and suggests minimal adverse effects, it is not clear whether the statistically significant positive symptom improvements (+1.5 PANSS points for CBD over PLB) were clinically significant.
The most recently published placebo-controlled RCT of CBD as add-on therapy to antipsychotic medication included 36 patients with schizophrenia treated over 6 weeks.26 In this study, there was no benefit of CBD, 600 mg/d, on any PANSS score outcome (total, general, positive, or negative symptoms). For the primary outcome of the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery, there were no significant drug × time effects, and post-hoc analyses showed that only patients treated with PLB improved with time. Sedation was more common among patients treated with CBD compared with PLB.
Making sense of the data
There have been mixed results from the few case reports and 3 RCTs of patients with schizophrenia who were treated with CBD. How can we resolve these disparate findings? A few possible interpretations of the data that warrant clarification through additional research include:
Dosing. In the first case report with positive results, CBD was dosed at 1,500 mg/d,22 whereas in the subsequent case series with mixed results, the maximum allowable dose of CBD was 1,280 mg/d.23 Likewise, in the RCTs, positive results were found when CBD was dosed at 800 to 1,000 mg/d,24,25 but not at 600 mg/d.26 The efficacy of CBD for schizophrenia might depend on higher doses.
Treatment resistance. In the second case series in which only 1 out of 3 patients responded to treatment with CBD,23 the patients had demonstrated previous nonresponse to at least 2 first-generation antipsychotics (FGAs) and risperidone, 6 mg/d. In the RCTs, all patients were antipsychotic-responsive.24-26 Cannabidiol may not be as effective for patients with treatment-refractory schizophrenia as it is for patients with schizophrenia who respond to antipsychotics.
Continue to: Clinical stability
Clinical stability. Within the RCTs, the greatest response was observed in the study that enrolled patients who were hospitalized with acute symptoms of schizophrenia.23 In the 2 studies that found either modest or no benefit with CBD, the patients had been stabilized on antipsychotic medications prior to randomization. Cannabidiol may offer limited benefit as add-on therapy to patients who have already responded to antipsychotic treatment, where there is “less room” for additional improvement.
Monotherapy. Both the case reports22,23 and the RCT with the most robust positive findings24 involved treatment with CBD as monotherapy. For some patients with schizophrenia, CBD might be effective as standalone therapy as an alternative to antipsychotics that is better tolerated. Adding CBD to antipsychotic therapy might be redundant and therefore less effective.
Answering questions about CBD
Cannabidiol is becoming increasingly popular for its purported health benefits. The mixed results of the few studies published on CBD for schizophrenia place clinicians in a difficult position when attempting to answer questions about how cannabinoids might fit into treatment of patients with psychosis. Consider the following:
Is cannabis helpful for patients with schizophrenia? No. Aside from the few case reports suggesting that FDA-approved THC (dronabinol) can improve symptoms in some patients,9,10 most of the evidence from anecdotal reports and both experimental and observational studies indicate that cannabis, THC, and synthetic cannabinoids have a harmful effect in patients with or at risk for psychosis.1-3
If you are considering recommending some form of cannabis to patients with schizophrenia, what kind should you recommend? Recommending or encouraging cannabis use for patients with psychosis is ill-advised. Although certain types of cannabis might contain more THC (eg, Cannabis indica vs Cannabis sativa) or variable amounts of CBD, in general the amount of CBD in whole leaf cannabis is minimal, with the ratio of THC to CBD increasingly significantly over the past decade.3,27 Most forms of cannabis should therefore be avoided by individuals with or at risk for psychotic disorders.
Continue to: What about CBD oil and other CBD products sold in dispensaries?
What about CBD oil and other CBD products sold in dispensaries? Cannabidiol is increasingly available in various forms based on its ability to be designated as a legal hemp product (containing <0.3% THC) at the federal level or as a cannabinoid in states where cannabis is legal. However, several studies have now shown that cannabis products sold online or in dispensaries are often labeled inaccurately, with both under- and over-reporting of THC and CBD content.28-30 Some CBD products have been found to have almost no CBD at all.29,30 The unreliability of product labeling makes it difficult to predict the effects of CBD products that are not subject to FDA purity standards for medications or dietary supplements. It also raises questions about the sources of CBD and the reliability of dosing in the studies discussed above.
Why might CBD work as an antipsychotic? Although CBD has minimal affinity for cannabinoid receptors, it appears to act as a partial agonist of dopamine D2 receptors and an agonist at 5-HT1A receptors, with overall effects that decrease mesolimbic dopamine activity.31,32 In addition, CBD increases the availability of the endogenous cannabinoid anandamide, which may have antipsychotic properties.14,33
Now that the FDA has approved CBD manufactured by a pharmaceutical company, should it be prescribed “off-label” for patients with schizophrenia? This is the “million dollar question,” with insufficient evidence to provide a clear answer. It should now be possible to prescribe FDA-approved CBD for off-label purposes, including the treatment of schizophrenia and other psychiatric disorders. No doubt, some clinicians are already doing so. This will predictably yield more anecdotal evidence about efficacy and adverse effects in the future, but there is not yet adequate evidence to support an FDA indication for CBD in schizophrenia. Additional studies of CBD for schizophrenia are ongoing.
Bottom Line
Cannabidiol (CBD) is becoming increasingly popular based on its purported health benefits, but the evidence supporting a therapeutic role in psychiatry is preliminary at best. Although CBD is now available by prescription as an FDA-approved drug for the treatment of 2 rare forms of epilepsy, its benefits in patients with schizophrenia are uncertain based on mixed results in clinical trials.
Related Resources
- Clinicaltrials.gov. Studies of “cannabidiol” and “schizophrenia.” U.S. National Library of Medicine. https://clinicaltrials.gov/ct2/results?cond=Schizophrenia&term=cannabidiol.
- Grinspoon P. Cannabidiol (CBD) – what we know and what we don’t. Harvard Health Blog. https://www.health.harvard.edu/blog/cannabidiol-cbd-what-we-know-and-what-wedont-2018082414476. Published August 24, 2018.
Drug Brand Names
Cannabidiol • Epidiolex
Dronabinol • Marinol
Risperidone • Risperdal
Over the past few decades, it has become increasingly clear that cannabis use can increase the risk of developing a psychotic disorder and worsen the course of existing schizophrenia in a dose-dependent fashion.1-3 Beyond psychosis, although many patients with mental illness use cannabis for recreational purposes or as purported “self-medication,” currently available evidence suggests that marijuana is more likely to represent a harm than a benefit for psychiatric disorders4 (Box4-8). Our current state of knowledge therefore suggests that psychiatrists should caution their patients against using cannabis and prioritize interventions to reduce or discontinue use, especially among those with psychotic disorders.
Box
Data from California in 2006—a decade after the state’s legalization of “medical marijuana”—revealed that 23% of patients in a sample enrolled in medical marijuana clinics were receiving cannabis to treat a mental disorder.5 That was a striking statistic given the dearth of evidence to support a benefit of cannabis for psychiatric conditions at the time, leaving clinicians who provided the necessary recommendations to obtain medical marijuana largely unable to give informed consent about the risks and benefits, much less recommendations about specific products, routes of administration, or dosing. In 2019, we know considerably more about the interaction between cannabinoids and mental health, but research findings thus far warrant more caution than enthusiasm, with one recent review concluding that “whenever an association is observed between cannabis use and psychiatric disorders, the relationship is generally an adverse one.”4
Some critics have argued that the medical marijuana industry represents little more than a front for recreational use. In California and other states that have legalized recreational use, that claim has been rendered all but moot, although the public remains curious about the potential health benefits of cannabinoids and will likely continue to look to clinicians for advice. For those seeking guidance from evidence-based research, the existing state of knowledge can seem like a “Wild West” of anecdotal subjective reports, biased opinions, and uncontrolled clinical studies. Cannabis remains a Schedule I drug at the federal level, and quality clinical research has been limited to a relatively modest number of randomized controlled trials (RCTs), mostly involving FDA-approved cannabinoids rather than smoked cannabis. Randomized controlled trials that have involved smoked marijuana have generally involved low-potency delta-9-tetrahydrocannabinol (THC) cannabis that may not reflect the same therapeutic and adverse effects of the increasingly high potency cannabis now available on the street and in dispensaries.
In psychiatry, a few RCTs are underway exploring cannabis as a viable treatment for mental disorders (eg, posttraumatic stress disorder), but none have yet been completed or published. At best, retrospective studies to date have failed to support a consistent benefit of cannabis for any psychiatric disorder and at worst increasingly suggest a negative impact on psychotic, mood, and anxiety disorders.4,6 Meanwhile, synthetic cannabinoid receptor agonists (eg, “Spice” products) have come to represent a clear public health risk, with both medical and psychiatric toxicity.7
A more cautiously optimistic case for the therapeutic potential of cannabinoids in psychiatry could be made for cannabidiol (CBD), which may possess anxiolytic, antipsychotic, and neuroprotective properties.8 Based on its purported health benefits, it is possible that CBD may even gain widespread popularity as a food supplement. Because a pharmaceutically-manufactured form of CBD was recently FDA-approved for the treatment of seizures associated with Lennox-Gastaut syndrome and Dravet syndrome, off-label prescribing of CBD for psychiatric disorders can be anticipated. While there is not yet sufficient evidence about risks and benefits to justify CBD being recommended broadly in psychiatry, that same informational vacuum has not stopped eager patients from seeking approval for cannabis, and some physicians from providing it.
Despite that conclusion, because cannabis is classified as a Schedule I drug by the US Drug Enforcement Agency, clinical research investigating the risks and benefits of cannabis has been limited. It therefore remains possible that cannabis, or individual cannabinoids such as cannabidiol (CBD), may yet find a therapeutic niche in psychiatry. This article reviews evidence on CBD for the treatment of schizophrenia.
Cannabinergic drugs as potential antipsychotics
Although the bulk of evidence indicates a harmful effect of cannabis in individuals with or at risk for psychosis, there have been a few published cases of schizophrenia improving with dronabinol, an FDA-approved, synthetic form of delta-9-tetrahydrocannabinol (THC).9,10 THC is the constituent of cannabis that produces euphoric effects. These provocative findings have not been replicated in controlled clinical trials, but suggest at least the theoretical possibility of idiosyncratic benefits from THC for some individuals within the psychotic spectrum.
Still, given that most available evidence supports that THC has a harmful effect on psychosis and psychosis risk, researchers have instead performed randomized controlled trials (RCTs) to investigate a possible therapeutic role for medications that oppose the agonist effects of THC at cannabinoid type 1 (CB1) receptors. To date, 2 RCTs comparing rimonabant, a CB1 inverse agonist, with placebo (PLB) in patients with schizophrenia have failed to demonstrate any benefit for psychotic symptoms or cognitive deficits.11,12 A third trial examining rimonabant for people diagnosed with schizophrenia who were overweight found significant benefits for anxiety and depressive symptoms, but none for positive symptoms or the primary outcome of weight loss.13 While these results are discouraging, the role of THC in precipitating psychosis suggests that novel agents opposing the actions of THC on the cannabinoid system could have antipsychotic properties.14
Cannabidiol: An antipsychotic medication?
In contrast to THC, CBD has minimal euphorigenic properties and has recently been heralded in the popular press as a “miracle drug” with benefits for medical and psychiatric disorders alike.15 It has even been speculated that it could become a popular food supplement.16 In 2018, the FDA gave full approval to a pharmaceutically manufactured form of CBD (brand name: Epidiolex) as a novel treatment for 2 rare and severe forms of pediatric epilepsy, Lennox-Gastaut syndrome and Dravet syndrome,17 based on RCTs supporting its efficacy for these often refractory and life-threatening conditions.18-20
In psychiatry, there have not yet been enough robust clinical studies to support broad therapeutic claims for CBD as a treatment for any mental disorder.21 However, there is growing evidence that CBD has potential as an antipsychotic medication. In 1995, the first case report was published describing the efficacy of CBD, 1,500 mg/d, as standalone therapy in a single individual with schizophrenia.22 In 2006, the same research group followed up with a case series in which only 1 out of 3 patients with treatment-refractory schizophrenia improved with flexible dosing of CBD to a maximum dose of 1,280 mg/d.23
There have been 3 published RCTs exploring the efficacy of CBD in schizophrenia (Table24-26). The first study, published in 2012, included 39 adults with schizophrenia who were randomized to 800 mg/d of CBD or amisulpride (AMS), a second-generation antipsychotic that is popular in Europe but is not available in the United States.24 Over 4 weeks of randomized treatment, CBD resulted in as much improvement in overall symptoms and positive symptoms as AMS, and improvement of negative symptoms was significantly greater with CBD. Compared with patients treated with antipsychotic medication, patients who were treated with CBD had fewer extrapyramidal symptoms, less weight gain, and less prolactin elevation. This initial trial suggests that CBD might be as efficacious in schizophrenia as antipsychotic medication, without its burdensome adverse effects. However, this is the only RCT of CBD monotherapy published to date.
Continue to: Two other recently published RCTs...
Two other recently published RCTs compared CBD with PLB as add-on therapy to antipsychotics. McGuire et al25 compared CBD, 1,000 mg/d, to PLB over 6 weeks in 88 patients with schizophrenia. Positive symptom improvement was statistically greater with CBD than with PLB, although the magnitude of clinical change was modest (using the Positive and Negative Syndrome Scale [PANSS] positive symptom subscale: −3.2 points for CBD vs −1.7 points for PLB). Changes in PANSS total score and subscales for general and negative symptoms were not significantly different between treatment groups. There was also no significant difference in overall change in neurocognitive symptoms, although post-hoc analysis revealed significantly greater improvement in motor speed for patients treated with CBD. More than twice the number of patients treated with CBD were rated as “much improved” by the Clinical Global Impressions scale compared with patients treated with PLB, but this was not a statistically significant finding, and most patients experienced only “minimal” or “no improvement.” In terms of adverse events, there were no significant differences between patients in the CBD and PLB groups. Although this study is technically “positive” for CBD and suggests minimal adverse effects, it is not clear whether the statistically significant positive symptom improvements (+1.5 PANSS points for CBD over PLB) were clinically significant.
The most recently published placebo-controlled RCT of CBD as add-on therapy to antipsychotic medication included 36 patients with schizophrenia treated over 6 weeks.26 In this study, there was no benefit of CBD, 600 mg/d, on any PANSS score outcome (total, general, positive, or negative symptoms). For the primary outcome of the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery, there were no significant drug × time effects, and post-hoc analyses showed that only patients treated with PLB improved with time. Sedation was more common among patients treated with CBD compared with PLB.
Making sense of the data
There have been mixed results from the few case reports and 3 RCTs of patients with schizophrenia who were treated with CBD. How can we resolve these disparate findings? A few possible interpretations of the data that warrant clarification through additional research include:
Dosing. In the first case report with positive results, CBD was dosed at 1,500 mg/d,22 whereas in the subsequent case series with mixed results, the maximum allowable dose of CBD was 1,280 mg/d.23 Likewise, in the RCTs, positive results were found when CBD was dosed at 800 to 1,000 mg/d,24,25 but not at 600 mg/d.26 The efficacy of CBD for schizophrenia might depend on higher doses.
Treatment resistance. In the second case series in which only 1 out of 3 patients responded to treatment with CBD,23 the patients had demonstrated previous nonresponse to at least 2 first-generation antipsychotics (FGAs) and risperidone, 6 mg/d. In the RCTs, all patients were antipsychotic-responsive.24-26 Cannabidiol may not be as effective for patients with treatment-refractory schizophrenia as it is for patients with schizophrenia who respond to antipsychotics.
Continue to: Clinical stability
Clinical stability. Within the RCTs, the greatest response was observed in the study that enrolled patients who were hospitalized with acute symptoms of schizophrenia.23 In the 2 studies that found either modest or no benefit with CBD, the patients had been stabilized on antipsychotic medications prior to randomization. Cannabidiol may offer limited benefit as add-on therapy to patients who have already responded to antipsychotic treatment, where there is “less room” for additional improvement.
Monotherapy. Both the case reports22,23 and the RCT with the most robust positive findings24 involved treatment with CBD as monotherapy. For some patients with schizophrenia, CBD might be effective as standalone therapy as an alternative to antipsychotics that is better tolerated. Adding CBD to antipsychotic therapy might be redundant and therefore less effective.
Answering questions about CBD
Cannabidiol is becoming increasingly popular for its purported health benefits. The mixed results of the few studies published on CBD for schizophrenia place clinicians in a difficult position when attempting to answer questions about how cannabinoids might fit into treatment of patients with psychosis. Consider the following:
Is cannabis helpful for patients with schizophrenia? No. Aside from the few case reports suggesting that FDA-approved THC (dronabinol) can improve symptoms in some patients,9,10 most of the evidence from anecdotal reports and both experimental and observational studies indicate that cannabis, THC, and synthetic cannabinoids have a harmful effect in patients with or at risk for psychosis.1-3
If you are considering recommending some form of cannabis to patients with schizophrenia, what kind should you recommend? Recommending or encouraging cannabis use for patients with psychosis is ill-advised. Although certain types of cannabis might contain more THC (eg, Cannabis indica vs Cannabis sativa) or variable amounts of CBD, in general the amount of CBD in whole leaf cannabis is minimal, with the ratio of THC to CBD increasingly significantly over the past decade.3,27 Most forms of cannabis should therefore be avoided by individuals with or at risk for psychotic disorders.
Continue to: What about CBD oil and other CBD products sold in dispensaries?
What about CBD oil and other CBD products sold in dispensaries? Cannabidiol is increasingly available in various forms based on its ability to be designated as a legal hemp product (containing <0.3% THC) at the federal level or as a cannabinoid in states where cannabis is legal. However, several studies have now shown that cannabis products sold online or in dispensaries are often labeled inaccurately, with both under- and over-reporting of THC and CBD content.28-30 Some CBD products have been found to have almost no CBD at all.29,30 The unreliability of product labeling makes it difficult to predict the effects of CBD products that are not subject to FDA purity standards for medications or dietary supplements. It also raises questions about the sources of CBD and the reliability of dosing in the studies discussed above.
Why might CBD work as an antipsychotic? Although CBD has minimal affinity for cannabinoid receptors, it appears to act as a partial agonist of dopamine D2 receptors and an agonist at 5-HT1A receptors, with overall effects that decrease mesolimbic dopamine activity.31,32 In addition, CBD increases the availability of the endogenous cannabinoid anandamide, which may have antipsychotic properties.14,33
Now that the FDA has approved CBD manufactured by a pharmaceutical company, should it be prescribed “off-label” for patients with schizophrenia? This is the “million dollar question,” with insufficient evidence to provide a clear answer. It should now be possible to prescribe FDA-approved CBD for off-label purposes, including the treatment of schizophrenia and other psychiatric disorders. No doubt, some clinicians are already doing so. This will predictably yield more anecdotal evidence about efficacy and adverse effects in the future, but there is not yet adequate evidence to support an FDA indication for CBD in schizophrenia. Additional studies of CBD for schizophrenia are ongoing.
Bottom Line
Cannabidiol (CBD) is becoming increasingly popular based on its purported health benefits, but the evidence supporting a therapeutic role in psychiatry is preliminary at best. Although CBD is now available by prescription as an FDA-approved drug for the treatment of 2 rare forms of epilepsy, its benefits in patients with schizophrenia are uncertain based on mixed results in clinical trials.
Related Resources
- Clinicaltrials.gov. Studies of “cannabidiol” and “schizophrenia.” U.S. National Library of Medicine. https://clinicaltrials.gov/ct2/results?cond=Schizophrenia&term=cannabidiol.
- Grinspoon P. Cannabidiol (CBD) – what we know and what we don’t. Harvard Health Blog. https://www.health.harvard.edu/blog/cannabidiol-cbd-what-we-know-and-what-wedont-2018082414476. Published August 24, 2018.
Drug Brand Names
Cannabidiol • Epidiolex
Dronabinol • Marinol
Risperidone • Risperdal
1. Pierre JM. Cannabis, synthetic cannabinoids, and psychosis risk: what the evidence says. Current Psychiatry. 2011;10(9):49-58.
2. Radhakrishan R, Wilkinson ST, D’Souza DC. Gone to pot – a review of the association between cannabis and psychosis. Front Psychiatry. 2014;5:54.
3. Pierre JM. Risks of increasingly potent cannabis: joint effects of potency and frequency. Current Psychiatry. 2016;16(2):14-20.
4. Hanna RC, Perez JM, Ghose S. Cannabis and development of dual diagnoses: a literature review. Am J Drug Alcohol Abuse. 2017;43(4):442-255.
5. Nunberg H, Kilmer B, Pacula RL, et al. An analysis of applicants presenting to a medical marijuana specialty practice in California. J Drug Policy Anal. 2011;4(1):1.
6. Wilkinson ST, Radhakrishnan, D’Souza DC. A systematic review of the evidence for medical marijuana in psychiatric indications. J Clin Psychiatry. 2016;77(8):1050-1064.
7. Tournebize J, Gibaja V, Kahn JP. Acute effects of synthetic cannabinoids: Update 2015. Subst Abus. 2016;38(3):344-366.
8. Crippa JA, Guimarães FS, Campos A, et al. Translational investigation of the therapeutic potential of cannabidiol (CBD): toward a new age. Front Immunol. 2018;9:2009.
9. Schwarz G, Karajgi B. Improvement in refractory psychosis with dronabinol: four case reports. J Clin Psychiatry. 2010;71(11):1552-1553.
10. Schwarz G, Karajgi B, McCarthy R. Synthetic delta-9-tetrahydrocannabinol (dronabinol) can improve the symptoms of schizophrenia. J Clin Psychopharmacol. 2009;29(3):255-258.
11. Meltzer HY, Arvanitis L, Bauer D, et al. Placebo-controlled evaluation of four novel compounds for the treatment of schizophrenia and schizoaffective disorder. Am J Psychiatry. 2004;161(6):975-984.
12. Boggs DL, Kelly DL, McMahon RP, et al. Rimonabant for neurocognition in schizophrenia: a 16-week double blind placebo controlled trial. Schizophr Res. 2012;134(2-3):207-210.
13. Kelly DL, Gorelick DA, Conley RR, et al. Effects of cannabinoid-1 receptor antagonist rimonabant on psychiatric symptoms in overweight people with schizophrenia: a randomized, double-blind, pilot study. J Clin Psychopharmacol. 2011;31(1):86-91.
14. Leweke FM, Mueller JK, Lange B, et al. Therapeutic potential of cannabinoids in psychosis. Biol Psychiatry. 2016;79(7):604-612.
15. Halperin A. What is CBD? The ‘miracle’ cannabis compound that doesn’t get you high. The Guardian. https://www.theguardian.com/society/2018/may/28/what-is-cbd-cannabidiol-cannabis-medical-uses. Published May 28, 2018. Accessed April 3, 2019.
16. Pierre J. Coca, cola, and cannabis: psychoactive drugs as beverages. Psychology Today (blog) Psych Unseen. https://www.psychologytoday.com/us/blog/psych-unseen/201810/coca-cola-and-cannabis-psychoactive-drugs-beverages. Published October 1, 2018. Accessed April 3, 2019.
17. U.S. Food and Drug Administration. FDA approves first drug comprised of an active ingredient derived from marijuana to treat rare, severe forms of epilepsy. FDA News Release. https://www.fda.gov/newsevents/newsroom/pressannouncements/ucm611046.htm. Published June 25, 2018. Accessed April 3, 2019.
18. Devinsky O, Cross JH, Laux L, et al. Trial of cannabidiol for drug-resistant seizures in the Dravet syndrome. N Engl J Med. 2017;376:2011-2020.
19. Thiele EA, March ED, French JA, et al. Cannabidiol in patients with seizures associated with Lennox-Gastaut syndrome (GWPCARE4): a randomised, double-blind, placebo-controlled phase 3 trial. Lancet. 2018;391(10125):1085-1096.
20. Devinsky O, Patel AD, Cross JH, et al. Effect of cannabidiol on drop seizures in the Lennox-Gastaut syndrome. N Engl J Med. 2018;378:1888-1897.
21. Khoury JM, Neves MCLD, Rogue MAV, et al. Is there a role of cannabidiol in psychiatry? World J Biol Psychiatry. 2017:1-16.
22. Zuardi AW, Morais SL, Guimares FS, et al. Antipsychotic effect of cannabidiol. J Clin Psychiatry. 1995;56(10):485-486.
23. Zuardi AW, Hallak JEC, Dursun SM. Cannabidiol monotherapy for treatment-resistant schizophrenia. J Psychopharmacol. 2006;20(5):683-686.
24. Leweke FM, Piomelli D, Pahlisch F, et al. Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Transl Psychiatry. 2012;2:e94. doi: 10.1038/tp.2012.15.
25. McGuire P, Robson P, Cubala WJ, et al. Cannabidiol (CBD) as an adjunctive therapy in schizophrenia: a multicenter randomized controlled trial. Am J Psychiatry. 2018;175(3):225-231.
26. Boggs DL, Surti I, Gupta A, et al. The effects of cannabidiol (CBD) on cognition and symptoms in outpatients with chronic schizophrenia a randomized placebo controlled trial. Psychopharmacol. 2018;235(7):1923-1932.
27. ElSohly MA, Mehmedic Z, Foster S, et al. Changes in cannabis potency over the last 2 decades (1995-2014): analysis of current data in the United States. Biol Psychiatry. 2016; 79(7):613-619.
28. Vandrey R, Raber JC, Raber ME, et al. Cannabinoid dose and label accuracy in edible medical cannabis products. JAMA. 2015;313(24):2491-2492.
29. Ruth AC, Gryniewicz-Ruzicka CM, Trehy ML, et al. Consistency of label claims of internet-purchased hemp oil and cannabis products as determined using IMS and LC-MS: a marketplace study. J Reg Sci. 2016;3:1-6.
30. Bonn-Miller MO, Loflin MJE, Thomas BF, et al. Labeling accuracy of cannabidiol extracts sold online. JAMA. 2017;318(17):1708-1709.
31. Seeman P. Cannabidiol is a partial agonist at dopamine D2High receptors, predicting its antipsychotic clinical dose. Transl Psychiatry. 2016;6(10):e920. doi: 10.1038/tp.2016.195.
32. Renard J, Norris C, Rushlow W, et al. Neuronal and molecular effects of cannabidiol on the mesolimbic dopamine system: implications for novel schizophrenia treatments. Neurosci Biobehav Rev. 2017;157-165.
33. Gururajan A, Malone DT. Does cannabidiol have a role in the treatment of schizophrenia? Schizophr Res. 2016;176(2-3):281-290.
1. Pierre JM. Cannabis, synthetic cannabinoids, and psychosis risk: what the evidence says. Current Psychiatry. 2011;10(9):49-58.
2. Radhakrishan R, Wilkinson ST, D’Souza DC. Gone to pot – a review of the association between cannabis and psychosis. Front Psychiatry. 2014;5:54.
3. Pierre JM. Risks of increasingly potent cannabis: joint effects of potency and frequency. Current Psychiatry. 2016;16(2):14-20.
4. Hanna RC, Perez JM, Ghose S. Cannabis and development of dual diagnoses: a literature review. Am J Drug Alcohol Abuse. 2017;43(4):442-255.
5. Nunberg H, Kilmer B, Pacula RL, et al. An analysis of applicants presenting to a medical marijuana specialty practice in California. J Drug Policy Anal. 2011;4(1):1.
6. Wilkinson ST, Radhakrishnan, D’Souza DC. A systematic review of the evidence for medical marijuana in psychiatric indications. J Clin Psychiatry. 2016;77(8):1050-1064.
7. Tournebize J, Gibaja V, Kahn JP. Acute effects of synthetic cannabinoids: Update 2015. Subst Abus. 2016;38(3):344-366.
8. Crippa JA, Guimarães FS, Campos A, et al. Translational investigation of the therapeutic potential of cannabidiol (CBD): toward a new age. Front Immunol. 2018;9:2009.
9. Schwarz G, Karajgi B. Improvement in refractory psychosis with dronabinol: four case reports. J Clin Psychiatry. 2010;71(11):1552-1553.
10. Schwarz G, Karajgi B, McCarthy R. Synthetic delta-9-tetrahydrocannabinol (dronabinol) can improve the symptoms of schizophrenia. J Clin Psychopharmacol. 2009;29(3):255-258.
11. Meltzer HY, Arvanitis L, Bauer D, et al. Placebo-controlled evaluation of four novel compounds for the treatment of schizophrenia and schizoaffective disorder. Am J Psychiatry. 2004;161(6):975-984.
12. Boggs DL, Kelly DL, McMahon RP, et al. Rimonabant for neurocognition in schizophrenia: a 16-week double blind placebo controlled trial. Schizophr Res. 2012;134(2-3):207-210.
13. Kelly DL, Gorelick DA, Conley RR, et al. Effects of cannabinoid-1 receptor antagonist rimonabant on psychiatric symptoms in overweight people with schizophrenia: a randomized, double-blind, pilot study. J Clin Psychopharmacol. 2011;31(1):86-91.
14. Leweke FM, Mueller JK, Lange B, et al. Therapeutic potential of cannabinoids in psychosis. Biol Psychiatry. 2016;79(7):604-612.
15. Halperin A. What is CBD? The ‘miracle’ cannabis compound that doesn’t get you high. The Guardian. https://www.theguardian.com/society/2018/may/28/what-is-cbd-cannabidiol-cannabis-medical-uses. Published May 28, 2018. Accessed April 3, 2019.
16. Pierre J. Coca, cola, and cannabis: psychoactive drugs as beverages. Psychology Today (blog) Psych Unseen. https://www.psychologytoday.com/us/blog/psych-unseen/201810/coca-cola-and-cannabis-psychoactive-drugs-beverages. Published October 1, 2018. Accessed April 3, 2019.
17. U.S. Food and Drug Administration. FDA approves first drug comprised of an active ingredient derived from marijuana to treat rare, severe forms of epilepsy. FDA News Release. https://www.fda.gov/newsevents/newsroom/pressannouncements/ucm611046.htm. Published June 25, 2018. Accessed April 3, 2019.
18. Devinsky O, Cross JH, Laux L, et al. Trial of cannabidiol for drug-resistant seizures in the Dravet syndrome. N Engl J Med. 2017;376:2011-2020.
19. Thiele EA, March ED, French JA, et al. Cannabidiol in patients with seizures associated with Lennox-Gastaut syndrome (GWPCARE4): a randomised, double-blind, placebo-controlled phase 3 trial. Lancet. 2018;391(10125):1085-1096.
20. Devinsky O, Patel AD, Cross JH, et al. Effect of cannabidiol on drop seizures in the Lennox-Gastaut syndrome. N Engl J Med. 2018;378:1888-1897.
21. Khoury JM, Neves MCLD, Rogue MAV, et al. Is there a role of cannabidiol in psychiatry? World J Biol Psychiatry. 2017:1-16.
22. Zuardi AW, Morais SL, Guimares FS, et al. Antipsychotic effect of cannabidiol. J Clin Psychiatry. 1995;56(10):485-486.
23. Zuardi AW, Hallak JEC, Dursun SM. Cannabidiol monotherapy for treatment-resistant schizophrenia. J Psychopharmacol. 2006;20(5):683-686.
24. Leweke FM, Piomelli D, Pahlisch F, et al. Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Transl Psychiatry. 2012;2:e94. doi: 10.1038/tp.2012.15.
25. McGuire P, Robson P, Cubala WJ, et al. Cannabidiol (CBD) as an adjunctive therapy in schizophrenia: a multicenter randomized controlled trial. Am J Psychiatry. 2018;175(3):225-231.
26. Boggs DL, Surti I, Gupta A, et al. The effects of cannabidiol (CBD) on cognition and symptoms in outpatients with chronic schizophrenia a randomized placebo controlled trial. Psychopharmacol. 2018;235(7):1923-1932.
27. ElSohly MA, Mehmedic Z, Foster S, et al. Changes in cannabis potency over the last 2 decades (1995-2014): analysis of current data in the United States. Biol Psychiatry. 2016; 79(7):613-619.
28. Vandrey R, Raber JC, Raber ME, et al. Cannabinoid dose and label accuracy in edible medical cannabis products. JAMA. 2015;313(24):2491-2492.
29. Ruth AC, Gryniewicz-Ruzicka CM, Trehy ML, et al. Consistency of label claims of internet-purchased hemp oil and cannabis products as determined using IMS and LC-MS: a marketplace study. J Reg Sci. 2016;3:1-6.
30. Bonn-Miller MO, Loflin MJE, Thomas BF, et al. Labeling accuracy of cannabidiol extracts sold online. JAMA. 2017;318(17):1708-1709.
31. Seeman P. Cannabidiol is a partial agonist at dopamine D2High receptors, predicting its antipsychotic clinical dose. Transl Psychiatry. 2016;6(10):e920. doi: 10.1038/tp.2016.195.
32. Renard J, Norris C, Rushlow W, et al. Neuronal and molecular effects of cannabidiol on the mesolimbic dopamine system: implications for novel schizophrenia treatments. Neurosci Biobehav Rev. 2017;157-165.
33. Gururajan A, Malone DT. Does cannabidiol have a role in the treatment of schizophrenia? Schizophr Res. 2016;176(2-3):281-290.
Marijuana during prenatal OUD treatment increases premature birth
BALTIMORE – Marijuana is a not a good idea during pregnancy, and it’s an even worse idea when women are being treated for opioid addiction, according to an investigation from East Tennessee State University, Mountain Home.
Marijuana use may become more common as legalization rolls out across the country, and legalization, in turn, may add to the perception that pot is harmless, and maybe a good way to take the edge off during pregnancy and prevent morning sickness, said neonatologist Darshan Shaw, MD, of the department of pediatrics at the university.
Dr. Shaw wondered how that trend might impact treatment of opioid use disorder (OUD) during pregnancy, which has also become more common. The take-home is that “if you have a pregnant patient on medically assistant therapy” for opioid addition, “you should warn them against use of marijuana. It increases the risk of prematurity and low birth weight,” he said at the Pediatric Academic Societies annual meeting.
He and his team reviewed 2,375 opioid-exposed pregnancies at six hospitals in south-central Appalachia from July 2011 to June 2016. All of the women had used opioids during pregnancy, some illegally and others for opioid use disorder (OUD) treatment or other medical issues; 108 had urine screens that were positive for tetrahydrocannabinol (THC) at the time of delivery.
Infants were born a mean of 3 days earlier in the marijuana group, and a mean of 265 g lighter. They were also more likely to be born before 37 weeks’ gestation (14% versus 6.5%); born weighing less than 2,500 g (17.6% versus 7.3%); and more likely to be admitted to the neonatal ICU (17.5% versus 7.1%).
On logistic regression to control for parity, maternal status, and tobacco and benzodiazepine use, prenatal marijuana exposure more than doubled the risk of prematurity (odds ratio, 2.35; 95% confidence interval, 1.3-4.23); tobacco and benzodiazepines did not increase the risk. Marijuana also doubled the risk of low birth weight (OR, 2.02; 95% CI, 1.18-3.47), about the same as tobacco and benzodiazepines.
The study had limitations. There was no controlling for a major confounder: the amount of opioids woman took while pregnant. These data were not available, Dr. Shaw said.
Neonatal abstinence syndrome was more common in the marijuana group (33.3% versus 18.1%), so it’s possible that women who used marijuana also used more opioids. “We suspect that opioid exposure was not uniform among all infants,” he said. There were also no data on the amount or way marijuana was used.
Marijuana-positive women were more likely to be unmarried, nulliparous, and use tobacco and benzodiazepines.
There was no industry funding for the work, and Dr. Shaw had no disclosures.
BALTIMORE – Marijuana is a not a good idea during pregnancy, and it’s an even worse idea when women are being treated for opioid addiction, according to an investigation from East Tennessee State University, Mountain Home.
Marijuana use may become more common as legalization rolls out across the country, and legalization, in turn, may add to the perception that pot is harmless, and maybe a good way to take the edge off during pregnancy and prevent morning sickness, said neonatologist Darshan Shaw, MD, of the department of pediatrics at the university.
Dr. Shaw wondered how that trend might impact treatment of opioid use disorder (OUD) during pregnancy, which has also become more common. The take-home is that “if you have a pregnant patient on medically assistant therapy” for opioid addition, “you should warn them against use of marijuana. It increases the risk of prematurity and low birth weight,” he said at the Pediatric Academic Societies annual meeting.
He and his team reviewed 2,375 opioid-exposed pregnancies at six hospitals in south-central Appalachia from July 2011 to June 2016. All of the women had used opioids during pregnancy, some illegally and others for opioid use disorder (OUD) treatment or other medical issues; 108 had urine screens that were positive for tetrahydrocannabinol (THC) at the time of delivery.
Infants were born a mean of 3 days earlier in the marijuana group, and a mean of 265 g lighter. They were also more likely to be born before 37 weeks’ gestation (14% versus 6.5%); born weighing less than 2,500 g (17.6% versus 7.3%); and more likely to be admitted to the neonatal ICU (17.5% versus 7.1%).
On logistic regression to control for parity, maternal status, and tobacco and benzodiazepine use, prenatal marijuana exposure more than doubled the risk of prematurity (odds ratio, 2.35; 95% confidence interval, 1.3-4.23); tobacco and benzodiazepines did not increase the risk. Marijuana also doubled the risk of low birth weight (OR, 2.02; 95% CI, 1.18-3.47), about the same as tobacco and benzodiazepines.
The study had limitations. There was no controlling for a major confounder: the amount of opioids woman took while pregnant. These data were not available, Dr. Shaw said.
Neonatal abstinence syndrome was more common in the marijuana group (33.3% versus 18.1%), so it’s possible that women who used marijuana also used more opioids. “We suspect that opioid exposure was not uniform among all infants,” he said. There were also no data on the amount or way marijuana was used.
Marijuana-positive women were more likely to be unmarried, nulliparous, and use tobacco and benzodiazepines.
There was no industry funding for the work, and Dr. Shaw had no disclosures.
BALTIMORE – Marijuana is a not a good idea during pregnancy, and it’s an even worse idea when women are being treated for opioid addiction, according to an investigation from East Tennessee State University, Mountain Home.
Marijuana use may become more common as legalization rolls out across the country, and legalization, in turn, may add to the perception that pot is harmless, and maybe a good way to take the edge off during pregnancy and prevent morning sickness, said neonatologist Darshan Shaw, MD, of the department of pediatrics at the university.
Dr. Shaw wondered how that trend might impact treatment of opioid use disorder (OUD) during pregnancy, which has also become more common. The take-home is that “if you have a pregnant patient on medically assistant therapy” for opioid addition, “you should warn them against use of marijuana. It increases the risk of prematurity and low birth weight,” he said at the Pediatric Academic Societies annual meeting.
He and his team reviewed 2,375 opioid-exposed pregnancies at six hospitals in south-central Appalachia from July 2011 to June 2016. All of the women had used opioids during pregnancy, some illegally and others for opioid use disorder (OUD) treatment or other medical issues; 108 had urine screens that were positive for tetrahydrocannabinol (THC) at the time of delivery.
Infants were born a mean of 3 days earlier in the marijuana group, and a mean of 265 g lighter. They were also more likely to be born before 37 weeks’ gestation (14% versus 6.5%); born weighing less than 2,500 g (17.6% versus 7.3%); and more likely to be admitted to the neonatal ICU (17.5% versus 7.1%).
On logistic regression to control for parity, maternal status, and tobacco and benzodiazepine use, prenatal marijuana exposure more than doubled the risk of prematurity (odds ratio, 2.35; 95% confidence interval, 1.3-4.23); tobacco and benzodiazepines did not increase the risk. Marijuana also doubled the risk of low birth weight (OR, 2.02; 95% CI, 1.18-3.47), about the same as tobacco and benzodiazepines.
The study had limitations. There was no controlling for a major confounder: the amount of opioids woman took while pregnant. These data were not available, Dr. Shaw said.
Neonatal abstinence syndrome was more common in the marijuana group (33.3% versus 18.1%), so it’s possible that women who used marijuana also used more opioids. “We suspect that opioid exposure was not uniform among all infants,” he said. There were also no data on the amount or way marijuana was used.
Marijuana-positive women were more likely to be unmarried, nulliparous, and use tobacco and benzodiazepines.
There was no industry funding for the work, and Dr. Shaw had no disclosures.
REPORTING FROM PAS 2019
Key clinical point: Warn pregnant women being treated for opioid use disorder to stay away from marijuana.
Major finding: Marijuana use more than doubled the risk of prematurity and low birth weight.
Study details: Review of 2,375 opioid-exposed pregnancies at six hospitals
Disclosures: There was no industry funding for the work, and the lead investigator had no disclosures.
