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Medical Cannabis for Chronic Pain Tied to Arrhythmia Risk
TOPLINE:
, mainly atrial fibrillation/flutter, a Danish registry study suggested. Cannabis use has been associated with increased cardiovascular (CV) risk, but data on CV side effects with use of medical cannabis for chronic pain are limited.
METHODOLOGY:
- To investigate, researchers identified 5391 patients with chronic pain (median age 59; 63% women) initiating first-time treatment with medical cannabis during 2018-2021 and matched them (1:5) to 26,941 control patients on age, sex, chronic pain diagnosis, and concomitant use of other noncannabis pain medication.
- They calculated and compared absolute risks for first-time arrhythmia (atrial fibrillation/flutter, conduction disorders, paroxysmal tachycardias, and ventricular arrhythmias) and acute coronary syndrome (ACS) between groups.
TAKEAWAY:
- Within 180 days, 42 medical cannabis users and 107 control participants developed arrhythmia, most commonly atrial fibrillation/flutter.
- Medical cannabis users had a slightly elevated risk for new-onset arrhythmia compared with nonusers (180-day absolute risk, 0.8% vs 0.4%).
- The 180-day risk ratio with cannabis use was 2.07 (95% CI, 1.34-2.80), and the 1-year risk ratio was 1.36 (95% CI, 1.00-1.73).
- Adults with cancer or cardiometabolic disease had the highest risk for arrhythmia with cannabis use (180-day absolute risk difference, 1.1% and 0.8%). There was no significant association between medical cannabis use and ACS risk.
IN PRACTICE:
“With the investigated cohort’s low age and low prevalence of comorbidity in mind, the notable relative risk increase of new-onset arrhythmia, mainly driven by atrial fibrillation/flutter, could be a reason for concern, albeit the absolute risks in this study population were modest,” the authors wrote.
“Medical cannabis may not be a ‘one-size-fits-all’ therapeutic option for certain medical conditions and should be contextualized based on patient comorbidities and potential vulnerability to side effects,” added the author of an editorial.
SOURCE:
The study, led by Anders Holt, MD, Copenhagen University and Herlev-Gentofte Hospital, Hellerup, Denmark, was published online on January 11, 2024, in the European Heart Journal, with an editorial by Robert Page II, PharmD, MSPH, University of Colorado, Aurora.
LIMITATIONS:
Residual confounding is possible. The registers lack information on disease severity, clinical measures, blood tests, and lifestyle factors. The route of cannabis administration was not known.
DISCLOSURES:
The study was funded by external and independent medical research grants. Holt had no relevant disclosures. Some coauthors reported research grants and speakers’ fees from various drug companies.
A version of this article appeared on Medscape.com.
TOPLINE:
, mainly atrial fibrillation/flutter, a Danish registry study suggested. Cannabis use has been associated with increased cardiovascular (CV) risk, but data on CV side effects with use of medical cannabis for chronic pain are limited.
METHODOLOGY:
- To investigate, researchers identified 5391 patients with chronic pain (median age 59; 63% women) initiating first-time treatment with medical cannabis during 2018-2021 and matched them (1:5) to 26,941 control patients on age, sex, chronic pain diagnosis, and concomitant use of other noncannabis pain medication.
- They calculated and compared absolute risks for first-time arrhythmia (atrial fibrillation/flutter, conduction disorders, paroxysmal tachycardias, and ventricular arrhythmias) and acute coronary syndrome (ACS) between groups.
TAKEAWAY:
- Within 180 days, 42 medical cannabis users and 107 control participants developed arrhythmia, most commonly atrial fibrillation/flutter.
- Medical cannabis users had a slightly elevated risk for new-onset arrhythmia compared with nonusers (180-day absolute risk, 0.8% vs 0.4%).
- The 180-day risk ratio with cannabis use was 2.07 (95% CI, 1.34-2.80), and the 1-year risk ratio was 1.36 (95% CI, 1.00-1.73).
- Adults with cancer or cardiometabolic disease had the highest risk for arrhythmia with cannabis use (180-day absolute risk difference, 1.1% and 0.8%). There was no significant association between medical cannabis use and ACS risk.
IN PRACTICE:
“With the investigated cohort’s low age and low prevalence of comorbidity in mind, the notable relative risk increase of new-onset arrhythmia, mainly driven by atrial fibrillation/flutter, could be a reason for concern, albeit the absolute risks in this study population were modest,” the authors wrote.
“Medical cannabis may not be a ‘one-size-fits-all’ therapeutic option for certain medical conditions and should be contextualized based on patient comorbidities and potential vulnerability to side effects,” added the author of an editorial.
SOURCE:
The study, led by Anders Holt, MD, Copenhagen University and Herlev-Gentofte Hospital, Hellerup, Denmark, was published online on January 11, 2024, in the European Heart Journal, with an editorial by Robert Page II, PharmD, MSPH, University of Colorado, Aurora.
LIMITATIONS:
Residual confounding is possible. The registers lack information on disease severity, clinical measures, blood tests, and lifestyle factors. The route of cannabis administration was not known.
DISCLOSURES:
The study was funded by external and independent medical research grants. Holt had no relevant disclosures. Some coauthors reported research grants and speakers’ fees from various drug companies.
A version of this article appeared on Medscape.com.
TOPLINE:
, mainly atrial fibrillation/flutter, a Danish registry study suggested. Cannabis use has been associated with increased cardiovascular (CV) risk, but data on CV side effects with use of medical cannabis for chronic pain are limited.
METHODOLOGY:
- To investigate, researchers identified 5391 patients with chronic pain (median age 59; 63% women) initiating first-time treatment with medical cannabis during 2018-2021 and matched them (1:5) to 26,941 control patients on age, sex, chronic pain diagnosis, and concomitant use of other noncannabis pain medication.
- They calculated and compared absolute risks for first-time arrhythmia (atrial fibrillation/flutter, conduction disorders, paroxysmal tachycardias, and ventricular arrhythmias) and acute coronary syndrome (ACS) between groups.
TAKEAWAY:
- Within 180 days, 42 medical cannabis users and 107 control participants developed arrhythmia, most commonly atrial fibrillation/flutter.
- Medical cannabis users had a slightly elevated risk for new-onset arrhythmia compared with nonusers (180-day absolute risk, 0.8% vs 0.4%).
- The 180-day risk ratio with cannabis use was 2.07 (95% CI, 1.34-2.80), and the 1-year risk ratio was 1.36 (95% CI, 1.00-1.73).
- Adults with cancer or cardiometabolic disease had the highest risk for arrhythmia with cannabis use (180-day absolute risk difference, 1.1% and 0.8%). There was no significant association between medical cannabis use and ACS risk.
IN PRACTICE:
“With the investigated cohort’s low age and low prevalence of comorbidity in mind, the notable relative risk increase of new-onset arrhythmia, mainly driven by atrial fibrillation/flutter, could be a reason for concern, albeit the absolute risks in this study population were modest,” the authors wrote.
“Medical cannabis may not be a ‘one-size-fits-all’ therapeutic option for certain medical conditions and should be contextualized based on patient comorbidities and potential vulnerability to side effects,” added the author of an editorial.
SOURCE:
The study, led by Anders Holt, MD, Copenhagen University and Herlev-Gentofte Hospital, Hellerup, Denmark, was published online on January 11, 2024, in the European Heart Journal, with an editorial by Robert Page II, PharmD, MSPH, University of Colorado, Aurora.
LIMITATIONS:
Residual confounding is possible. The registers lack information on disease severity, clinical measures, blood tests, and lifestyle factors. The route of cannabis administration was not known.
DISCLOSURES:
The study was funded by external and independent medical research grants. Holt had no relevant disclosures. Some coauthors reported research grants and speakers’ fees from various drug companies.
A version of this article appeared on Medscape.com.
Higher-Dose Atypical Antipsychotics Risky in Young Adults
High doses of a second-generation antipsychotic are associated with a significantly increased risk for death in young adults, adding to longstanding safety concerns regarding the use of higher doses of antipsychotic medication in this age group.
In a large cohort study, people aged 18-24 years had a significantly higher risk for death when starting a second-generation antipsychotic at doses greater than 100-mg chlorpromazine equivalents, but no increased mortality risk with lower doses.
There was no association with mortality risk in children aged 5-17 years with either dose.
“This finding suggests that antipsychotic medication–related fatalities are rare in healthy children without psychosis,” lead investigator Wayne Ray, PhD, from Vanderbilt University School of Medicine in Nashville, Tennessee, and colleagues wrote in a recent study that was published online in JAMA Psychiatry.
“In contrast, young adults aged 18-24 years treated with doses greater than 100-mg chlorpromazine equivalents had 127.5 additional deaths for every 100,000 person-years of exposure, suggesting further investigations of antipsychotic medication safety in this population are needed.”
Large, Retrospective Study
The researchers compared mortality for more than 2 million Medicaid patients aged 5-24 years (mean age, 13 years; 51% men) starting treatment with a second-generation antipsychotic vs control psychiatric medications. None of them had a diagnosis of severe somatic illness, schizophrenia, or related psychosis.
From January 2004 through September 2013, more than 21 million prescriptions were filled — roughly 5.4 million for antipsychotic doses of 100 mg or less, 2.8 million for doses greater than 100 mg, and 13.5 million for control medications.
The most commonly prescribed antipsychotic medication was risperidone, followed by aripiprazole, quetiapine, ziprasidone, and olanzapine. The most commonly prescribed control medication was clonidine, followed by atomoxetine, guanfacine, and sertraline.
In the overall study population, there was no significant association with risk for death for antipsychotic doses less than or equal to 100-mg chlorpromazine equivalents (hazard ratio [HR], 1.08; 95% CI, 0.89-1.32). However, mortality risk was increased at doses greater than 100 mg (HR, 1.37; 95% CI, 1.11-1.70).
Looking at mortality risk by age, for children aged 5-17 years, there was no significant association with either antipsychotic dose, whereas young adults aged 18-24 years had increased risk for doses greater than 100 mg (HR, 1.68; 95% CI, 1.23-2.29).
Start Low, Go Slow
“Start low and go slow is always a good rule of thumb when it comes to the use of these and any medicines, especially among especially among children and adolescents,” Caleb Alexander, MD, codirector of the Center for Drug Safety and Effectiveness at Johns Hopkins University in Baltimore, Maryland, who wasn’t involved in the study, told this news organization.
Higher-dose antipsychotic treatment was significantly associated with overdose deaths (HR, 1.57; 95% CI, 1.02-2.42) and other unintentional injury deaths (HR, 1.57; 95% CI, 1.12-2.22), but not with nonoverdose suicide deaths or cardiovascular/metabolic deaths.
Death certificates listed opioid involvement in more than half of overdose deaths in those taking higher antipsychotic doses as well as those taking control medications.
“That’s a good reminder that the risk of these medicines may increase markedly when they’re combined with other treatments, such as prescription opioids,” Dr. Alexander said.
Also weighing in on the research, Anish Dube, MD, chair of the American Psychiatric Association’s Council on Children, Adolescents, and their Families, said the study is “notable for both the increased risk of death among young adults 18-24 prescribed treatment with antipsychotics at doses greater than 100-mg chlorpromazine equivalents, but also for the absence of such a finding with antipsychotic use in younger age groups,” he said.
“This suggests an interaction between other factors more common to young adults, such as substance use as mentioned by the authors, and concurrent treatment with antipsychotic medications at doses greater than 100-mg chlorpromazine equivalents,” said Dr. Dube.
“As the authors point out, additional research is needed to help clarify the observed increased risk of death at this developmental juncture so as to allow us to better predict which young adults may be especially vulnerable,” Dr. Dube said.
The findings also point to a need for caution when prescribing any antipsychotic medications off label, Dr. Dube added, especially among people aged 18-24 years, and other treatments should be considered when possible.
“Thankfully, with greater awareness and increased scrutiny, overall prescriptions for antipsychotic medications in the pediatric and young adult populations have likely decreased since the study period,” he said.
Limitations of the study include potential residual confounding, confining the study population to Medicaid recipients, restriction to second-generation antipsychotics, and exclusion of individuals with psychoses or severe somatic illness. Also, insufficient numbers of deaths from specific causes precluded an examination of individual antipsychotics or more detailed dose categories.
“No study is perfect,” said Dr. Alexander, “and some of the findings may be due to unmeasured differences between the groups that were being compared. That’s the elephant in the room.”
The study was funded by a grant from the National Institute for Child Health and Human Development. Dr. Ray, Dr. Alexander, and Dr. Dube have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
High doses of a second-generation antipsychotic are associated with a significantly increased risk for death in young adults, adding to longstanding safety concerns regarding the use of higher doses of antipsychotic medication in this age group.
In a large cohort study, people aged 18-24 years had a significantly higher risk for death when starting a second-generation antipsychotic at doses greater than 100-mg chlorpromazine equivalents, but no increased mortality risk with lower doses.
There was no association with mortality risk in children aged 5-17 years with either dose.
“This finding suggests that antipsychotic medication–related fatalities are rare in healthy children without psychosis,” lead investigator Wayne Ray, PhD, from Vanderbilt University School of Medicine in Nashville, Tennessee, and colleagues wrote in a recent study that was published online in JAMA Psychiatry.
“In contrast, young adults aged 18-24 years treated with doses greater than 100-mg chlorpromazine equivalents had 127.5 additional deaths for every 100,000 person-years of exposure, suggesting further investigations of antipsychotic medication safety in this population are needed.”
Large, Retrospective Study
The researchers compared mortality for more than 2 million Medicaid patients aged 5-24 years (mean age, 13 years; 51% men) starting treatment with a second-generation antipsychotic vs control psychiatric medications. None of them had a diagnosis of severe somatic illness, schizophrenia, or related psychosis.
From January 2004 through September 2013, more than 21 million prescriptions were filled — roughly 5.4 million for antipsychotic doses of 100 mg or less, 2.8 million for doses greater than 100 mg, and 13.5 million for control medications.
The most commonly prescribed antipsychotic medication was risperidone, followed by aripiprazole, quetiapine, ziprasidone, and olanzapine. The most commonly prescribed control medication was clonidine, followed by atomoxetine, guanfacine, and sertraline.
In the overall study population, there was no significant association with risk for death for antipsychotic doses less than or equal to 100-mg chlorpromazine equivalents (hazard ratio [HR], 1.08; 95% CI, 0.89-1.32). However, mortality risk was increased at doses greater than 100 mg (HR, 1.37; 95% CI, 1.11-1.70).
Looking at mortality risk by age, for children aged 5-17 years, there was no significant association with either antipsychotic dose, whereas young adults aged 18-24 years had increased risk for doses greater than 100 mg (HR, 1.68; 95% CI, 1.23-2.29).
Start Low, Go Slow
“Start low and go slow is always a good rule of thumb when it comes to the use of these and any medicines, especially among especially among children and adolescents,” Caleb Alexander, MD, codirector of the Center for Drug Safety and Effectiveness at Johns Hopkins University in Baltimore, Maryland, who wasn’t involved in the study, told this news organization.
Higher-dose antipsychotic treatment was significantly associated with overdose deaths (HR, 1.57; 95% CI, 1.02-2.42) and other unintentional injury deaths (HR, 1.57; 95% CI, 1.12-2.22), but not with nonoverdose suicide deaths or cardiovascular/metabolic deaths.
Death certificates listed opioid involvement in more than half of overdose deaths in those taking higher antipsychotic doses as well as those taking control medications.
“That’s a good reminder that the risk of these medicines may increase markedly when they’re combined with other treatments, such as prescription opioids,” Dr. Alexander said.
Also weighing in on the research, Anish Dube, MD, chair of the American Psychiatric Association’s Council on Children, Adolescents, and their Families, said the study is “notable for both the increased risk of death among young adults 18-24 prescribed treatment with antipsychotics at doses greater than 100-mg chlorpromazine equivalents, but also for the absence of such a finding with antipsychotic use in younger age groups,” he said.
“This suggests an interaction between other factors more common to young adults, such as substance use as mentioned by the authors, and concurrent treatment with antipsychotic medications at doses greater than 100-mg chlorpromazine equivalents,” said Dr. Dube.
“As the authors point out, additional research is needed to help clarify the observed increased risk of death at this developmental juncture so as to allow us to better predict which young adults may be especially vulnerable,” Dr. Dube said.
The findings also point to a need for caution when prescribing any antipsychotic medications off label, Dr. Dube added, especially among people aged 18-24 years, and other treatments should be considered when possible.
“Thankfully, with greater awareness and increased scrutiny, overall prescriptions for antipsychotic medications in the pediatric and young adult populations have likely decreased since the study period,” he said.
Limitations of the study include potential residual confounding, confining the study population to Medicaid recipients, restriction to second-generation antipsychotics, and exclusion of individuals with psychoses or severe somatic illness. Also, insufficient numbers of deaths from specific causes precluded an examination of individual antipsychotics or more detailed dose categories.
“No study is perfect,” said Dr. Alexander, “and some of the findings may be due to unmeasured differences between the groups that were being compared. That’s the elephant in the room.”
The study was funded by a grant from the National Institute for Child Health and Human Development. Dr. Ray, Dr. Alexander, and Dr. Dube have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
High doses of a second-generation antipsychotic are associated with a significantly increased risk for death in young adults, adding to longstanding safety concerns regarding the use of higher doses of antipsychotic medication in this age group.
In a large cohort study, people aged 18-24 years had a significantly higher risk for death when starting a second-generation antipsychotic at doses greater than 100-mg chlorpromazine equivalents, but no increased mortality risk with lower doses.
There was no association with mortality risk in children aged 5-17 years with either dose.
“This finding suggests that antipsychotic medication–related fatalities are rare in healthy children without psychosis,” lead investigator Wayne Ray, PhD, from Vanderbilt University School of Medicine in Nashville, Tennessee, and colleagues wrote in a recent study that was published online in JAMA Psychiatry.
“In contrast, young adults aged 18-24 years treated with doses greater than 100-mg chlorpromazine equivalents had 127.5 additional deaths for every 100,000 person-years of exposure, suggesting further investigations of antipsychotic medication safety in this population are needed.”
Large, Retrospective Study
The researchers compared mortality for more than 2 million Medicaid patients aged 5-24 years (mean age, 13 years; 51% men) starting treatment with a second-generation antipsychotic vs control psychiatric medications. None of them had a diagnosis of severe somatic illness, schizophrenia, or related psychosis.
From January 2004 through September 2013, more than 21 million prescriptions were filled — roughly 5.4 million for antipsychotic doses of 100 mg or less, 2.8 million for doses greater than 100 mg, and 13.5 million for control medications.
The most commonly prescribed antipsychotic medication was risperidone, followed by aripiprazole, quetiapine, ziprasidone, and olanzapine. The most commonly prescribed control medication was clonidine, followed by atomoxetine, guanfacine, and sertraline.
In the overall study population, there was no significant association with risk for death for antipsychotic doses less than or equal to 100-mg chlorpromazine equivalents (hazard ratio [HR], 1.08; 95% CI, 0.89-1.32). However, mortality risk was increased at doses greater than 100 mg (HR, 1.37; 95% CI, 1.11-1.70).
Looking at mortality risk by age, for children aged 5-17 years, there was no significant association with either antipsychotic dose, whereas young adults aged 18-24 years had increased risk for doses greater than 100 mg (HR, 1.68; 95% CI, 1.23-2.29).
Start Low, Go Slow
“Start low and go slow is always a good rule of thumb when it comes to the use of these and any medicines, especially among especially among children and adolescents,” Caleb Alexander, MD, codirector of the Center for Drug Safety and Effectiveness at Johns Hopkins University in Baltimore, Maryland, who wasn’t involved in the study, told this news organization.
Higher-dose antipsychotic treatment was significantly associated with overdose deaths (HR, 1.57; 95% CI, 1.02-2.42) and other unintentional injury deaths (HR, 1.57; 95% CI, 1.12-2.22), but not with nonoverdose suicide deaths or cardiovascular/metabolic deaths.
Death certificates listed opioid involvement in more than half of overdose deaths in those taking higher antipsychotic doses as well as those taking control medications.
“That’s a good reminder that the risk of these medicines may increase markedly when they’re combined with other treatments, such as prescription opioids,” Dr. Alexander said.
Also weighing in on the research, Anish Dube, MD, chair of the American Psychiatric Association’s Council on Children, Adolescents, and their Families, said the study is “notable for both the increased risk of death among young adults 18-24 prescribed treatment with antipsychotics at doses greater than 100-mg chlorpromazine equivalents, but also for the absence of such a finding with antipsychotic use in younger age groups,” he said.
“This suggests an interaction between other factors more common to young adults, such as substance use as mentioned by the authors, and concurrent treatment with antipsychotic medications at doses greater than 100-mg chlorpromazine equivalents,” said Dr. Dube.
“As the authors point out, additional research is needed to help clarify the observed increased risk of death at this developmental juncture so as to allow us to better predict which young adults may be especially vulnerable,” Dr. Dube said.
The findings also point to a need for caution when prescribing any antipsychotic medications off label, Dr. Dube added, especially among people aged 18-24 years, and other treatments should be considered when possible.
“Thankfully, with greater awareness and increased scrutiny, overall prescriptions for antipsychotic medications in the pediatric and young adult populations have likely decreased since the study period,” he said.
Limitations of the study include potential residual confounding, confining the study population to Medicaid recipients, restriction to second-generation antipsychotics, and exclusion of individuals with psychoses or severe somatic illness. Also, insufficient numbers of deaths from specific causes precluded an examination of individual antipsychotics or more detailed dose categories.
“No study is perfect,” said Dr. Alexander, “and some of the findings may be due to unmeasured differences between the groups that were being compared. That’s the elephant in the room.”
The study was funded by a grant from the National Institute for Child Health and Human Development. Dr. Ray, Dr. Alexander, and Dr. Dube have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
FROM JAMA PSYCHIATRY
Side Effects of Local Treatment for Advanced Prostate Cancer May Linger for Years
TOPLINE:
METHODOLOGY:
Recent evidence suggested that in men with advanced prostate cancer, local therapy with radical prostatectomy or radiation may improve survival outcomes; however, data on the long-term side effects from these local options were limited.
The retrospective cohort included 5502 men (mean age, 68 years) diagnosed with advanced (T4, N1, and/or M1) prostate cancer.
A total of 1705 men (31%) received initial local treatment, consisting of radical prostatectomy, (55%), radiation (39%), or both (5.6%), while 3797 (69%) opted for initial nonlocal treatment (hormone therapy, chemotherapy, or both).
The main outcomes were treatment-related adverse effects, including GI, chronic pain, sexual dysfunction, and urinary symptoms, assessed at three timepoints after initial treatment — up to 1 year, between 1 and 2 years, and between 2 and 5 years.
TAKEAWAY:
Overall, 916 men (75%) who had initial local treatment and 897 men (67%) with initial nonlocal therapy reported at least one adverse condition up to 5 years after initial treatment.
In the first year after initial treatment, local therapy was associated with a higher prevalence of GI (9% vs 3%), pain (60% vs 38%), sexual (37% vs 8%), and urinary (46.5% vs 18%) conditions. Men receiving local therapy were more likely to experience GI (adjusted odds ratio [aOR], 4.08), pain (aOR, 1.57), sexual (aOR, 2.96), and urinary (aOR, 2.25) conditions.
Between 2 and 5 years after local therapy, certain conditions remained more prevalent — 7.8% vs 4.2% for GI, 40% vs 13% for sexual, and 40.5% vs 26% for urinary issues. Men receiving local vs nonlocal therapy were more likely to experience GI (aOR, 2.39), sexual (aOR, 3.36), and urinary (aOR, 1.39) issues over the long term.
The researchers found no difference in the prevalence of constitutional conditions such as hot flashes (36.5% vs 34.4%) in the first year following initial local or nonlocal therapy. However, local treatment followed by any secondary treatment was associated with a higher likelihood of developing constitutional conditions at 1-2 years (aOR, 1.50) and 2-5 years (aOR, 1.78) after initial treatment.
IN PRACTICE:
“These results suggest that patients and clinicians should consider the adverse effects of local treatment” alongside the potential for enhanced survival when making treatment decisions in the setting of advanced prostate cancer, the authors explained. Careful informed decision-making by both patients and practitioners is especially important because “there are currently no established guidelines regarding the use of local treatment among men with advanced prostate cancer.”
SOURCE:
The study, with first author Saira Khan, PhD, MPH, Washington University School of Medicine in St. Louis, Missouri, was published online in JAMA Network Open.
LIMITATIONS:
The authors noted that the study was limited by its retrospective design. Men who received local treatment were, on average, younger; older or lesser healthy patients who received local treatment may experience worse adverse effects than observed in the study. The study was limited to US veterans.
DISCLOSURES:
The study was supported by a grant from the US Department of Defense. The authors have no relevant disclosures.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
Recent evidence suggested that in men with advanced prostate cancer, local therapy with radical prostatectomy or radiation may improve survival outcomes; however, data on the long-term side effects from these local options were limited.
The retrospective cohort included 5502 men (mean age, 68 years) diagnosed with advanced (T4, N1, and/or M1) prostate cancer.
A total of 1705 men (31%) received initial local treatment, consisting of radical prostatectomy, (55%), radiation (39%), or both (5.6%), while 3797 (69%) opted for initial nonlocal treatment (hormone therapy, chemotherapy, or both).
The main outcomes were treatment-related adverse effects, including GI, chronic pain, sexual dysfunction, and urinary symptoms, assessed at three timepoints after initial treatment — up to 1 year, between 1 and 2 years, and between 2 and 5 years.
TAKEAWAY:
Overall, 916 men (75%) who had initial local treatment and 897 men (67%) with initial nonlocal therapy reported at least one adverse condition up to 5 years after initial treatment.
In the first year after initial treatment, local therapy was associated with a higher prevalence of GI (9% vs 3%), pain (60% vs 38%), sexual (37% vs 8%), and urinary (46.5% vs 18%) conditions. Men receiving local therapy were more likely to experience GI (adjusted odds ratio [aOR], 4.08), pain (aOR, 1.57), sexual (aOR, 2.96), and urinary (aOR, 2.25) conditions.
Between 2 and 5 years after local therapy, certain conditions remained more prevalent — 7.8% vs 4.2% for GI, 40% vs 13% for sexual, and 40.5% vs 26% for urinary issues. Men receiving local vs nonlocal therapy were more likely to experience GI (aOR, 2.39), sexual (aOR, 3.36), and urinary (aOR, 1.39) issues over the long term.
The researchers found no difference in the prevalence of constitutional conditions such as hot flashes (36.5% vs 34.4%) in the first year following initial local or nonlocal therapy. However, local treatment followed by any secondary treatment was associated with a higher likelihood of developing constitutional conditions at 1-2 years (aOR, 1.50) and 2-5 years (aOR, 1.78) after initial treatment.
IN PRACTICE:
“These results suggest that patients and clinicians should consider the adverse effects of local treatment” alongside the potential for enhanced survival when making treatment decisions in the setting of advanced prostate cancer, the authors explained. Careful informed decision-making by both patients and practitioners is especially important because “there are currently no established guidelines regarding the use of local treatment among men with advanced prostate cancer.”
SOURCE:
The study, with first author Saira Khan, PhD, MPH, Washington University School of Medicine in St. Louis, Missouri, was published online in JAMA Network Open.
LIMITATIONS:
The authors noted that the study was limited by its retrospective design. Men who received local treatment were, on average, younger; older or lesser healthy patients who received local treatment may experience worse adverse effects than observed in the study. The study was limited to US veterans.
DISCLOSURES:
The study was supported by a grant from the US Department of Defense. The authors have no relevant disclosures.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
Recent evidence suggested that in men with advanced prostate cancer, local therapy with radical prostatectomy or radiation may improve survival outcomes; however, data on the long-term side effects from these local options were limited.
The retrospective cohort included 5502 men (mean age, 68 years) diagnosed with advanced (T4, N1, and/or M1) prostate cancer.
A total of 1705 men (31%) received initial local treatment, consisting of radical prostatectomy, (55%), radiation (39%), or both (5.6%), while 3797 (69%) opted for initial nonlocal treatment (hormone therapy, chemotherapy, or both).
The main outcomes were treatment-related adverse effects, including GI, chronic pain, sexual dysfunction, and urinary symptoms, assessed at three timepoints after initial treatment — up to 1 year, between 1 and 2 years, and between 2 and 5 years.
TAKEAWAY:
Overall, 916 men (75%) who had initial local treatment and 897 men (67%) with initial nonlocal therapy reported at least one adverse condition up to 5 years after initial treatment.
In the first year after initial treatment, local therapy was associated with a higher prevalence of GI (9% vs 3%), pain (60% vs 38%), sexual (37% vs 8%), and urinary (46.5% vs 18%) conditions. Men receiving local therapy were more likely to experience GI (adjusted odds ratio [aOR], 4.08), pain (aOR, 1.57), sexual (aOR, 2.96), and urinary (aOR, 2.25) conditions.
Between 2 and 5 years after local therapy, certain conditions remained more prevalent — 7.8% vs 4.2% for GI, 40% vs 13% for sexual, and 40.5% vs 26% for urinary issues. Men receiving local vs nonlocal therapy were more likely to experience GI (aOR, 2.39), sexual (aOR, 3.36), and urinary (aOR, 1.39) issues over the long term.
The researchers found no difference in the prevalence of constitutional conditions such as hot flashes (36.5% vs 34.4%) in the first year following initial local or nonlocal therapy. However, local treatment followed by any secondary treatment was associated with a higher likelihood of developing constitutional conditions at 1-2 years (aOR, 1.50) and 2-5 years (aOR, 1.78) after initial treatment.
IN PRACTICE:
“These results suggest that patients and clinicians should consider the adverse effects of local treatment” alongside the potential for enhanced survival when making treatment decisions in the setting of advanced prostate cancer, the authors explained. Careful informed decision-making by both patients and practitioners is especially important because “there are currently no established guidelines regarding the use of local treatment among men with advanced prostate cancer.”
SOURCE:
The study, with first author Saira Khan, PhD, MPH, Washington University School of Medicine in St. Louis, Missouri, was published online in JAMA Network Open.
LIMITATIONS:
The authors noted that the study was limited by its retrospective design. Men who received local treatment were, on average, younger; older or lesser healthy patients who received local treatment may experience worse adverse effects than observed in the study. The study was limited to US veterans.
DISCLOSURES:
The study was supported by a grant from the US Department of Defense. The authors have no relevant disclosures.
A version of this article appeared on Medscape.com.
African Psychedelic Tied to ‘Remarkable’ Improvement in TBI-Related Psych Symptoms, Functional Disability
The plant-based psychoactive compound ibogaine, combined with magnesium to protect the heart, is linked to improvement in severe psychiatric symptoms including depression, anxiety, and functioning in veterans with traumatic brain injury (TBI), early results from a small study showed.
“The most unique findings we observed are the improvements in disability and cognition. At the start of the study, participants had mild to moderate levels of disability. However, a month after treatment, their average disability rating indicated no disability and cognitive testing indicated improvements in concentration and memory,” study investigator Nolan Williams, MD, Stanford University, Stanford, California, told this news organization.
Also noteworthy were improvements across all participants in posttraumatic stress disorder (PTSD), depression, and anxiety — effects that lasted for at least 1 month after treatment, he said.
“These results are remarkable and exceeded our expectations. There is no drug today that can broadly relieve functional and neuropsychiatric symptoms of TBI as we observed with ibogaine,” Dr. Williams added.
The study was published online on January 5, 2024, in Nature Medicine.
‘The Storm Lifted’
Ibogaine is derived from the root bark of the Tabernanthe iboga shrub and related plants and is traditionally used in African spiritual and healing ceremonies.
It is known to interact with multiple neurotransmitter systems and has been studied primarily as a treatment of substance use disorders (SUDs). Some studies of ibogaine for SUDs have also noted improvements in self-reported measures of mood.
In the United States, ibogaine is classified as a Schedule I substance, but legal ibogaine treatments are offered in clinics in Canada and Mexico.
Dr. Williams noted that a handful of US veterans who went to Mexico for ibogaine treatment anecdotally reported improvements a variety of aspects of their lives.
The goal of the current study was to characterize those improvements with structured clinical and neurobiological assessments.
Participants included 30 US Special Operations Forces veterans (SOVs) with predominantly mild TBI from combat/blast exposures and psychiatric symptoms and functional limitations. All of them had independently scheduled themselves for treatment with magnesium and ibogaine at a clinic in Mexico.
Before treatment, the veterans had an average disability rating of 30.2 on the World Health Organization Disability Assessment Scale 2.0, equivalent to mild to moderate disability. One month after ibogaine treatment, that rating improved to 5.1, indicating no disability, the researchers reported.
One month after treatment, participants also experienced average reductions of 88% in PTSD symptoms, 87% in depression symptoms, and 81% in anxiety symptoms relative to before treatment.
Neuropsychological testing revealed improved concentration, information processing, memory, and impulsivity. There was also a substantial reduction in suicidal ideation.
“Before the treatment, I was living life in a blizzard with zero visibility and a cold, hopeless, listless feeling. After ibogaine, the storm lifted,” Sean, a 51-year-old veteran from Arizona with six combat deployments who participated in the study, said in a Stanford news release.
There were no serious side effects of ibogaine, and no instances of heart problems associated with the treatment.
Although the study findings are promising, additional research is needed to address some clear limitations, the researchers noted.
“Most importantly, the study was not controlled and so the relative contribution of any therapeutic benefits from non-ibogaine elements of the experience, such as complementary treatments, group activities, coaching, international travel, expectancy, or other nonspecific effects, cannot be determined,” they wrote.
In addition, follow-up was limited to 1 month, and longer-term data are needed to determine durability of the effects.
“We plan to study this compound further, as well as launch future studies to continue to understand how this drug can be used to treat TBI and possibly as a broader neuro-rehab drug. We will work towards a US-based set of trials to confirm efficacy with a multisite design,” said Dr. Williams.
Promising, but Very Preliminary
Commenting on the study for this news organization, Ramon Diaz-Arrastia, MD, PhD, professor of neurology and director of the Clinical TBI Research Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, said the results are “promising, but very preliminary.”
Dr. Diaz-Arrastia noted that this was an open-label, nonrandomized study, early phase 2a study with “highly subjective outcome measures and the likelihood of it being a placebo effect is very high.”
Nonetheless, “there is a lot of interest in these ‘psychedelic’ alkaloids, and ibogaine is a good candidate for further study,” Dr. Diaz-Arrastia said.
Also providing perspective, Alan K. Davis, PhD, director of the Center for Psychedelic Drug Research and Education, Ohio State University, Columbus, said “mounting evidence supports the importance of studying this treatment in rigorous clinical trials in the US.”
Dr. Davis and colleagues recently observed that treatment with two naturally occurring psychedelics — ibogaine and 5-MeO-DMT — was associated with reduced depressive and anxiety symptoms in trauma-exposed SOVs, as previously reported by this news organization.
This new study “basically is a replication of what we’ve already published on this topic, and we published data from much larger samples and longer follow up,” said Dr. Davis.
Dr. Davis said it’s “important for the public to know that there are important and serious risks associated with ibogaine therapy, including the possibility of cardiac problems and death. These risks are compounded when people are in clinics or settings where proper screening and medical oversight are not completed.”
“Furthermore, the long-term effectiveness of this treatment is not well established. It may only help in the short term for most people. For many, ongoing clinical aftercare therapy and other forms of treatment may be needed,” Dr. Davis noted.
The study was independently funded by philanthropic gifts from Steve and Genevieve Jurvetson and another anonymous donor. Williams is an inventor on a patent application related to the safety of MISTIC administration as described in the paper and a separate patent related to the use of ibogaine to treat disorders associated with brain aging. Dr. Davis is a board member at Source Resource Foundation and a lead trainer at Fluence. Dr. Diaz-Arrastia has no relevant disclosures.
A version of this article appeared on Medscape.com.
The plant-based psychoactive compound ibogaine, combined with magnesium to protect the heart, is linked to improvement in severe psychiatric symptoms including depression, anxiety, and functioning in veterans with traumatic brain injury (TBI), early results from a small study showed.
“The most unique findings we observed are the improvements in disability and cognition. At the start of the study, participants had mild to moderate levels of disability. However, a month after treatment, their average disability rating indicated no disability and cognitive testing indicated improvements in concentration and memory,” study investigator Nolan Williams, MD, Stanford University, Stanford, California, told this news organization.
Also noteworthy were improvements across all participants in posttraumatic stress disorder (PTSD), depression, and anxiety — effects that lasted for at least 1 month after treatment, he said.
“These results are remarkable and exceeded our expectations. There is no drug today that can broadly relieve functional and neuropsychiatric symptoms of TBI as we observed with ibogaine,” Dr. Williams added.
The study was published online on January 5, 2024, in Nature Medicine.
‘The Storm Lifted’
Ibogaine is derived from the root bark of the Tabernanthe iboga shrub and related plants and is traditionally used in African spiritual and healing ceremonies.
It is known to interact with multiple neurotransmitter systems and has been studied primarily as a treatment of substance use disorders (SUDs). Some studies of ibogaine for SUDs have also noted improvements in self-reported measures of mood.
In the United States, ibogaine is classified as a Schedule I substance, but legal ibogaine treatments are offered in clinics in Canada and Mexico.
Dr. Williams noted that a handful of US veterans who went to Mexico for ibogaine treatment anecdotally reported improvements a variety of aspects of their lives.
The goal of the current study was to characterize those improvements with structured clinical and neurobiological assessments.
Participants included 30 US Special Operations Forces veterans (SOVs) with predominantly mild TBI from combat/blast exposures and psychiatric symptoms and functional limitations. All of them had independently scheduled themselves for treatment with magnesium and ibogaine at a clinic in Mexico.
Before treatment, the veterans had an average disability rating of 30.2 on the World Health Organization Disability Assessment Scale 2.0, equivalent to mild to moderate disability. One month after ibogaine treatment, that rating improved to 5.1, indicating no disability, the researchers reported.
One month after treatment, participants also experienced average reductions of 88% in PTSD symptoms, 87% in depression symptoms, and 81% in anxiety symptoms relative to before treatment.
Neuropsychological testing revealed improved concentration, information processing, memory, and impulsivity. There was also a substantial reduction in suicidal ideation.
“Before the treatment, I was living life in a blizzard with zero visibility and a cold, hopeless, listless feeling. After ibogaine, the storm lifted,” Sean, a 51-year-old veteran from Arizona with six combat deployments who participated in the study, said in a Stanford news release.
There were no serious side effects of ibogaine, and no instances of heart problems associated with the treatment.
Although the study findings are promising, additional research is needed to address some clear limitations, the researchers noted.
“Most importantly, the study was not controlled and so the relative contribution of any therapeutic benefits from non-ibogaine elements of the experience, such as complementary treatments, group activities, coaching, international travel, expectancy, or other nonspecific effects, cannot be determined,” they wrote.
In addition, follow-up was limited to 1 month, and longer-term data are needed to determine durability of the effects.
“We plan to study this compound further, as well as launch future studies to continue to understand how this drug can be used to treat TBI and possibly as a broader neuro-rehab drug. We will work towards a US-based set of trials to confirm efficacy with a multisite design,” said Dr. Williams.
Promising, but Very Preliminary
Commenting on the study for this news organization, Ramon Diaz-Arrastia, MD, PhD, professor of neurology and director of the Clinical TBI Research Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, said the results are “promising, but very preliminary.”
Dr. Diaz-Arrastia noted that this was an open-label, nonrandomized study, early phase 2a study with “highly subjective outcome measures and the likelihood of it being a placebo effect is very high.”
Nonetheless, “there is a lot of interest in these ‘psychedelic’ alkaloids, and ibogaine is a good candidate for further study,” Dr. Diaz-Arrastia said.
Also providing perspective, Alan K. Davis, PhD, director of the Center for Psychedelic Drug Research and Education, Ohio State University, Columbus, said “mounting evidence supports the importance of studying this treatment in rigorous clinical trials in the US.”
Dr. Davis and colleagues recently observed that treatment with two naturally occurring psychedelics — ibogaine and 5-MeO-DMT — was associated with reduced depressive and anxiety symptoms in trauma-exposed SOVs, as previously reported by this news organization.
This new study “basically is a replication of what we’ve already published on this topic, and we published data from much larger samples and longer follow up,” said Dr. Davis.
Dr. Davis said it’s “important for the public to know that there are important and serious risks associated with ibogaine therapy, including the possibility of cardiac problems and death. These risks are compounded when people are in clinics or settings where proper screening and medical oversight are not completed.”
“Furthermore, the long-term effectiveness of this treatment is not well established. It may only help in the short term for most people. For many, ongoing clinical aftercare therapy and other forms of treatment may be needed,” Dr. Davis noted.
The study was independently funded by philanthropic gifts from Steve and Genevieve Jurvetson and another anonymous donor. Williams is an inventor on a patent application related to the safety of MISTIC administration as described in the paper and a separate patent related to the use of ibogaine to treat disorders associated with brain aging. Dr. Davis is a board member at Source Resource Foundation and a lead trainer at Fluence. Dr. Diaz-Arrastia has no relevant disclosures.
A version of this article appeared on Medscape.com.
The plant-based psychoactive compound ibogaine, combined with magnesium to protect the heart, is linked to improvement in severe psychiatric symptoms including depression, anxiety, and functioning in veterans with traumatic brain injury (TBI), early results from a small study showed.
“The most unique findings we observed are the improvements in disability and cognition. At the start of the study, participants had mild to moderate levels of disability. However, a month after treatment, their average disability rating indicated no disability and cognitive testing indicated improvements in concentration and memory,” study investigator Nolan Williams, MD, Stanford University, Stanford, California, told this news organization.
Also noteworthy were improvements across all participants in posttraumatic stress disorder (PTSD), depression, and anxiety — effects that lasted for at least 1 month after treatment, he said.
“These results are remarkable and exceeded our expectations. There is no drug today that can broadly relieve functional and neuropsychiatric symptoms of TBI as we observed with ibogaine,” Dr. Williams added.
The study was published online on January 5, 2024, in Nature Medicine.
‘The Storm Lifted’
Ibogaine is derived from the root bark of the Tabernanthe iboga shrub and related plants and is traditionally used in African spiritual and healing ceremonies.
It is known to interact with multiple neurotransmitter systems and has been studied primarily as a treatment of substance use disorders (SUDs). Some studies of ibogaine for SUDs have also noted improvements in self-reported measures of mood.
In the United States, ibogaine is classified as a Schedule I substance, but legal ibogaine treatments are offered in clinics in Canada and Mexico.
Dr. Williams noted that a handful of US veterans who went to Mexico for ibogaine treatment anecdotally reported improvements a variety of aspects of their lives.
The goal of the current study was to characterize those improvements with structured clinical and neurobiological assessments.
Participants included 30 US Special Operations Forces veterans (SOVs) with predominantly mild TBI from combat/blast exposures and psychiatric symptoms and functional limitations. All of them had independently scheduled themselves for treatment with magnesium and ibogaine at a clinic in Mexico.
Before treatment, the veterans had an average disability rating of 30.2 on the World Health Organization Disability Assessment Scale 2.0, equivalent to mild to moderate disability. One month after ibogaine treatment, that rating improved to 5.1, indicating no disability, the researchers reported.
One month after treatment, participants also experienced average reductions of 88% in PTSD symptoms, 87% in depression symptoms, and 81% in anxiety symptoms relative to before treatment.
Neuropsychological testing revealed improved concentration, information processing, memory, and impulsivity. There was also a substantial reduction in suicidal ideation.
“Before the treatment, I was living life in a blizzard with zero visibility and a cold, hopeless, listless feeling. After ibogaine, the storm lifted,” Sean, a 51-year-old veteran from Arizona with six combat deployments who participated in the study, said in a Stanford news release.
There were no serious side effects of ibogaine, and no instances of heart problems associated with the treatment.
Although the study findings are promising, additional research is needed to address some clear limitations, the researchers noted.
“Most importantly, the study was not controlled and so the relative contribution of any therapeutic benefits from non-ibogaine elements of the experience, such as complementary treatments, group activities, coaching, international travel, expectancy, or other nonspecific effects, cannot be determined,” they wrote.
In addition, follow-up was limited to 1 month, and longer-term data are needed to determine durability of the effects.
“We plan to study this compound further, as well as launch future studies to continue to understand how this drug can be used to treat TBI and possibly as a broader neuro-rehab drug. We will work towards a US-based set of trials to confirm efficacy with a multisite design,” said Dr. Williams.
Promising, but Very Preliminary
Commenting on the study for this news organization, Ramon Diaz-Arrastia, MD, PhD, professor of neurology and director of the Clinical TBI Research Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, said the results are “promising, but very preliminary.”
Dr. Diaz-Arrastia noted that this was an open-label, nonrandomized study, early phase 2a study with “highly subjective outcome measures and the likelihood of it being a placebo effect is very high.”
Nonetheless, “there is a lot of interest in these ‘psychedelic’ alkaloids, and ibogaine is a good candidate for further study,” Dr. Diaz-Arrastia said.
Also providing perspective, Alan K. Davis, PhD, director of the Center for Psychedelic Drug Research and Education, Ohio State University, Columbus, said “mounting evidence supports the importance of studying this treatment in rigorous clinical trials in the US.”
Dr. Davis and colleagues recently observed that treatment with two naturally occurring psychedelics — ibogaine and 5-MeO-DMT — was associated with reduced depressive and anxiety symptoms in trauma-exposed SOVs, as previously reported by this news organization.
This new study “basically is a replication of what we’ve already published on this topic, and we published data from much larger samples and longer follow up,” said Dr. Davis.
Dr. Davis said it’s “important for the public to know that there are important and serious risks associated with ibogaine therapy, including the possibility of cardiac problems and death. These risks are compounded when people are in clinics or settings where proper screening and medical oversight are not completed.”
“Furthermore, the long-term effectiveness of this treatment is not well established. It may only help in the short term for most people. For many, ongoing clinical aftercare therapy and other forms of treatment may be needed,” Dr. Davis noted.
The study was independently funded by philanthropic gifts from Steve and Genevieve Jurvetson and another anonymous donor. Williams is an inventor on a patent application related to the safety of MISTIC administration as described in the paper and a separate patent related to the use of ibogaine to treat disorders associated with brain aging. Dr. Davis is a board member at Source Resource Foundation and a lead trainer at Fluence. Dr. Diaz-Arrastia has no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM NATURE MEDICINE
Poor Oral Health Tied to Worse Brain Health
In a large observational study of middle-aged adults without stroke or dementia, poor oral health was strongly associated with multiple neuroimaging markers of white matter injury.
“Because the neuroimaging markers evaluated in this study precede and are established risk factors of stroke and dementia, our results suggest that oral health, an easily modifiable process, may be a promising target for very early interventions focused on improving brain health,” wrote the authors, led by Cyprien A. Rivier, MD, MS, with the Department of Neurology, Yale University School of Medicine, New Haven, Connecticut.
The study was published online on December 20, 2023, in Neurology.
Research data came from 40,175 adults (mean age, 55 years; 53% women) with no history of stroke or dementia who enrolled in the UK Biobank from 2006 to 2010 and had brain MRI between 2014 and 2016.
Altogether, 5470 (14%) participants had poor oral health, defined as the presence of dentures or loose teeth. Those with poor (vs optimal) oral health were older, more likely to be male, and had higher prevalence of hypertension, hypercholesterolemia, diabetes, overweight/obesity, and current or past smoking history.
In a multivariable model, poor oral health was associated with a 9% increase in white matter hyperintensity (WMH) volume (P < .001), a well-established marker of clinically silent cerebrovascular disease.
Poor oral health was also associated with a 10% change in aggregate fractional anisotropy (FA) score (P < .001) and a 5% change in aggregate mean diffusivity (MD) score (P < .001), two diffusion tensor imaging metrics that accurately represent white matter disintegrity.
Genetic analyses using Mendelian randomization confirmed these associations. Individuals who were genetically prone to poor oral health had a 30% increase in WMH volume (P < .001), 43% change in aggregate FA score (P < .001), and 10% change in aggregate MD score (P < .01), the researchers reported.
These findings, they noted, add to prior epidemiologic evidence for an association between poor oral health and a higher risk for clinical outcomes related to brain health, including cognitive decline.
‘Huge Dividends’
The authors of an accompanying editorial praised the authors for looking at the consequences of poor oral health in a “new and powerful way by using as their outcome MRI-defined white matter injury, which is associated with, but antedates by many years, cognitive decline and stroke.”
“The fact that these imaging changes are seen in asymptomatic persons offers the hope that if the association is causal, interventions to improve oral health could pay huge dividends in subsequent brain health,” wrote Steven J. Kittner, MD, MPH, and Breana L. Taylor, MD, with the Department of Neurology, University of Maryland School of Medicine in Baltimore.
“The mechanisms mediating the relationship between the oral health genetic risk score and white matter injury are likely to be complex, but the authors have taken an important step forward in addressing a hypothesis of immense public health importance,” they added.
Data from the World Health Organization suggested that oral diseases, which are largely preventable, affect nearly 3.5 billion people globally, with three out of four people affected in middle-income countries.
Funding for the study was provided in part by grants from the National Institutes of Health, the American Heart Association, and the Neurocritical Care Society Research Fellowship. The authors and editorialists disclosed no relevant conflicts of interest.
Megan Brooks has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
In a large observational study of middle-aged adults without stroke or dementia, poor oral health was strongly associated with multiple neuroimaging markers of white matter injury.
“Because the neuroimaging markers evaluated in this study precede and are established risk factors of stroke and dementia, our results suggest that oral health, an easily modifiable process, may be a promising target for very early interventions focused on improving brain health,” wrote the authors, led by Cyprien A. Rivier, MD, MS, with the Department of Neurology, Yale University School of Medicine, New Haven, Connecticut.
The study was published online on December 20, 2023, in Neurology.
Research data came from 40,175 adults (mean age, 55 years; 53% women) with no history of stroke or dementia who enrolled in the UK Biobank from 2006 to 2010 and had brain MRI between 2014 and 2016.
Altogether, 5470 (14%) participants had poor oral health, defined as the presence of dentures or loose teeth. Those with poor (vs optimal) oral health were older, more likely to be male, and had higher prevalence of hypertension, hypercholesterolemia, diabetes, overweight/obesity, and current or past smoking history.
In a multivariable model, poor oral health was associated with a 9% increase in white matter hyperintensity (WMH) volume (P < .001), a well-established marker of clinically silent cerebrovascular disease.
Poor oral health was also associated with a 10% change in aggregate fractional anisotropy (FA) score (P < .001) and a 5% change in aggregate mean diffusivity (MD) score (P < .001), two diffusion tensor imaging metrics that accurately represent white matter disintegrity.
Genetic analyses using Mendelian randomization confirmed these associations. Individuals who were genetically prone to poor oral health had a 30% increase in WMH volume (P < .001), 43% change in aggregate FA score (P < .001), and 10% change in aggregate MD score (P < .01), the researchers reported.
These findings, they noted, add to prior epidemiologic evidence for an association between poor oral health and a higher risk for clinical outcomes related to brain health, including cognitive decline.
‘Huge Dividends’
The authors of an accompanying editorial praised the authors for looking at the consequences of poor oral health in a “new and powerful way by using as their outcome MRI-defined white matter injury, which is associated with, but antedates by many years, cognitive decline and stroke.”
“The fact that these imaging changes are seen in asymptomatic persons offers the hope that if the association is causal, interventions to improve oral health could pay huge dividends in subsequent brain health,” wrote Steven J. Kittner, MD, MPH, and Breana L. Taylor, MD, with the Department of Neurology, University of Maryland School of Medicine in Baltimore.
“The mechanisms mediating the relationship between the oral health genetic risk score and white matter injury are likely to be complex, but the authors have taken an important step forward in addressing a hypothesis of immense public health importance,” they added.
Data from the World Health Organization suggested that oral diseases, which are largely preventable, affect nearly 3.5 billion people globally, with three out of four people affected in middle-income countries.
Funding for the study was provided in part by grants from the National Institutes of Health, the American Heart Association, and the Neurocritical Care Society Research Fellowship. The authors and editorialists disclosed no relevant conflicts of interest.
Megan Brooks has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
In a large observational study of middle-aged adults without stroke or dementia, poor oral health was strongly associated with multiple neuroimaging markers of white matter injury.
“Because the neuroimaging markers evaluated in this study precede and are established risk factors of stroke and dementia, our results suggest that oral health, an easily modifiable process, may be a promising target for very early interventions focused on improving brain health,” wrote the authors, led by Cyprien A. Rivier, MD, MS, with the Department of Neurology, Yale University School of Medicine, New Haven, Connecticut.
The study was published online on December 20, 2023, in Neurology.
Research data came from 40,175 adults (mean age, 55 years; 53% women) with no history of stroke or dementia who enrolled in the UK Biobank from 2006 to 2010 and had brain MRI between 2014 and 2016.
Altogether, 5470 (14%) participants had poor oral health, defined as the presence of dentures or loose teeth. Those with poor (vs optimal) oral health were older, more likely to be male, and had higher prevalence of hypertension, hypercholesterolemia, diabetes, overweight/obesity, and current or past smoking history.
In a multivariable model, poor oral health was associated with a 9% increase in white matter hyperintensity (WMH) volume (P < .001), a well-established marker of clinically silent cerebrovascular disease.
Poor oral health was also associated with a 10% change in aggregate fractional anisotropy (FA) score (P < .001) and a 5% change in aggregate mean diffusivity (MD) score (P < .001), two diffusion tensor imaging metrics that accurately represent white matter disintegrity.
Genetic analyses using Mendelian randomization confirmed these associations. Individuals who were genetically prone to poor oral health had a 30% increase in WMH volume (P < .001), 43% change in aggregate FA score (P < .001), and 10% change in aggregate MD score (P < .01), the researchers reported.
These findings, they noted, add to prior epidemiologic evidence for an association between poor oral health and a higher risk for clinical outcomes related to brain health, including cognitive decline.
‘Huge Dividends’
The authors of an accompanying editorial praised the authors for looking at the consequences of poor oral health in a “new and powerful way by using as their outcome MRI-defined white matter injury, which is associated with, but antedates by many years, cognitive decline and stroke.”
“The fact that these imaging changes are seen in asymptomatic persons offers the hope that if the association is causal, interventions to improve oral health could pay huge dividends in subsequent brain health,” wrote Steven J. Kittner, MD, MPH, and Breana L. Taylor, MD, with the Department of Neurology, University of Maryland School of Medicine in Baltimore.
“The mechanisms mediating the relationship between the oral health genetic risk score and white matter injury are likely to be complex, but the authors have taken an important step forward in addressing a hypothesis of immense public health importance,” they added.
Data from the World Health Organization suggested that oral diseases, which are largely preventable, affect nearly 3.5 billion people globally, with three out of four people affected in middle-income countries.
Funding for the study was provided in part by grants from the National Institutes of Health, the American Heart Association, and the Neurocritical Care Society Research Fellowship. The authors and editorialists disclosed no relevant conflicts of interest.
Megan Brooks has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Noninvasive Brain Stimulation a Breakthrough for Hypnotherapy?
Less than 2 minutes of transcranial magnetic stimulation (TMS) targeting specific areas of the brain can boost an individual’s ability to be hypnotized, in new findings that could increase the efficacy of therapeutic hypnosis and expand the pool of patients who can benefit from it.
“We were able to increase hypnotizability, a neuropsychological trait previously shown to be as stable as IQ in adulthood,” said co-senior author David Spiegel, MD, professor of psychiatry and behavioral sciences, Stanford University, Palo Alto, California.
“Our findings would allow us to combine neurostimulation with hypnosis to expand the number of people able to benefit from hypnosis and enhance their responsiveness to treatment,” Dr. Spiegel added.
The study was published online on January 4, 2024, in Nature Mental Health.
A Breakthrough for Hypnotherapy?
About two thirds of the general adult population are estimated to be at least somewhat hypnotizable, and 15% are highly hypnotizable.
Through brain imaging, the Stanford team found that high hypnotizability is associated with greater functional connectivity between the left dorsolateral prefrontal cortex (DLPFC) and the dorsal anterior cingulate cortex.
In the double-blind study, they randomly assigned 80 patients (mean age, 48 years; 94% women) with fibromyalgia syndrome to active, or sham, continuous theta-burst stimulation over a personalized neuroimaging-derived left DLPFC target — a technique known as Stanford Hypnosis Integrated with Functional Connectivity-targeted Transcranial Stimulation (SHIFT). Individuals who were naturally highly hypnotizable were excluded.
“A novel aspect of this trial is that we used the person’s own brain networks, based on brain imaging, to target the right spot,” Co-senior author Nolan Williams, MD, with Stanford University, California, said in a news release.
The team chose patients with chronic pain because hypnosis has been shown to be a “highly effective analgesic that has a far better risk/benefit ratio than widely overutilized opioids that have serious fatal overdose potential,” Spiegel told this news organization.
The pre-to-post SHIFT change in hypnotic induction profile scores, a standardized measure of hypnotizability, was significantly greater in the active vs sham group after just 92 seconds of stimulation (P = .046).
Only the active SHIFT group showed a significant increase in hypnotizability following stimulation, an effect that lasted for about 1 hour.
“Increasing hypnotizability in people who are low-to-medium hypnotizable individuals could improve both the efficacy and effectiveness of therapeutic hypnosis as a clinical intervention,” the researchers wrote.
They note that because this was a “mechanistic study,” it did not explore the impact of increased hypnotizability on disease symptoms. They also note that further studies are needed to assess the dose-response relationships of SHIFT.
Transformative Research
“This line of research is fascinating,” Shaheen Lakhan, MD, PhD, neurologist, and researcher in Boston, told this news organization.
“We are nearing an era of personalized, noninvasive brain modulation. The ability to individually modulate the DLPFC opens new possibilities for brain health beyond hypnotizability for fibromyalgia,” said Dr. Lakhan, who wasn’t involved in the study.
“The DLPFC is involved in executive functions (and disorders) like attention (ADHD), emotional regulation (depression), motivation (schizophrenia), and impulse control (addiction),” he noted.
“Soon we may no longer need large expensive devices like transcranial magnetic stimulators as in this research study. Smartphones could deliver tailored digital therapeutics by engaging specific brain circuits,” Dr. Lakhan predicted.
“Imagine using an app to receive treatment customized to your unique brain and needs — all without anything implanted and delivered anywhere. The potential to precisely modulate the brain’s wiring to enhance cognition and mental health, without surgery or physical constraints, is incredibly promising. The possibilities are intriguing and could truly transform how we address brain diseases,” he added.
The study was supported by a grant from the National Center for Complementary and Integrative Health (NCCIH), part of the National Institutes of Health (NIH). Dr. Williams is a named inventor on Stanford-owned intellectual property relating to accelerated TMS pulse pattern sequences and neuroimaging-based TMS targeting; has served on scientific advisory boards for Otsuka, NeuraWell, Magnus Medical, and Nooma as a paid advisor; and holds equity/stock options in Magnus Medical, NeuraWell, and Nooma. Dr. Spiegel is a cofounder of Reveri Health, Inc., an interactive hypnosis app (not utilized in the current study).
A version of this article appeared on Medscape.com.
Less than 2 minutes of transcranial magnetic stimulation (TMS) targeting specific areas of the brain can boost an individual’s ability to be hypnotized, in new findings that could increase the efficacy of therapeutic hypnosis and expand the pool of patients who can benefit from it.
“We were able to increase hypnotizability, a neuropsychological trait previously shown to be as stable as IQ in adulthood,” said co-senior author David Spiegel, MD, professor of psychiatry and behavioral sciences, Stanford University, Palo Alto, California.
“Our findings would allow us to combine neurostimulation with hypnosis to expand the number of people able to benefit from hypnosis and enhance their responsiveness to treatment,” Dr. Spiegel added.
The study was published online on January 4, 2024, in Nature Mental Health.
A Breakthrough for Hypnotherapy?
About two thirds of the general adult population are estimated to be at least somewhat hypnotizable, and 15% are highly hypnotizable.
Through brain imaging, the Stanford team found that high hypnotizability is associated with greater functional connectivity between the left dorsolateral prefrontal cortex (DLPFC) and the dorsal anterior cingulate cortex.
In the double-blind study, they randomly assigned 80 patients (mean age, 48 years; 94% women) with fibromyalgia syndrome to active, or sham, continuous theta-burst stimulation over a personalized neuroimaging-derived left DLPFC target — a technique known as Stanford Hypnosis Integrated with Functional Connectivity-targeted Transcranial Stimulation (SHIFT). Individuals who were naturally highly hypnotizable were excluded.
“A novel aspect of this trial is that we used the person’s own brain networks, based on brain imaging, to target the right spot,” Co-senior author Nolan Williams, MD, with Stanford University, California, said in a news release.
The team chose patients with chronic pain because hypnosis has been shown to be a “highly effective analgesic that has a far better risk/benefit ratio than widely overutilized opioids that have serious fatal overdose potential,” Spiegel told this news organization.
The pre-to-post SHIFT change in hypnotic induction profile scores, a standardized measure of hypnotizability, was significantly greater in the active vs sham group after just 92 seconds of stimulation (P = .046).
Only the active SHIFT group showed a significant increase in hypnotizability following stimulation, an effect that lasted for about 1 hour.
“Increasing hypnotizability in people who are low-to-medium hypnotizable individuals could improve both the efficacy and effectiveness of therapeutic hypnosis as a clinical intervention,” the researchers wrote.
They note that because this was a “mechanistic study,” it did not explore the impact of increased hypnotizability on disease symptoms. They also note that further studies are needed to assess the dose-response relationships of SHIFT.
Transformative Research
“This line of research is fascinating,” Shaheen Lakhan, MD, PhD, neurologist, and researcher in Boston, told this news organization.
“We are nearing an era of personalized, noninvasive brain modulation. The ability to individually modulate the DLPFC opens new possibilities for brain health beyond hypnotizability for fibromyalgia,” said Dr. Lakhan, who wasn’t involved in the study.
“The DLPFC is involved in executive functions (and disorders) like attention (ADHD), emotional regulation (depression), motivation (schizophrenia), and impulse control (addiction),” he noted.
“Soon we may no longer need large expensive devices like transcranial magnetic stimulators as in this research study. Smartphones could deliver tailored digital therapeutics by engaging specific brain circuits,” Dr. Lakhan predicted.
“Imagine using an app to receive treatment customized to your unique brain and needs — all without anything implanted and delivered anywhere. The potential to precisely modulate the brain’s wiring to enhance cognition and mental health, without surgery or physical constraints, is incredibly promising. The possibilities are intriguing and could truly transform how we address brain diseases,” he added.
The study was supported by a grant from the National Center for Complementary and Integrative Health (NCCIH), part of the National Institutes of Health (NIH). Dr. Williams is a named inventor on Stanford-owned intellectual property relating to accelerated TMS pulse pattern sequences and neuroimaging-based TMS targeting; has served on scientific advisory boards for Otsuka, NeuraWell, Magnus Medical, and Nooma as a paid advisor; and holds equity/stock options in Magnus Medical, NeuraWell, and Nooma. Dr. Spiegel is a cofounder of Reveri Health, Inc., an interactive hypnosis app (not utilized in the current study).
A version of this article appeared on Medscape.com.
Less than 2 minutes of transcranial magnetic stimulation (TMS) targeting specific areas of the brain can boost an individual’s ability to be hypnotized, in new findings that could increase the efficacy of therapeutic hypnosis and expand the pool of patients who can benefit from it.
“We were able to increase hypnotizability, a neuropsychological trait previously shown to be as stable as IQ in adulthood,” said co-senior author David Spiegel, MD, professor of psychiatry and behavioral sciences, Stanford University, Palo Alto, California.
“Our findings would allow us to combine neurostimulation with hypnosis to expand the number of people able to benefit from hypnosis and enhance their responsiveness to treatment,” Dr. Spiegel added.
The study was published online on January 4, 2024, in Nature Mental Health.
A Breakthrough for Hypnotherapy?
About two thirds of the general adult population are estimated to be at least somewhat hypnotizable, and 15% are highly hypnotizable.
Through brain imaging, the Stanford team found that high hypnotizability is associated with greater functional connectivity between the left dorsolateral prefrontal cortex (DLPFC) and the dorsal anterior cingulate cortex.
In the double-blind study, they randomly assigned 80 patients (mean age, 48 years; 94% women) with fibromyalgia syndrome to active, or sham, continuous theta-burst stimulation over a personalized neuroimaging-derived left DLPFC target — a technique known as Stanford Hypnosis Integrated with Functional Connectivity-targeted Transcranial Stimulation (SHIFT). Individuals who were naturally highly hypnotizable were excluded.
“A novel aspect of this trial is that we used the person’s own brain networks, based on brain imaging, to target the right spot,” Co-senior author Nolan Williams, MD, with Stanford University, California, said in a news release.
The team chose patients with chronic pain because hypnosis has been shown to be a “highly effective analgesic that has a far better risk/benefit ratio than widely overutilized opioids that have serious fatal overdose potential,” Spiegel told this news organization.
The pre-to-post SHIFT change in hypnotic induction profile scores, a standardized measure of hypnotizability, was significantly greater in the active vs sham group after just 92 seconds of stimulation (P = .046).
Only the active SHIFT group showed a significant increase in hypnotizability following stimulation, an effect that lasted for about 1 hour.
“Increasing hypnotizability in people who are low-to-medium hypnotizable individuals could improve both the efficacy and effectiveness of therapeutic hypnosis as a clinical intervention,” the researchers wrote.
They note that because this was a “mechanistic study,” it did not explore the impact of increased hypnotizability on disease symptoms. They also note that further studies are needed to assess the dose-response relationships of SHIFT.
Transformative Research
“This line of research is fascinating,” Shaheen Lakhan, MD, PhD, neurologist, and researcher in Boston, told this news organization.
“We are nearing an era of personalized, noninvasive brain modulation. The ability to individually modulate the DLPFC opens new possibilities for brain health beyond hypnotizability for fibromyalgia,” said Dr. Lakhan, who wasn’t involved in the study.
“The DLPFC is involved in executive functions (and disorders) like attention (ADHD), emotional regulation (depression), motivation (schizophrenia), and impulse control (addiction),” he noted.
“Soon we may no longer need large expensive devices like transcranial magnetic stimulators as in this research study. Smartphones could deliver tailored digital therapeutics by engaging specific brain circuits,” Dr. Lakhan predicted.
“Imagine using an app to receive treatment customized to your unique brain and needs — all without anything implanted and delivered anywhere. The potential to precisely modulate the brain’s wiring to enhance cognition and mental health, without surgery or physical constraints, is incredibly promising. The possibilities are intriguing and could truly transform how we address brain diseases,” he added.
The study was supported by a grant from the National Center for Complementary and Integrative Health (NCCIH), part of the National Institutes of Health (NIH). Dr. Williams is a named inventor on Stanford-owned intellectual property relating to accelerated TMS pulse pattern sequences and neuroimaging-based TMS targeting; has served on scientific advisory boards for Otsuka, NeuraWell, Magnus Medical, and Nooma as a paid advisor; and holds equity/stock options in Magnus Medical, NeuraWell, and Nooma. Dr. Spiegel is a cofounder of Reveri Health, Inc., an interactive hypnosis app (not utilized in the current study).
A version of this article appeared on Medscape.com.
New Prior Auth Policy Tied to Delays, Discontinuation of Oral Cancer Meds
TOPLINE:
Imposing a new prior authorization requirement increased the likelihood that older patients with cancer will delay or stop filling their prescription for oral anticancer drugs, a new study showed.
METHODOLOGY:
- Prior authorization requirements, especially in oncology, continue to increase, but how these policies affect patients’ access to care remains less clear.
- Researchers analyzed Medicare Part D claims from 2010 to 2020 to assess the effects of prior authorization changes on prescriptions fills for 1 of 11 oral anticancer drugs.
- The study included 2495 patients filling a prescription for these medications prior to their health plan imposing a new prior authorization policy and 22,641 patients filling prescriptions for the same drugs with no change in prior authorization policy (control).
- Beneficiaries had at least three 30-day fills in the 120 days before the new prior authorization policy was established on January 1 and continued to be enrolled in the same plan 120 days after the policy change.
- The researchers focused on how often patients discontinued their therapy within 120 days following a prior authorization policy change, as well as the time to fill a prescription after this change.
TAKEAWAY:
- Patients subjected to a new prior authorization policy on an established drug had a sevenfold higher likelihood of stopping the drug within 120 days than those who had no change in prior authorization requirements (adjusted odds ratio, 7.1).
- The adjusted probability of discontinuing an oral cancer regimen within 120 days after an index date of January 1 (when most health plan policy changes occur) was 5.8% for those with a new prior authorization policy vs 1.4% for the control group.
- A new prior authorization requirement was also associated with an average 10-day delay to refill the first prescription following the policy change (P < .001).
- The probability of a delay of more than 30 days was 22% after a policy change vs 7% after no policy change.
IN PRACTICE:
“Our results suggest concerns about delayed and foregone care related to prior authorization are warranted,” the authors said. Overall, this study found that “prior authorization wasted time and undermined the policy priorities of access to care and oral anticancer drug adherence for patients who were regular users of a particular medication.”
SOURCE:
The study by Michael Anna Kyle, PhD, RN, and Nancy Keating, MD, MPH, with Harvard Medical School, Boston, was published online in the Journal of Clinical Oncology.
LIMITATIONS:
The study did not look at patients starting new oral anticancer drugs, which may come with more complex prior authorization processes and create more significant access issues. The results are also limited to patients taking 1 of 11 oral anticancer agents in Medicare Part D.
DISCLOSURES:
Funding for the study was provided by the National Cancer Institute. The authors reported no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
Imposing a new prior authorization requirement increased the likelihood that older patients with cancer will delay or stop filling their prescription for oral anticancer drugs, a new study showed.
METHODOLOGY:
- Prior authorization requirements, especially in oncology, continue to increase, but how these policies affect patients’ access to care remains less clear.
- Researchers analyzed Medicare Part D claims from 2010 to 2020 to assess the effects of prior authorization changes on prescriptions fills for 1 of 11 oral anticancer drugs.
- The study included 2495 patients filling a prescription for these medications prior to their health plan imposing a new prior authorization policy and 22,641 patients filling prescriptions for the same drugs with no change in prior authorization policy (control).
- Beneficiaries had at least three 30-day fills in the 120 days before the new prior authorization policy was established on January 1 and continued to be enrolled in the same plan 120 days after the policy change.
- The researchers focused on how often patients discontinued their therapy within 120 days following a prior authorization policy change, as well as the time to fill a prescription after this change.
TAKEAWAY:
- Patients subjected to a new prior authorization policy on an established drug had a sevenfold higher likelihood of stopping the drug within 120 days than those who had no change in prior authorization requirements (adjusted odds ratio, 7.1).
- The adjusted probability of discontinuing an oral cancer regimen within 120 days after an index date of January 1 (when most health plan policy changes occur) was 5.8% for those with a new prior authorization policy vs 1.4% for the control group.
- A new prior authorization requirement was also associated with an average 10-day delay to refill the first prescription following the policy change (P < .001).
- The probability of a delay of more than 30 days was 22% after a policy change vs 7% after no policy change.
IN PRACTICE:
“Our results suggest concerns about delayed and foregone care related to prior authorization are warranted,” the authors said. Overall, this study found that “prior authorization wasted time and undermined the policy priorities of access to care and oral anticancer drug adherence for patients who were regular users of a particular medication.”
SOURCE:
The study by Michael Anna Kyle, PhD, RN, and Nancy Keating, MD, MPH, with Harvard Medical School, Boston, was published online in the Journal of Clinical Oncology.
LIMITATIONS:
The study did not look at patients starting new oral anticancer drugs, which may come with more complex prior authorization processes and create more significant access issues. The results are also limited to patients taking 1 of 11 oral anticancer agents in Medicare Part D.
DISCLOSURES:
Funding for the study was provided by the National Cancer Institute. The authors reported no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
Imposing a new prior authorization requirement increased the likelihood that older patients with cancer will delay or stop filling their prescription for oral anticancer drugs, a new study showed.
METHODOLOGY:
- Prior authorization requirements, especially in oncology, continue to increase, but how these policies affect patients’ access to care remains less clear.
- Researchers analyzed Medicare Part D claims from 2010 to 2020 to assess the effects of prior authorization changes on prescriptions fills for 1 of 11 oral anticancer drugs.
- The study included 2495 patients filling a prescription for these medications prior to their health plan imposing a new prior authorization policy and 22,641 patients filling prescriptions for the same drugs with no change in prior authorization policy (control).
- Beneficiaries had at least three 30-day fills in the 120 days before the new prior authorization policy was established on January 1 and continued to be enrolled in the same plan 120 days after the policy change.
- The researchers focused on how often patients discontinued their therapy within 120 days following a prior authorization policy change, as well as the time to fill a prescription after this change.
TAKEAWAY:
- Patients subjected to a new prior authorization policy on an established drug had a sevenfold higher likelihood of stopping the drug within 120 days than those who had no change in prior authorization requirements (adjusted odds ratio, 7.1).
- The adjusted probability of discontinuing an oral cancer regimen within 120 days after an index date of January 1 (when most health plan policy changes occur) was 5.8% for those with a new prior authorization policy vs 1.4% for the control group.
- A new prior authorization requirement was also associated with an average 10-day delay to refill the first prescription following the policy change (P < .001).
- The probability of a delay of more than 30 days was 22% after a policy change vs 7% after no policy change.
IN PRACTICE:
“Our results suggest concerns about delayed and foregone care related to prior authorization are warranted,” the authors said. Overall, this study found that “prior authorization wasted time and undermined the policy priorities of access to care and oral anticancer drug adherence for patients who were regular users of a particular medication.”
SOURCE:
The study by Michael Anna Kyle, PhD, RN, and Nancy Keating, MD, MPH, with Harvard Medical School, Boston, was published online in the Journal of Clinical Oncology.
LIMITATIONS:
The study did not look at patients starting new oral anticancer drugs, which may come with more complex prior authorization processes and create more significant access issues. The results are also limited to patients taking 1 of 11 oral anticancer agents in Medicare Part D.
DISCLOSURES:
Funding for the study was provided by the National Cancer Institute. The authors reported no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
Is There a Safe Alcohol Limit in Early Liver Disease?
TOPLINE:
Daily consumption of up to half of a standard US drink (7.4 gram/day) does not appear to increase mortality risk in adults with steatotic liver disease (SLD) who have low risk for advanced fibrosis.
METHODOLOGY:
- Researchers used data from the National Health and Nutrition Examination Survey III (1988-1994) to elucidate the dose-dependent association of alcohol use with SLD progression.
- They identified 2834 adults with confirmed SLD (51.8% male, 34.2% non-Hispanic White), including 591 (20.8%) with intermediate or high risk for advanced fibrosis, defined as a Fibrosis-4 index (FIB-4) score of 1.3 or higher.
- Multivariable Cox regression with restricted cubic spines was used to investigate nonlinear associations between alcohol use and mortality.
TAKEAWAY:
- During median follow-up of 26 years, the mortality rate per 100,000 persons was 4342 in the group with intermediate and high risk for advanced fibrosis versus 1099 in the low-risk group.
- After adjustment for demographics and metabolic variables, there was a nonlinear association between alcohol intake and mortality in the low-risk group (P = .001 for nonlinearity).
- In the low-risk group, the mortality risk threshold was < 7.4 gram/day, which equals half a 12-ounce beer or half a glass of wine. Each additional gram above this level led to a higher death rate.
- No safe alcohol limit was evident in the intermediate- and high-risk group; their mortality risk rose with any alcohol intake.
IN PRACTICE:
“Individuals with SLD should be advised to maintain regular health monitoring and lifestyle management. Recent guidelines have recommended the FIB-4 score as a first-line assessment tool given its low cost, high accuracy, and noninvasiveness,” the authors write. “In this cohort study, we proposed using the FIB-4 score to guide clinicians in advising patients with SLD who choose not to abstain completely from alcohol.”
SOURCE:
The study, with the first author Yee Hui Yeo, MD, at Cedars-Sinai Medical Center, Los Angeles, California, was published online on December 14, 2023, in JAMA Network Open.
LIMITATIONS:
The study relied on self-reported alcohol intake and lacked data on drinking patterns. All variables were only available at baseline, with no tracking of alcohol intake changes during follow-up. Individual risks may vary and require case-by-case discussion as the data are population based.
DISCLOSURES:
The study did not list funding. The authors report no conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
Daily consumption of up to half of a standard US drink (7.4 gram/day) does not appear to increase mortality risk in adults with steatotic liver disease (SLD) who have low risk for advanced fibrosis.
METHODOLOGY:
- Researchers used data from the National Health and Nutrition Examination Survey III (1988-1994) to elucidate the dose-dependent association of alcohol use with SLD progression.
- They identified 2834 adults with confirmed SLD (51.8% male, 34.2% non-Hispanic White), including 591 (20.8%) with intermediate or high risk for advanced fibrosis, defined as a Fibrosis-4 index (FIB-4) score of 1.3 or higher.
- Multivariable Cox regression with restricted cubic spines was used to investigate nonlinear associations between alcohol use and mortality.
TAKEAWAY:
- During median follow-up of 26 years, the mortality rate per 100,000 persons was 4342 in the group with intermediate and high risk for advanced fibrosis versus 1099 in the low-risk group.
- After adjustment for demographics and metabolic variables, there was a nonlinear association between alcohol intake and mortality in the low-risk group (P = .001 for nonlinearity).
- In the low-risk group, the mortality risk threshold was < 7.4 gram/day, which equals half a 12-ounce beer or half a glass of wine. Each additional gram above this level led to a higher death rate.
- No safe alcohol limit was evident in the intermediate- and high-risk group; their mortality risk rose with any alcohol intake.
IN PRACTICE:
“Individuals with SLD should be advised to maintain regular health monitoring and lifestyle management. Recent guidelines have recommended the FIB-4 score as a first-line assessment tool given its low cost, high accuracy, and noninvasiveness,” the authors write. “In this cohort study, we proposed using the FIB-4 score to guide clinicians in advising patients with SLD who choose not to abstain completely from alcohol.”
SOURCE:
The study, with the first author Yee Hui Yeo, MD, at Cedars-Sinai Medical Center, Los Angeles, California, was published online on December 14, 2023, in JAMA Network Open.
LIMITATIONS:
The study relied on self-reported alcohol intake and lacked data on drinking patterns. All variables were only available at baseline, with no tracking of alcohol intake changes during follow-up. Individual risks may vary and require case-by-case discussion as the data are population based.
DISCLOSURES:
The study did not list funding. The authors report no conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
Daily consumption of up to half of a standard US drink (7.4 gram/day) does not appear to increase mortality risk in adults with steatotic liver disease (SLD) who have low risk for advanced fibrosis.
METHODOLOGY:
- Researchers used data from the National Health and Nutrition Examination Survey III (1988-1994) to elucidate the dose-dependent association of alcohol use with SLD progression.
- They identified 2834 adults with confirmed SLD (51.8% male, 34.2% non-Hispanic White), including 591 (20.8%) with intermediate or high risk for advanced fibrosis, defined as a Fibrosis-4 index (FIB-4) score of 1.3 or higher.
- Multivariable Cox regression with restricted cubic spines was used to investigate nonlinear associations between alcohol use and mortality.
TAKEAWAY:
- During median follow-up of 26 years, the mortality rate per 100,000 persons was 4342 in the group with intermediate and high risk for advanced fibrosis versus 1099 in the low-risk group.
- After adjustment for demographics and metabolic variables, there was a nonlinear association between alcohol intake and mortality in the low-risk group (P = .001 for nonlinearity).
- In the low-risk group, the mortality risk threshold was < 7.4 gram/day, which equals half a 12-ounce beer or half a glass of wine. Each additional gram above this level led to a higher death rate.
- No safe alcohol limit was evident in the intermediate- and high-risk group; their mortality risk rose with any alcohol intake.
IN PRACTICE:
“Individuals with SLD should be advised to maintain regular health monitoring and lifestyle management. Recent guidelines have recommended the FIB-4 score as a first-line assessment tool given its low cost, high accuracy, and noninvasiveness,” the authors write. “In this cohort study, we proposed using the FIB-4 score to guide clinicians in advising patients with SLD who choose not to abstain completely from alcohol.”
SOURCE:
The study, with the first author Yee Hui Yeo, MD, at Cedars-Sinai Medical Center, Los Angeles, California, was published online on December 14, 2023, in JAMA Network Open.
LIMITATIONS:
The study relied on self-reported alcohol intake and lacked data on drinking patterns. All variables were only available at baseline, with no tracking of alcohol intake changes during follow-up. Individual risks may vary and require case-by-case discussion as the data are population based.
DISCLOSURES:
The study did not list funding. The authors report no conflicts of interest.
A version of this article appeared on Medscape.com.
Regular Physical Activity Linked to Larger Brain Volume
TOPLINE:
, new data suggest.
METHODOLOGY:
- The potential neuroprotective effects of regular physical activity on brain structure are unclear despite reported links between physical activity and reduced dementia risk.
- To investigate, researchers analyzed MRI brain scans from 10,125 healthy adults (mean age, 53 years; 52% male) who self-reported their level of physical activity.
- Moderate to vigorous physical activities, defined as those increasing respiration and pulse rate for at least 10 continuous minutes, was modeled with brain volumes, adjusting for covariates.
- The threshold for defining physically active (vs nonactive) adults was intentionally set at 2.5 days per week, a level far lower than current guidelines.
TAKEAWAY:
- Three quarters of the cohort reported engaging in moderate to vigorous physical activity approximately 4 days per week.
- Physically active adults tended to be younger, with a higher proportion of White individuals, and with lower rates of hypertension and type 2 diabetes.
- After adjusting for multiple factors, increased days of moderate to vigorous activity correlated with larger normalized brain volume in multiple regions including total gray matter; white matter; hippocampus; and frontal, parietal, and occipital lobes.
IN PRACTICE:
“We found that even moderate levels of physical activity, such as taking fewer than 4,000 steps a day, can have a positive effect on brain health. This is much less than the often-suggested 10,000 steps, making it a more achievable goal for many people,” co-author David Merrill, MD, with Pacific Brain Health Center, Santa Monica, California, said in a statement.
SOURCE:
The study, with first author Cyrus A. Raji, MD, PhD, Washington University School of Medicine, St. Louis, was published online in the Journal of Alzheimer’s Disease.
LIMITATIONS:
Participants self-reported physical activity in the past 2 weeks, which does not reflect a lifetime of activity levels. The correlation identified between physical activity and brain volumes may not be solely attributable to physical activity alone.
DISCLOSURES:
The study received funding from several health centers and foundations. Dr. Raji consults for Brainreader ApS, Neurevolution LLC, Apollo Health, Voxelwise Imaging Technology, and Pacific Neuroscience Foundation and is an editorial board member of the Journal of Alzheimer’s Disease but was not involved in the peer-review process.
A version of this article appeared on Medscape.com.
TOPLINE:
, new data suggest.
METHODOLOGY:
- The potential neuroprotective effects of regular physical activity on brain structure are unclear despite reported links between physical activity and reduced dementia risk.
- To investigate, researchers analyzed MRI brain scans from 10,125 healthy adults (mean age, 53 years; 52% male) who self-reported their level of physical activity.
- Moderate to vigorous physical activities, defined as those increasing respiration and pulse rate for at least 10 continuous minutes, was modeled with brain volumes, adjusting for covariates.
- The threshold for defining physically active (vs nonactive) adults was intentionally set at 2.5 days per week, a level far lower than current guidelines.
TAKEAWAY:
- Three quarters of the cohort reported engaging in moderate to vigorous physical activity approximately 4 days per week.
- Physically active adults tended to be younger, with a higher proportion of White individuals, and with lower rates of hypertension and type 2 diabetes.
- After adjusting for multiple factors, increased days of moderate to vigorous activity correlated with larger normalized brain volume in multiple regions including total gray matter; white matter; hippocampus; and frontal, parietal, and occipital lobes.
IN PRACTICE:
“We found that even moderate levels of physical activity, such as taking fewer than 4,000 steps a day, can have a positive effect on brain health. This is much less than the often-suggested 10,000 steps, making it a more achievable goal for many people,” co-author David Merrill, MD, with Pacific Brain Health Center, Santa Monica, California, said in a statement.
SOURCE:
The study, with first author Cyrus A. Raji, MD, PhD, Washington University School of Medicine, St. Louis, was published online in the Journal of Alzheimer’s Disease.
LIMITATIONS:
Participants self-reported physical activity in the past 2 weeks, which does not reflect a lifetime of activity levels. The correlation identified between physical activity and brain volumes may not be solely attributable to physical activity alone.
DISCLOSURES:
The study received funding from several health centers and foundations. Dr. Raji consults for Brainreader ApS, Neurevolution LLC, Apollo Health, Voxelwise Imaging Technology, and Pacific Neuroscience Foundation and is an editorial board member of the Journal of Alzheimer’s Disease but was not involved in the peer-review process.
A version of this article appeared on Medscape.com.
TOPLINE:
, new data suggest.
METHODOLOGY:
- The potential neuroprotective effects of regular physical activity on brain structure are unclear despite reported links between physical activity and reduced dementia risk.
- To investigate, researchers analyzed MRI brain scans from 10,125 healthy adults (mean age, 53 years; 52% male) who self-reported their level of physical activity.
- Moderate to vigorous physical activities, defined as those increasing respiration and pulse rate for at least 10 continuous minutes, was modeled with brain volumes, adjusting for covariates.
- The threshold for defining physically active (vs nonactive) adults was intentionally set at 2.5 days per week, a level far lower than current guidelines.
TAKEAWAY:
- Three quarters of the cohort reported engaging in moderate to vigorous physical activity approximately 4 days per week.
- Physically active adults tended to be younger, with a higher proportion of White individuals, and with lower rates of hypertension and type 2 diabetes.
- After adjusting for multiple factors, increased days of moderate to vigorous activity correlated with larger normalized brain volume in multiple regions including total gray matter; white matter; hippocampus; and frontal, parietal, and occipital lobes.
IN PRACTICE:
“We found that even moderate levels of physical activity, such as taking fewer than 4,000 steps a day, can have a positive effect on brain health. This is much less than the often-suggested 10,000 steps, making it a more achievable goal for many people,” co-author David Merrill, MD, with Pacific Brain Health Center, Santa Monica, California, said in a statement.
SOURCE:
The study, with first author Cyrus A. Raji, MD, PhD, Washington University School of Medicine, St. Louis, was published online in the Journal of Alzheimer’s Disease.
LIMITATIONS:
Participants self-reported physical activity in the past 2 weeks, which does not reflect a lifetime of activity levels. The correlation identified between physical activity and brain volumes may not be solely attributable to physical activity alone.
DISCLOSURES:
The study received funding from several health centers and foundations. Dr. Raji consults for Brainreader ApS, Neurevolution LLC, Apollo Health, Voxelwise Imaging Technology, and Pacific Neuroscience Foundation and is an editorial board member of the Journal of Alzheimer’s Disease but was not involved in the peer-review process.
A version of this article appeared on Medscape.com.
How an Obesity Drug Could Help Alcohol Use Disorder
The glucagon-like peptide 1 (GLP-1) receptor agonist semaglutide has made headlines as a US Food and Drug Administration (FDA)–approved treatment for type 2 diabetes (Ozempic) and obesity (Wegovy).
Recently,
“There is some really interesting preclinical research in rodents and monkeys that shows that GLP-1 agonist molecules, like semaglutide, have the effect of reducing the consumption of not just food, but also alcohol, nicotine, cocaine and amphetamines,” Kyle Simmons, PhD, professor of pharmacology and physiology at Oklahoma State University Center for Health Sciences in Tulsa, said in an interview.
Some of that early research was conducted by Elisabet Jerlhag Holm, PhD, and colleagues at University of Gothenburg, Sweden.
“We have worked on GLP-1 and alcohol since 2012, and observe promising effects,” Holm told this news organization.
Her team published two studies earlier this year — one in one in Frontiers in Pharmacology and the other in eBioMedicine — demonstrating that semaglutide, in low doses, reduces alcohol intake in male and female rats.
“We have shown that semaglutide binds to the nucleus accumbens — an area of the brain associated with reward. We have also shown that semaglutide alters the dopamine metabolism when alcohol is on board. This provides a tentative mechanism,” Dr. Holm said.
First Human Data
The preclinical data fueled interest in testing the value of the GLP-1 agonist in patient populations with addiction.
Dr. Simmons and colleagues have now published what is believed to be the first evidence in humans that semaglutide specifically reduces the symptoms of alcohol use disorder (AUD).
In a report published online on November 27 in The Journal of Clinical Psychiatry, they describe six patients (of whom five are female; mean age, 43 years) who received semaglutide treatment in the course of pharmacotherapy for weight loss.
All six screened positive for AUD on the Alcohol Use Disorders Identification Test (AUDIT), and all six showed significant improvement in their alcohol-related symptoms after starting semaglutide.
An AUDIT score > 8 is considered positive. The mean AUDIT score at baseline was 14. It fell to 4.5 on average after semaglutide treatment. The mean 9.5-point decrease in AUDIT scores with semaglutide was statistically significant (P < .001).
The patients were followed up from a few weeks to almost 9 months, and all of them had a reduction in AUD symptoms. At the various follow-up time points, all six patients had AUDIT scores consistent with “low-risk” drinking.
Strong Response at Low Doses
“There was a very strong response, even at a very low dose,” lead author Jesse Richards, DO, director of obesity medicine and assistant professor of medicine University of Oklahoma School of Community Medicine, Tulsa, said in an interview.
Three patients were treated with 0.5 mg of semaglutide weekly, two with 0.25 mg weekly, and one with 1 mg weekly. These doses are lower than those currently approved for treatment of type 2 diabetes and obesity.
Dr. Holm is not surprised by the results in these six patients. “Based on our preclinical data, this outcome is expected. The data are promising and bigger studies needed,” she said.
Simmons is currently leading a randomized placebo-controlled trial to further test the impact of semaglutide on AUD.
The STAR (Semaglutide Therapy for Alcohol Reduction) study is funded by the Hardesty Family Foundation and Oklahoma State University Center for Health Sciences.
A sister study is also currently underway in Baltimore, funded by the National Institute on Drug Abuse.
Hopefully, these studies will be able to “definitively tell us whether semaglutide is safe and effective for treatment” for AUD, Dr. Simmons said in a statement.
Despite being a major cause of preventable death worldwide, AUD currently has only three FDA-approved pharmacotherapies. However, there has been limited uptake of these drugs.
“There remains a significant treatment gap and need for new and novel or perhaps better tolerated or different mechanism treatment options for patients,” Dr. Richards said.
The preclinical and early clinical data provide a “signal” of a treatment effect for semaglutide in AUD, Dr. Richards said. The randomized controlled trials now underway should be concluding in the next 1-2 years, “at which point we’ll have a much better sense of the safety and efficacy of this drug for AUD,” he said.
The case series had no specific funding. Dr. Richards is on speakers bureaus for Rhythm Pharmaceuticals and Novo Nordisk and is on an advisory board for Rhythm Pharmaceuticals. Simmons is the recipient of a grant from the Hardesty Family Foundation to support an ongoing clinical trial of semaglutide in the treatment of AUD. Dr. Holm has no relevant disclosures.
A version of this article appeared on Medscape.com.
The glucagon-like peptide 1 (GLP-1) receptor agonist semaglutide has made headlines as a US Food and Drug Administration (FDA)–approved treatment for type 2 diabetes (Ozempic) and obesity (Wegovy).
Recently,
“There is some really interesting preclinical research in rodents and monkeys that shows that GLP-1 agonist molecules, like semaglutide, have the effect of reducing the consumption of not just food, but also alcohol, nicotine, cocaine and amphetamines,” Kyle Simmons, PhD, professor of pharmacology and physiology at Oklahoma State University Center for Health Sciences in Tulsa, said in an interview.
Some of that early research was conducted by Elisabet Jerlhag Holm, PhD, and colleagues at University of Gothenburg, Sweden.
“We have worked on GLP-1 and alcohol since 2012, and observe promising effects,” Holm told this news organization.
Her team published two studies earlier this year — one in one in Frontiers in Pharmacology and the other in eBioMedicine — demonstrating that semaglutide, in low doses, reduces alcohol intake in male and female rats.
“We have shown that semaglutide binds to the nucleus accumbens — an area of the brain associated with reward. We have also shown that semaglutide alters the dopamine metabolism when alcohol is on board. This provides a tentative mechanism,” Dr. Holm said.
First Human Data
The preclinical data fueled interest in testing the value of the GLP-1 agonist in patient populations with addiction.
Dr. Simmons and colleagues have now published what is believed to be the first evidence in humans that semaglutide specifically reduces the symptoms of alcohol use disorder (AUD).
In a report published online on November 27 in The Journal of Clinical Psychiatry, they describe six patients (of whom five are female; mean age, 43 years) who received semaglutide treatment in the course of pharmacotherapy for weight loss.
All six screened positive for AUD on the Alcohol Use Disorders Identification Test (AUDIT), and all six showed significant improvement in their alcohol-related symptoms after starting semaglutide.
An AUDIT score > 8 is considered positive. The mean AUDIT score at baseline was 14. It fell to 4.5 on average after semaglutide treatment. The mean 9.5-point decrease in AUDIT scores with semaglutide was statistically significant (P < .001).
The patients were followed up from a few weeks to almost 9 months, and all of them had a reduction in AUD symptoms. At the various follow-up time points, all six patients had AUDIT scores consistent with “low-risk” drinking.
Strong Response at Low Doses
“There was a very strong response, even at a very low dose,” lead author Jesse Richards, DO, director of obesity medicine and assistant professor of medicine University of Oklahoma School of Community Medicine, Tulsa, said in an interview.
Three patients were treated with 0.5 mg of semaglutide weekly, two with 0.25 mg weekly, and one with 1 mg weekly. These doses are lower than those currently approved for treatment of type 2 diabetes and obesity.
Dr. Holm is not surprised by the results in these six patients. “Based on our preclinical data, this outcome is expected. The data are promising and bigger studies needed,” she said.
Simmons is currently leading a randomized placebo-controlled trial to further test the impact of semaglutide on AUD.
The STAR (Semaglutide Therapy for Alcohol Reduction) study is funded by the Hardesty Family Foundation and Oklahoma State University Center for Health Sciences.
A sister study is also currently underway in Baltimore, funded by the National Institute on Drug Abuse.
Hopefully, these studies will be able to “definitively tell us whether semaglutide is safe and effective for treatment” for AUD, Dr. Simmons said in a statement.
Despite being a major cause of preventable death worldwide, AUD currently has only three FDA-approved pharmacotherapies. However, there has been limited uptake of these drugs.
“There remains a significant treatment gap and need for new and novel or perhaps better tolerated or different mechanism treatment options for patients,” Dr. Richards said.
The preclinical and early clinical data provide a “signal” of a treatment effect for semaglutide in AUD, Dr. Richards said. The randomized controlled trials now underway should be concluding in the next 1-2 years, “at which point we’ll have a much better sense of the safety and efficacy of this drug for AUD,” he said.
The case series had no specific funding. Dr. Richards is on speakers bureaus for Rhythm Pharmaceuticals and Novo Nordisk and is on an advisory board for Rhythm Pharmaceuticals. Simmons is the recipient of a grant from the Hardesty Family Foundation to support an ongoing clinical trial of semaglutide in the treatment of AUD. Dr. Holm has no relevant disclosures.
A version of this article appeared on Medscape.com.
The glucagon-like peptide 1 (GLP-1) receptor agonist semaglutide has made headlines as a US Food and Drug Administration (FDA)–approved treatment for type 2 diabetes (Ozempic) and obesity (Wegovy).
Recently,
“There is some really interesting preclinical research in rodents and monkeys that shows that GLP-1 agonist molecules, like semaglutide, have the effect of reducing the consumption of not just food, but also alcohol, nicotine, cocaine and amphetamines,” Kyle Simmons, PhD, professor of pharmacology and physiology at Oklahoma State University Center for Health Sciences in Tulsa, said in an interview.
Some of that early research was conducted by Elisabet Jerlhag Holm, PhD, and colleagues at University of Gothenburg, Sweden.
“We have worked on GLP-1 and alcohol since 2012, and observe promising effects,” Holm told this news organization.
Her team published two studies earlier this year — one in one in Frontiers in Pharmacology and the other in eBioMedicine — demonstrating that semaglutide, in low doses, reduces alcohol intake in male and female rats.
“We have shown that semaglutide binds to the nucleus accumbens — an area of the brain associated with reward. We have also shown that semaglutide alters the dopamine metabolism when alcohol is on board. This provides a tentative mechanism,” Dr. Holm said.
First Human Data
The preclinical data fueled interest in testing the value of the GLP-1 agonist in patient populations with addiction.
Dr. Simmons and colleagues have now published what is believed to be the first evidence in humans that semaglutide specifically reduces the symptoms of alcohol use disorder (AUD).
In a report published online on November 27 in The Journal of Clinical Psychiatry, they describe six patients (of whom five are female; mean age, 43 years) who received semaglutide treatment in the course of pharmacotherapy for weight loss.
All six screened positive for AUD on the Alcohol Use Disorders Identification Test (AUDIT), and all six showed significant improvement in their alcohol-related symptoms after starting semaglutide.
An AUDIT score > 8 is considered positive. The mean AUDIT score at baseline was 14. It fell to 4.5 on average after semaglutide treatment. The mean 9.5-point decrease in AUDIT scores with semaglutide was statistically significant (P < .001).
The patients were followed up from a few weeks to almost 9 months, and all of them had a reduction in AUD symptoms. At the various follow-up time points, all six patients had AUDIT scores consistent with “low-risk” drinking.
Strong Response at Low Doses
“There was a very strong response, even at a very low dose,” lead author Jesse Richards, DO, director of obesity medicine and assistant professor of medicine University of Oklahoma School of Community Medicine, Tulsa, said in an interview.
Three patients were treated with 0.5 mg of semaglutide weekly, two with 0.25 mg weekly, and one with 1 mg weekly. These doses are lower than those currently approved for treatment of type 2 diabetes and obesity.
Dr. Holm is not surprised by the results in these six patients. “Based on our preclinical data, this outcome is expected. The data are promising and bigger studies needed,” she said.
Simmons is currently leading a randomized placebo-controlled trial to further test the impact of semaglutide on AUD.
The STAR (Semaglutide Therapy for Alcohol Reduction) study is funded by the Hardesty Family Foundation and Oklahoma State University Center for Health Sciences.
A sister study is also currently underway in Baltimore, funded by the National Institute on Drug Abuse.
Hopefully, these studies will be able to “definitively tell us whether semaglutide is safe and effective for treatment” for AUD, Dr. Simmons said in a statement.
Despite being a major cause of preventable death worldwide, AUD currently has only three FDA-approved pharmacotherapies. However, there has been limited uptake of these drugs.
“There remains a significant treatment gap and need for new and novel or perhaps better tolerated or different mechanism treatment options for patients,” Dr. Richards said.
The preclinical and early clinical data provide a “signal” of a treatment effect for semaglutide in AUD, Dr. Richards said. The randomized controlled trials now underway should be concluding in the next 1-2 years, “at which point we’ll have a much better sense of the safety and efficacy of this drug for AUD,” he said.
The case series had no specific funding. Dr. Richards is on speakers bureaus for Rhythm Pharmaceuticals and Novo Nordisk and is on an advisory board for Rhythm Pharmaceuticals. Simmons is the recipient of a grant from the Hardesty Family Foundation to support an ongoing clinical trial of semaglutide in the treatment of AUD. Dr. Holm has no relevant disclosures.
A version of this article appeared on Medscape.com.