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‘Substantial’ variation in responses to BP meds
A new study has shown a substantial variation in the blood pressure response to various antihypertensive medications between individuals, raising the possibility of future personalized therapy.
“We found that using the optimal antihypertensive drug for a particular patient resulted in an average of a 4.4 mm Hg greater reduction of blood pressure compared with a random choice of the other drugs. That is quite a substantial difference, and could be equivalent to adding in another drug,” lead author Johan Sundström, MD, Uppsala (Sweden) University Hospital, told this news organization.
“These preliminary findings suggest that some people may be better treated with one antihypertensive drug rather than another. This is opening up the field of hypertension for personalized medicine,” he added.
The study was published online in the Journal of the American Medical Association.
The authors noted that despite global access to multiple classes of highly effective blood pressure-lowering drugs, only one in four women and one in five men with hypertension reach treatment targets. While most hypertension guidelines advocate combination pharmacotherapy, many patients in routine care continue to be treated with monotherapy, with adverse effects and nonadherence being important clinical problems.
“One drug often does not give enough blood pressure reduction, but patients are often reluctant to up-titrate to two drugs,” Dr. Sundström said. “While we know that the four recommended classes of antihypertensives lower blood pressure equally well on average, we don’t know if their efficacy is the same in individual patients.
“We wondered whether there could be different optimal drugs for different people, and if we could identify the optimal drug for each person then maybe more patients could get to target levels with just one drug,” he said.
The researchers conducted a randomized, double-blind, repeated crossover trial at an outpatient research clinic in Sweden, studying 280 men and women with grade 1 hypertension at low risk for cardiovascular events.
Each participant was scheduled for 2 months’ treatment in random order with each of four different classes of antihypertensive drugs: an ACE inhibitor, lisinopril; an angiotensin II blocker, candesartan; a thiazide diuretic, hydrochlorothiazide; a calcium channel blocker, amlodipine.
There were then repeated treatment periods for two drug classes to try to account for any effect of a particular event that might have affected the blood pressure at one point in time. Ambulatory daytime systolic blood pressure was measured at the end of each treatment period.
Results showed that variation in systolic blood pressure was large between treatments on average, between participants on average, within participants taking the same treatment, and between treatments in the same participant.
Overall, personalized treatment using the optimal single-drug therapy led to a 4.4–mm Hg lower systolic blood pressure in the trial population than a random choice of any of the other drug classes.
Taking into consideration that lisinopril was found to be on average the most efficacious of the drugs at the selected doses, personalized treatment compared with lisinopril still led to a 3.1–mm Hg improvement in systolic blood pressure.
The researchers noted that the mean additional blood pressure reduction achievable by using the optimal agent was of a magnitude twice that achieved by doubling the dose of a first drug, and more than half that of adding a second drug on average.
While there were only small differences between certain drugs (e.g., candesartan vs. lisinopril; amlodipine vs. hydrochlorothiazide), for all other comparisons tested, the choice was important, with particularly large gains to be made by personalizing the choice between candesartan vs. amlodipine and between lisinopril vs. amlodipine.
In addition, some people showed very large differences in response to different drugs, whereas others did not have much difference at all.
How to identify the optimal drug?
“The million-dollar question is how we identify the best drug for each individual patient,” Dr. Sundström said. “This study has opened Pandora’s box. We now need to figure out how to go forward and how we tailor treatment in each patient.”
In the study, the researchers suggest that personalizing therapy could be achieved either by identifying the phenotypic characteristics that are associated with enhanced response to one treatment vs. another or by directly measuring the individual’s responses to a series of treatments to ascertain which is most effective.
Addressing the first scenario, Dr. Sundström explained: “We can analyze the characteristics of patients who did best on each drug. There are many variables we can look at here such as age, diet, baseline blood pressure, exercise levels, smoking status, race, body weight, salt intake, and findings from genetic tests. We are going to try to look into these to see if we can find any predictors of response to various different drugs.”
For the second strategy, he suggested that patients starting pharmacologic therapy could try a few different treatments. “For example, we could give patients two different drugs and ask them to alternate treatment periods with each of them and measure their blood pressure with a home monitoring kit and record adverse effects.”
Nonadherence “is such a big problem with antihypertensives,” he added. “This approach may allow patients to be more empowered when choosing the right treatment, which should help adherence in the longer term.”
‘Proof-of-principle’
Commenting on the study in an accompanying editorial, Robert M. Carey, MD, University of Virginia Health System, Charlottesville, wrote: “At this stage, the findings are more theoretical than immediately practical for the implementation of personalized antihypertensive drug therapy, but the study does provide proof-of-principle and the authors suggest a few scenarios in which a personalized approach could be used in the future.”
He said the practical ramifications of personally targeted therapy remain unclear, given that determination of an individual’s response to a series of short test treatments before selecting long-term therapy may be considered too cumbersome, and currently few phenotypic markers are currently available that would be likely to accurately predict the individual response to a particular therapy.
Dr. Carey concluded that the results of this study “encourage the further pursuit of larger randomized trials using similar repeated crossover designs to validate this concept and eventually in trials with longer follow-up data to determine whether there is improvement in long-term clinical outcomes compared with current strategies.”
He added that the results support the possibility that personalized medical treatment of hypertension “may ultimately supplement or even supplant the current method of antihypertensive drug decision-making in the future.”
This study was supported by the Swedish Research Council; Kjell and Märta Beijer Foundation; and Anders Wiklöf. Dr. Sundström reported owning stock in Symptoms Europe AB and Anagram Kommunikation AB. Coauthor Emil Hagström, MD, PhD, reported receiving grants from Pfizer and Amgen and personal fees from Amgen, Novo Nordisk, Bayer, AstraZeneca, Amarin, and Novartis. Coauthor Ollie Östlund, PhD, reported fees from Uppsala University paid to his institution, Uppsala Clinical Research Center, for its participation in the PHYSIC trial during the conduct of the study. Dr. Carey reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study has shown a substantial variation in the blood pressure response to various antihypertensive medications between individuals, raising the possibility of future personalized therapy.
“We found that using the optimal antihypertensive drug for a particular patient resulted in an average of a 4.4 mm Hg greater reduction of blood pressure compared with a random choice of the other drugs. That is quite a substantial difference, and could be equivalent to adding in another drug,” lead author Johan Sundström, MD, Uppsala (Sweden) University Hospital, told this news organization.
“These preliminary findings suggest that some people may be better treated with one antihypertensive drug rather than another. This is opening up the field of hypertension for personalized medicine,” he added.
The study was published online in the Journal of the American Medical Association.
The authors noted that despite global access to multiple classes of highly effective blood pressure-lowering drugs, only one in four women and one in five men with hypertension reach treatment targets. While most hypertension guidelines advocate combination pharmacotherapy, many patients in routine care continue to be treated with monotherapy, with adverse effects and nonadherence being important clinical problems.
“One drug often does not give enough blood pressure reduction, but patients are often reluctant to up-titrate to two drugs,” Dr. Sundström said. “While we know that the four recommended classes of antihypertensives lower blood pressure equally well on average, we don’t know if their efficacy is the same in individual patients.
“We wondered whether there could be different optimal drugs for different people, and if we could identify the optimal drug for each person then maybe more patients could get to target levels with just one drug,” he said.
The researchers conducted a randomized, double-blind, repeated crossover trial at an outpatient research clinic in Sweden, studying 280 men and women with grade 1 hypertension at low risk for cardiovascular events.
Each participant was scheduled for 2 months’ treatment in random order with each of four different classes of antihypertensive drugs: an ACE inhibitor, lisinopril; an angiotensin II blocker, candesartan; a thiazide diuretic, hydrochlorothiazide; a calcium channel blocker, amlodipine.
There were then repeated treatment periods for two drug classes to try to account for any effect of a particular event that might have affected the blood pressure at one point in time. Ambulatory daytime systolic blood pressure was measured at the end of each treatment period.
Results showed that variation in systolic blood pressure was large between treatments on average, between participants on average, within participants taking the same treatment, and between treatments in the same participant.
Overall, personalized treatment using the optimal single-drug therapy led to a 4.4–mm Hg lower systolic blood pressure in the trial population than a random choice of any of the other drug classes.
Taking into consideration that lisinopril was found to be on average the most efficacious of the drugs at the selected doses, personalized treatment compared with lisinopril still led to a 3.1–mm Hg improvement in systolic blood pressure.
The researchers noted that the mean additional blood pressure reduction achievable by using the optimal agent was of a magnitude twice that achieved by doubling the dose of a first drug, and more than half that of adding a second drug on average.
While there were only small differences between certain drugs (e.g., candesartan vs. lisinopril; amlodipine vs. hydrochlorothiazide), for all other comparisons tested, the choice was important, with particularly large gains to be made by personalizing the choice between candesartan vs. amlodipine and between lisinopril vs. amlodipine.
In addition, some people showed very large differences in response to different drugs, whereas others did not have much difference at all.
How to identify the optimal drug?
“The million-dollar question is how we identify the best drug for each individual patient,” Dr. Sundström said. “This study has opened Pandora’s box. We now need to figure out how to go forward and how we tailor treatment in each patient.”
In the study, the researchers suggest that personalizing therapy could be achieved either by identifying the phenotypic characteristics that are associated with enhanced response to one treatment vs. another or by directly measuring the individual’s responses to a series of treatments to ascertain which is most effective.
Addressing the first scenario, Dr. Sundström explained: “We can analyze the characteristics of patients who did best on each drug. There are many variables we can look at here such as age, diet, baseline blood pressure, exercise levels, smoking status, race, body weight, salt intake, and findings from genetic tests. We are going to try to look into these to see if we can find any predictors of response to various different drugs.”
For the second strategy, he suggested that patients starting pharmacologic therapy could try a few different treatments. “For example, we could give patients two different drugs and ask them to alternate treatment periods with each of them and measure their blood pressure with a home monitoring kit and record adverse effects.”
Nonadherence “is such a big problem with antihypertensives,” he added. “This approach may allow patients to be more empowered when choosing the right treatment, which should help adherence in the longer term.”
‘Proof-of-principle’
Commenting on the study in an accompanying editorial, Robert M. Carey, MD, University of Virginia Health System, Charlottesville, wrote: “At this stage, the findings are more theoretical than immediately practical for the implementation of personalized antihypertensive drug therapy, but the study does provide proof-of-principle and the authors suggest a few scenarios in which a personalized approach could be used in the future.”
He said the practical ramifications of personally targeted therapy remain unclear, given that determination of an individual’s response to a series of short test treatments before selecting long-term therapy may be considered too cumbersome, and currently few phenotypic markers are currently available that would be likely to accurately predict the individual response to a particular therapy.
Dr. Carey concluded that the results of this study “encourage the further pursuit of larger randomized trials using similar repeated crossover designs to validate this concept and eventually in trials with longer follow-up data to determine whether there is improvement in long-term clinical outcomes compared with current strategies.”
He added that the results support the possibility that personalized medical treatment of hypertension “may ultimately supplement or even supplant the current method of antihypertensive drug decision-making in the future.”
This study was supported by the Swedish Research Council; Kjell and Märta Beijer Foundation; and Anders Wiklöf. Dr. Sundström reported owning stock in Symptoms Europe AB and Anagram Kommunikation AB. Coauthor Emil Hagström, MD, PhD, reported receiving grants from Pfizer and Amgen and personal fees from Amgen, Novo Nordisk, Bayer, AstraZeneca, Amarin, and Novartis. Coauthor Ollie Östlund, PhD, reported fees from Uppsala University paid to his institution, Uppsala Clinical Research Center, for its participation in the PHYSIC trial during the conduct of the study. Dr. Carey reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study has shown a substantial variation in the blood pressure response to various antihypertensive medications between individuals, raising the possibility of future personalized therapy.
“We found that using the optimal antihypertensive drug for a particular patient resulted in an average of a 4.4 mm Hg greater reduction of blood pressure compared with a random choice of the other drugs. That is quite a substantial difference, and could be equivalent to adding in another drug,” lead author Johan Sundström, MD, Uppsala (Sweden) University Hospital, told this news organization.
“These preliminary findings suggest that some people may be better treated with one antihypertensive drug rather than another. This is opening up the field of hypertension for personalized medicine,” he added.
The study was published online in the Journal of the American Medical Association.
The authors noted that despite global access to multiple classes of highly effective blood pressure-lowering drugs, only one in four women and one in five men with hypertension reach treatment targets. While most hypertension guidelines advocate combination pharmacotherapy, many patients in routine care continue to be treated with monotherapy, with adverse effects and nonadherence being important clinical problems.
“One drug often does not give enough blood pressure reduction, but patients are often reluctant to up-titrate to two drugs,” Dr. Sundström said. “While we know that the four recommended classes of antihypertensives lower blood pressure equally well on average, we don’t know if their efficacy is the same in individual patients.
“We wondered whether there could be different optimal drugs for different people, and if we could identify the optimal drug for each person then maybe more patients could get to target levels with just one drug,” he said.
The researchers conducted a randomized, double-blind, repeated crossover trial at an outpatient research clinic in Sweden, studying 280 men and women with grade 1 hypertension at low risk for cardiovascular events.
Each participant was scheduled for 2 months’ treatment in random order with each of four different classes of antihypertensive drugs: an ACE inhibitor, lisinopril; an angiotensin II blocker, candesartan; a thiazide diuretic, hydrochlorothiazide; a calcium channel blocker, amlodipine.
There were then repeated treatment periods for two drug classes to try to account for any effect of a particular event that might have affected the blood pressure at one point in time. Ambulatory daytime systolic blood pressure was measured at the end of each treatment period.
Results showed that variation in systolic blood pressure was large between treatments on average, between participants on average, within participants taking the same treatment, and between treatments in the same participant.
Overall, personalized treatment using the optimal single-drug therapy led to a 4.4–mm Hg lower systolic blood pressure in the trial population than a random choice of any of the other drug classes.
Taking into consideration that lisinopril was found to be on average the most efficacious of the drugs at the selected doses, personalized treatment compared with lisinopril still led to a 3.1–mm Hg improvement in systolic blood pressure.
The researchers noted that the mean additional blood pressure reduction achievable by using the optimal agent was of a magnitude twice that achieved by doubling the dose of a first drug, and more than half that of adding a second drug on average.
While there were only small differences between certain drugs (e.g., candesartan vs. lisinopril; amlodipine vs. hydrochlorothiazide), for all other comparisons tested, the choice was important, with particularly large gains to be made by personalizing the choice between candesartan vs. amlodipine and between lisinopril vs. amlodipine.
In addition, some people showed very large differences in response to different drugs, whereas others did not have much difference at all.
How to identify the optimal drug?
“The million-dollar question is how we identify the best drug for each individual patient,” Dr. Sundström said. “This study has opened Pandora’s box. We now need to figure out how to go forward and how we tailor treatment in each patient.”
In the study, the researchers suggest that personalizing therapy could be achieved either by identifying the phenotypic characteristics that are associated with enhanced response to one treatment vs. another or by directly measuring the individual’s responses to a series of treatments to ascertain which is most effective.
Addressing the first scenario, Dr. Sundström explained: “We can analyze the characteristics of patients who did best on each drug. There are many variables we can look at here such as age, diet, baseline blood pressure, exercise levels, smoking status, race, body weight, salt intake, and findings from genetic tests. We are going to try to look into these to see if we can find any predictors of response to various different drugs.”
For the second strategy, he suggested that patients starting pharmacologic therapy could try a few different treatments. “For example, we could give patients two different drugs and ask them to alternate treatment periods with each of them and measure their blood pressure with a home monitoring kit and record adverse effects.”
Nonadherence “is such a big problem with antihypertensives,” he added. “This approach may allow patients to be more empowered when choosing the right treatment, which should help adherence in the longer term.”
‘Proof-of-principle’
Commenting on the study in an accompanying editorial, Robert M. Carey, MD, University of Virginia Health System, Charlottesville, wrote: “At this stage, the findings are more theoretical than immediately practical for the implementation of personalized antihypertensive drug therapy, but the study does provide proof-of-principle and the authors suggest a few scenarios in which a personalized approach could be used in the future.”
He said the practical ramifications of personally targeted therapy remain unclear, given that determination of an individual’s response to a series of short test treatments before selecting long-term therapy may be considered too cumbersome, and currently few phenotypic markers are currently available that would be likely to accurately predict the individual response to a particular therapy.
Dr. Carey concluded that the results of this study “encourage the further pursuit of larger randomized trials using similar repeated crossover designs to validate this concept and eventually in trials with longer follow-up data to determine whether there is improvement in long-term clinical outcomes compared with current strategies.”
He added that the results support the possibility that personalized medical treatment of hypertension “may ultimately supplement or even supplant the current method of antihypertensive drug decision-making in the future.”
This study was supported by the Swedish Research Council; Kjell and Märta Beijer Foundation; and Anders Wiklöf. Dr. Sundström reported owning stock in Symptoms Europe AB and Anagram Kommunikation AB. Coauthor Emil Hagström, MD, PhD, reported receiving grants from Pfizer and Amgen and personal fees from Amgen, Novo Nordisk, Bayer, AstraZeneca, Amarin, and Novartis. Coauthor Ollie Östlund, PhD, reported fees from Uppsala University paid to his institution, Uppsala Clinical Research Center, for its participation in the PHYSIC trial during the conduct of the study. Dr. Carey reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Vaginal microbiome does not affect infant gut microbiome
The findings suggest that practices such as vaginal seeding are ineffective.
A longitudinal, prospective cohort study of more than 600 pregnant Canadian women and their newborns showed significant differences in an infant’s stool composition by delivery mode at 10 days post partum, but the differences could not be explained by the mother’s vaginal microbiome, and they effectively disappeared by 3 months.
The findings were surprising, Scott Dos Santos, a PhD candidate at the University of Saskatchewan in Saskatoon, told this news organization. “The bacteria living in the maternal vagina are the first microbes that vaginally delivered infants are exposed to. … so it sounds intuitive that different kinds of vaginal microbiomes could end up influencing the development of a baby’s gut microbiome in different ways. But the maternal vaginal microbiome didn’t seem to have any role in predicting what the infant stool microbiome looked like.”
Therefore, women should not be concerned about cesarean delivery having an adverse effect on their baby’s gut microbiome, said Mr. Dos Santos. Moreover, “vaginal seeding is not safe or advised. Professional bodies, including the Society of Obstetricians and Gynecologists of Canada and the American College of Obstetricians and Gynecologists, strongly advise against this practice.”
The study was published online in Frontiers in Cellular and Infection Microbiology.
Independent communities
The investigators analyzed vaginal and stool microbiome profiles from 442 mother-infant dyads. The mothers were healthy, low-risk women who delivered at term. They were recruited into the Maternal Microbiome LEGACY Project from three hospitals in British Columbia.
The mean age of the mothers at delivery was 34.6 years, which is typical of the study hospitals’ delivery populations. Participants identified themselves as White (54.7%), Asian (21.2%), South Asian (8.3%), and of other ethnicities.
A nurse, midwife, or clinician collected maternal vaginal swabs of the posterior fornix and lateral vaginal wall at first presentation to the labor and delivery area. Neonatal meconium, which was defined as the first stool specimen collected within 72 hours of birth, and two infant stool samples were collected at follow-up visits at 10 days and 3 months post partum.
A principal component analysis of infant stool microbiomes showed no significant clustering of microbiome profiles at 10 days or 3 months by maternal community state types (that is, microbial species).
Correspondence analyses also showed no coclustering of maternal and infant clusters at either time. In addition, there were no differences in the distribution of maternal vaginal microbiome clusters among infant stool microbiome clusters, regardless of delivery mode.
Vaginal microbiome clusters were distributed across infant stool clusters in proportion to their frequency in the overall maternal population, indicating that the two communities were independent of each other.
Intrapartum antibiotic administration was identified as a confounder of infant stool microbiome differences and was associated with lower abundances of Escherichia coli, Bacteroides vulgatus, Bifidobacterium longum, and Parabacteroides distasonis.
“Our findings demonstrate that maternal vaginal microbiome composition at delivery does not affect infant stool microbiome composition and development, suggesting that practices to amend infant stool microbiome composition focus on factors other than maternal vaginal microbes,” the authors conclude.
More evidence needed
Commenting on the study, Emily H. Adhikari, MD, assistant professor of obstetrics and gynecology at UT Southwestern Medical Center in Dallas, and medical director of perinatal infectious diseases for the Parkland Health and Hospital System, said, “These findings contribute significantly more data to an understudied area of research into factors that affect the infant gut microbiome from the earliest hours of life. Prior studies have been small and often conflicting, and the authors reference recent larger studies, which corroborate their findings.”
The data regarding whether delivery mode or antibiotic-associated differences in infant microbiomes persist remain controversial, said Dr. Adhikari. “More evidence is needed involving a more ethnically diverse sampling of patients.” In addition, prospectively evaluating vaginal seeding in a rigorously designed clinical trial setting is “imperative to understand any potential benefit and certainly to understand the potential harms of the practice. To date, this does not exist.”
The study was funded by a Canadian Institutes of Health Research grant. Mr. Dos Santos and Dr. Adhikari have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The findings suggest that practices such as vaginal seeding are ineffective.
A longitudinal, prospective cohort study of more than 600 pregnant Canadian women and their newborns showed significant differences in an infant’s stool composition by delivery mode at 10 days post partum, but the differences could not be explained by the mother’s vaginal microbiome, and they effectively disappeared by 3 months.
The findings were surprising, Scott Dos Santos, a PhD candidate at the University of Saskatchewan in Saskatoon, told this news organization. “The bacteria living in the maternal vagina are the first microbes that vaginally delivered infants are exposed to. … so it sounds intuitive that different kinds of vaginal microbiomes could end up influencing the development of a baby’s gut microbiome in different ways. But the maternal vaginal microbiome didn’t seem to have any role in predicting what the infant stool microbiome looked like.”
Therefore, women should not be concerned about cesarean delivery having an adverse effect on their baby’s gut microbiome, said Mr. Dos Santos. Moreover, “vaginal seeding is not safe or advised. Professional bodies, including the Society of Obstetricians and Gynecologists of Canada and the American College of Obstetricians and Gynecologists, strongly advise against this practice.”
The study was published online in Frontiers in Cellular and Infection Microbiology.
Independent communities
The investigators analyzed vaginal and stool microbiome profiles from 442 mother-infant dyads. The mothers were healthy, low-risk women who delivered at term. They were recruited into the Maternal Microbiome LEGACY Project from three hospitals in British Columbia.
The mean age of the mothers at delivery was 34.6 years, which is typical of the study hospitals’ delivery populations. Participants identified themselves as White (54.7%), Asian (21.2%), South Asian (8.3%), and of other ethnicities.
A nurse, midwife, or clinician collected maternal vaginal swabs of the posterior fornix and lateral vaginal wall at first presentation to the labor and delivery area. Neonatal meconium, which was defined as the first stool specimen collected within 72 hours of birth, and two infant stool samples were collected at follow-up visits at 10 days and 3 months post partum.
A principal component analysis of infant stool microbiomes showed no significant clustering of microbiome profiles at 10 days or 3 months by maternal community state types (that is, microbial species).
Correspondence analyses also showed no coclustering of maternal and infant clusters at either time. In addition, there were no differences in the distribution of maternal vaginal microbiome clusters among infant stool microbiome clusters, regardless of delivery mode.
Vaginal microbiome clusters were distributed across infant stool clusters in proportion to their frequency in the overall maternal population, indicating that the two communities were independent of each other.
Intrapartum antibiotic administration was identified as a confounder of infant stool microbiome differences and was associated with lower abundances of Escherichia coli, Bacteroides vulgatus, Bifidobacterium longum, and Parabacteroides distasonis.
“Our findings demonstrate that maternal vaginal microbiome composition at delivery does not affect infant stool microbiome composition and development, suggesting that practices to amend infant stool microbiome composition focus on factors other than maternal vaginal microbes,” the authors conclude.
More evidence needed
Commenting on the study, Emily H. Adhikari, MD, assistant professor of obstetrics and gynecology at UT Southwestern Medical Center in Dallas, and medical director of perinatal infectious diseases for the Parkland Health and Hospital System, said, “These findings contribute significantly more data to an understudied area of research into factors that affect the infant gut microbiome from the earliest hours of life. Prior studies have been small and often conflicting, and the authors reference recent larger studies, which corroborate their findings.”
The data regarding whether delivery mode or antibiotic-associated differences in infant microbiomes persist remain controversial, said Dr. Adhikari. “More evidence is needed involving a more ethnically diverse sampling of patients.” In addition, prospectively evaluating vaginal seeding in a rigorously designed clinical trial setting is “imperative to understand any potential benefit and certainly to understand the potential harms of the practice. To date, this does not exist.”
The study was funded by a Canadian Institutes of Health Research grant. Mr. Dos Santos and Dr. Adhikari have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The findings suggest that practices such as vaginal seeding are ineffective.
A longitudinal, prospective cohort study of more than 600 pregnant Canadian women and their newborns showed significant differences in an infant’s stool composition by delivery mode at 10 days post partum, but the differences could not be explained by the mother’s vaginal microbiome, and they effectively disappeared by 3 months.
The findings were surprising, Scott Dos Santos, a PhD candidate at the University of Saskatchewan in Saskatoon, told this news organization. “The bacteria living in the maternal vagina are the first microbes that vaginally delivered infants are exposed to. … so it sounds intuitive that different kinds of vaginal microbiomes could end up influencing the development of a baby’s gut microbiome in different ways. But the maternal vaginal microbiome didn’t seem to have any role in predicting what the infant stool microbiome looked like.”
Therefore, women should not be concerned about cesarean delivery having an adverse effect on their baby’s gut microbiome, said Mr. Dos Santos. Moreover, “vaginal seeding is not safe or advised. Professional bodies, including the Society of Obstetricians and Gynecologists of Canada and the American College of Obstetricians and Gynecologists, strongly advise against this practice.”
The study was published online in Frontiers in Cellular and Infection Microbiology.
Independent communities
The investigators analyzed vaginal and stool microbiome profiles from 442 mother-infant dyads. The mothers were healthy, low-risk women who delivered at term. They were recruited into the Maternal Microbiome LEGACY Project from three hospitals in British Columbia.
The mean age of the mothers at delivery was 34.6 years, which is typical of the study hospitals’ delivery populations. Participants identified themselves as White (54.7%), Asian (21.2%), South Asian (8.3%), and of other ethnicities.
A nurse, midwife, or clinician collected maternal vaginal swabs of the posterior fornix and lateral vaginal wall at first presentation to the labor and delivery area. Neonatal meconium, which was defined as the first stool specimen collected within 72 hours of birth, and two infant stool samples were collected at follow-up visits at 10 days and 3 months post partum.
A principal component analysis of infant stool microbiomes showed no significant clustering of microbiome profiles at 10 days or 3 months by maternal community state types (that is, microbial species).
Correspondence analyses also showed no coclustering of maternal and infant clusters at either time. In addition, there were no differences in the distribution of maternal vaginal microbiome clusters among infant stool microbiome clusters, regardless of delivery mode.
Vaginal microbiome clusters were distributed across infant stool clusters in proportion to their frequency in the overall maternal population, indicating that the two communities were independent of each other.
Intrapartum antibiotic administration was identified as a confounder of infant stool microbiome differences and was associated with lower abundances of Escherichia coli, Bacteroides vulgatus, Bifidobacterium longum, and Parabacteroides distasonis.
“Our findings demonstrate that maternal vaginal microbiome composition at delivery does not affect infant stool microbiome composition and development, suggesting that practices to amend infant stool microbiome composition focus on factors other than maternal vaginal microbes,” the authors conclude.
More evidence needed
Commenting on the study, Emily H. Adhikari, MD, assistant professor of obstetrics and gynecology at UT Southwestern Medical Center in Dallas, and medical director of perinatal infectious diseases for the Parkland Health and Hospital System, said, “These findings contribute significantly more data to an understudied area of research into factors that affect the infant gut microbiome from the earliest hours of life. Prior studies have been small and often conflicting, and the authors reference recent larger studies, which corroborate their findings.”
The data regarding whether delivery mode or antibiotic-associated differences in infant microbiomes persist remain controversial, said Dr. Adhikari. “More evidence is needed involving a more ethnically diverse sampling of patients.” In addition, prospectively evaluating vaginal seeding in a rigorously designed clinical trial setting is “imperative to understand any potential benefit and certainly to understand the potential harms of the practice. To date, this does not exist.”
The study was funded by a Canadian Institutes of Health Research grant. Mr. Dos Santos and Dr. Adhikari have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
Alzheimer’s drug may ease hair pulling, skin-picking disorders
Results from the double-blind, placebo-controlled trial showed that 61% of participants who received memantine were “much or very much improved,” versus 8% in the placebo group.
“Memantine was far more effective than placebo,” lead investigator Jon Grant, MD, MPH, professor of psychiatry and behavioral neuroscience at the University of Chicago, said in an interview. “However, while subjects responded favorably, that didn’t necessarily mean there were no symptoms.”
The study was published online in the American Journal of Psychiatry.
Underrecognized, disabling
The investigators noted that trichotillomania and skin-picking disorder are underrecognized and are often disabling conditions. However, the researchers pointed out that with prevalence rates of 1.7% for trichotillomania and 2.1% for skin-picking disorder, they are not uncommon.
Behavioral therapy that attempts to reverse these habits is considered first-line treatment, but trained therapists are difficult to find. In addition, the investigators wrote that currently, there are no Food and Drug Administration–approved medications for either disorder, and pharmacologic clinical trials are relatively uncommon.
The existing data from double-blind, placebo-controlled studies support the use of the antipsychotic olanzapine, the tricyclic antidepressant clomipramine, and the supplement N-acetyl-L-cysteine (NAC). Dr. Grant also noted that previous drug trials involving patients with trichotillomania have been very short in duration.
Prior research has implicated the glutamate system in repetitive motor habits and the urges that drive them. Memantine, a glutamate receptor antagonist, targets excessive glutamatergic drive. To investigate whether this medication may be beneficial for patients with trichotillomania and skin-picking disorders, the investigators conducted a randomized placebo-controlled trial.
The study included 100 adults (86 women; mean age, 31.4) with trichotillomania, skin-picking disorder, or both; participants received memantine (n = 55) or placebo (n = 45) for 8 weeks; they received memantine 10 mg or placebo for the first 2 weeks, then 20 mg for the next 6 weeks.
The researchers, who were blinded to assignment, assessed participants every 2 weeks using the National Institute of Mental Health Trichotillomania Symptom Severity Scale, which was modified to include questions for skin-picking disorder.
The team also tracked symptoms and behaviors using additional scales, including the Sheehan Disability Scale and the Clinical Global Impressions severity scale.
At the study’s conclusion, 79 patients remained. Of those, 26 of the 43 participants in the memantine group were “very much” or “much” improved (61%), versus 3 of 36 (8%) in the placebo group. (P < .0001)
Six participants in the memantine group experienced complete remission of symptoms, compared with one in the placebo group. There were no differences between the study groups in terms of adverse events.
Study limitations included the relatively short length of the trial for what should be considered a chronic disease, as well as the inclusion of only mildly to moderately symptomatic participants.
Dr. Grant said that he would like to study how memantine works in combination with behavioral therapy.
‘Two great options’
Katharine Phillips, MD, professor of psychiatry at Weill Cornell Medicine, New York, said she has been using memantine for “quite some time” to treat her patients with skin-picking disorder, adding that she uses higher doses of the drug than were tested in the study.
She noted that both NAC and memantine affect glutamate, an amino acid in the brain that is likely involved in repetitive physical or motor habits, such as hair pulling and skin picking.
“The good news is that we have two great options” for the treatment of trichotillomania and skin-picking disorder, said Dr. Phillips, and that both are easy to tolerate.
Future research should focus on longer trials of memantine and at higher doses, as well as other glutamate modulators, she said.
The study was funded by departmental research funds at the University of Chicago. Dr. Grant reported receiving research funding from Biohaven Pharmaceuticals and Janssen, as well as yearly compensation from Springer Publishing for his role as editor-in-chief of the Journal of Gambling Studies. He has also received royalties from American Psychiatric Publishing, McGraw Hill, Oxford University Press, and WW Norton. Dr. Phillips reported receiving royalties from American Psychiatric Publishing and an honorarium from the Merck Manual.
A version of this article first appeared on Medscape.com.
Results from the double-blind, placebo-controlled trial showed that 61% of participants who received memantine were “much or very much improved,” versus 8% in the placebo group.
“Memantine was far more effective than placebo,” lead investigator Jon Grant, MD, MPH, professor of psychiatry and behavioral neuroscience at the University of Chicago, said in an interview. “However, while subjects responded favorably, that didn’t necessarily mean there were no symptoms.”
The study was published online in the American Journal of Psychiatry.
Underrecognized, disabling
The investigators noted that trichotillomania and skin-picking disorder are underrecognized and are often disabling conditions. However, the researchers pointed out that with prevalence rates of 1.7% for trichotillomania and 2.1% for skin-picking disorder, they are not uncommon.
Behavioral therapy that attempts to reverse these habits is considered first-line treatment, but trained therapists are difficult to find. In addition, the investigators wrote that currently, there are no Food and Drug Administration–approved medications for either disorder, and pharmacologic clinical trials are relatively uncommon.
The existing data from double-blind, placebo-controlled studies support the use of the antipsychotic olanzapine, the tricyclic antidepressant clomipramine, and the supplement N-acetyl-L-cysteine (NAC). Dr. Grant also noted that previous drug trials involving patients with trichotillomania have been very short in duration.
Prior research has implicated the glutamate system in repetitive motor habits and the urges that drive them. Memantine, a glutamate receptor antagonist, targets excessive glutamatergic drive. To investigate whether this medication may be beneficial for patients with trichotillomania and skin-picking disorders, the investigators conducted a randomized placebo-controlled trial.
The study included 100 adults (86 women; mean age, 31.4) with trichotillomania, skin-picking disorder, or both; participants received memantine (n = 55) or placebo (n = 45) for 8 weeks; they received memantine 10 mg or placebo for the first 2 weeks, then 20 mg for the next 6 weeks.
The researchers, who were blinded to assignment, assessed participants every 2 weeks using the National Institute of Mental Health Trichotillomania Symptom Severity Scale, which was modified to include questions for skin-picking disorder.
The team also tracked symptoms and behaviors using additional scales, including the Sheehan Disability Scale and the Clinical Global Impressions severity scale.
At the study’s conclusion, 79 patients remained. Of those, 26 of the 43 participants in the memantine group were “very much” or “much” improved (61%), versus 3 of 36 (8%) in the placebo group. (P < .0001)
Six participants in the memantine group experienced complete remission of symptoms, compared with one in the placebo group. There were no differences between the study groups in terms of adverse events.
Study limitations included the relatively short length of the trial for what should be considered a chronic disease, as well as the inclusion of only mildly to moderately symptomatic participants.
Dr. Grant said that he would like to study how memantine works in combination with behavioral therapy.
‘Two great options’
Katharine Phillips, MD, professor of psychiatry at Weill Cornell Medicine, New York, said she has been using memantine for “quite some time” to treat her patients with skin-picking disorder, adding that she uses higher doses of the drug than were tested in the study.
She noted that both NAC and memantine affect glutamate, an amino acid in the brain that is likely involved in repetitive physical or motor habits, such as hair pulling and skin picking.
“The good news is that we have two great options” for the treatment of trichotillomania and skin-picking disorder, said Dr. Phillips, and that both are easy to tolerate.
Future research should focus on longer trials of memantine and at higher doses, as well as other glutamate modulators, she said.
The study was funded by departmental research funds at the University of Chicago. Dr. Grant reported receiving research funding from Biohaven Pharmaceuticals and Janssen, as well as yearly compensation from Springer Publishing for his role as editor-in-chief of the Journal of Gambling Studies. He has also received royalties from American Psychiatric Publishing, McGraw Hill, Oxford University Press, and WW Norton. Dr. Phillips reported receiving royalties from American Psychiatric Publishing and an honorarium from the Merck Manual.
A version of this article first appeared on Medscape.com.
Results from the double-blind, placebo-controlled trial showed that 61% of participants who received memantine were “much or very much improved,” versus 8% in the placebo group.
“Memantine was far more effective than placebo,” lead investigator Jon Grant, MD, MPH, professor of psychiatry and behavioral neuroscience at the University of Chicago, said in an interview. “However, while subjects responded favorably, that didn’t necessarily mean there were no symptoms.”
The study was published online in the American Journal of Psychiatry.
Underrecognized, disabling
The investigators noted that trichotillomania and skin-picking disorder are underrecognized and are often disabling conditions. However, the researchers pointed out that with prevalence rates of 1.7% for trichotillomania and 2.1% for skin-picking disorder, they are not uncommon.
Behavioral therapy that attempts to reverse these habits is considered first-line treatment, but trained therapists are difficult to find. In addition, the investigators wrote that currently, there are no Food and Drug Administration–approved medications for either disorder, and pharmacologic clinical trials are relatively uncommon.
The existing data from double-blind, placebo-controlled studies support the use of the antipsychotic olanzapine, the tricyclic antidepressant clomipramine, and the supplement N-acetyl-L-cysteine (NAC). Dr. Grant also noted that previous drug trials involving patients with trichotillomania have been very short in duration.
Prior research has implicated the glutamate system in repetitive motor habits and the urges that drive them. Memantine, a glutamate receptor antagonist, targets excessive glutamatergic drive. To investigate whether this medication may be beneficial for patients with trichotillomania and skin-picking disorders, the investigators conducted a randomized placebo-controlled trial.
The study included 100 adults (86 women; mean age, 31.4) with trichotillomania, skin-picking disorder, or both; participants received memantine (n = 55) or placebo (n = 45) for 8 weeks; they received memantine 10 mg or placebo for the first 2 weeks, then 20 mg for the next 6 weeks.
The researchers, who were blinded to assignment, assessed participants every 2 weeks using the National Institute of Mental Health Trichotillomania Symptom Severity Scale, which was modified to include questions for skin-picking disorder.
The team also tracked symptoms and behaviors using additional scales, including the Sheehan Disability Scale and the Clinical Global Impressions severity scale.
At the study’s conclusion, 79 patients remained. Of those, 26 of the 43 participants in the memantine group were “very much” or “much” improved (61%), versus 3 of 36 (8%) in the placebo group. (P < .0001)
Six participants in the memantine group experienced complete remission of symptoms, compared with one in the placebo group. There were no differences between the study groups in terms of adverse events.
Study limitations included the relatively short length of the trial for what should be considered a chronic disease, as well as the inclusion of only mildly to moderately symptomatic participants.
Dr. Grant said that he would like to study how memantine works in combination with behavioral therapy.
‘Two great options’
Katharine Phillips, MD, professor of psychiatry at Weill Cornell Medicine, New York, said she has been using memantine for “quite some time” to treat her patients with skin-picking disorder, adding that she uses higher doses of the drug than were tested in the study.
She noted that both NAC and memantine affect glutamate, an amino acid in the brain that is likely involved in repetitive physical or motor habits, such as hair pulling and skin picking.
“The good news is that we have two great options” for the treatment of trichotillomania and skin-picking disorder, said Dr. Phillips, and that both are easy to tolerate.
Future research should focus on longer trials of memantine and at higher doses, as well as other glutamate modulators, she said.
The study was funded by departmental research funds at the University of Chicago. Dr. Grant reported receiving research funding from Biohaven Pharmaceuticals and Janssen, as well as yearly compensation from Springer Publishing for his role as editor-in-chief of the Journal of Gambling Studies. He has also received royalties from American Psychiatric Publishing, McGraw Hill, Oxford University Press, and WW Norton. Dr. Phillips reported receiving royalties from American Psychiatric Publishing and an honorarium from the Merck Manual.
A version of this article first appeared on Medscape.com.
FROM THE AMERICAN JOURNAL OF PSYCHIATRY
Integrating addiction medicine with primary care cost effective: Study
Integrating buprenorphine and harm eduction tools into primary care may improve clinical outcomes, increase costs only modestly, and be cost effective in health systems, authors conclude in an original investigation in JAMA Network Open.
A team led by Raagini Jawa, MD, MPH, with the Center for Research on Healthcare, University of Pittsburgh, set out to analyze costs of the interventions versus increased benefit in extending life expectancy.
Their analysis found that, compared with the status quo, integrating buprenorphine and harm reduction kits (syringes, wound care supplies, etc.) reduced drug use–related deaths by 33% and was cost effective.
“Our results suggest that integrated addiction care in primary care has the potential to save lives and increase nonemergency health care use, which is consistent with prior literature,” the authors write. “Colocated addiction services within primary care is pragmatic and effective and has comparable quality to specialty care. We found that onsite BUP [buprenorphine prescribing] plus HR [harm reduction] provides better outcomes than BUP alone at a lower cost.”
Three strategies compared
Using a microsimulation model of 2.25 million people in the United States who inject opioids, with an average age of 44 (69% of them male), the researchers tested three strategies:
- Status quo. PCP refers to addiction care.
- BUP. PCP services plus onsite buprenorphine prescribing with referral to off-site harm reduction kits.
- BUP plus HR. PCP services plus on-site buprenorphine prescribing and harm reduction kits.
The model is the Reducing Infections Related to Drug Use Cost-Effectiveness (REDUCE) microsimulation model, which tracks serious injection-related infections, overdose, hospitalization, and death.
The status quo (referral for treatment) resulted in 1,162 overdose deaths per 10,000 people (95% credible interval, 1,144-2,303), whereas both BUP and BUP plus HR resulted in about 160 fewer deaths per 10,000 people (95% Crl for BUP, 802-1718; 95% CrI for BUP plus HR, 692-1,810).
Compared with the status quo strategy, life expectancy was lengthened with the BUP strategy by 2.65 years and BUP plus HR by 2.71 years.
Researchers found the average discounted lifetime cost per person of both the BUP strategy and the BUP plus HR strategy were higher than the average status quo.
“The dominating strategy was BUP plus HR,” the authors write. “Compared with status quo, BUP plus HR was cost effective (incremental cost-effectiveness ratio [ICER], $34,400 per life year).”
Cost for primary care practices
Comparatively, over a 5-year period, BUP plus HR was found to cost an individual PCP practice approximately $13,000.
That cost includes direct costs for resources and opportunity costs, the authors write. These costs could be offset by health care system savings.
“These costs included those for X-waiver training, which has been eliminated; thus, we expect this to cost less. Put another way, our findings inform ways to reinvest health care dollars as financial incentives for PCPs to adopt this new paradigm. Public health departments could provide grants or harm reduction kit supplies directly to PCPs to offset these costs as they do in some places with syringe service programs and/or increase Medicaid reimbursements for providing addiction care in primary care,” they write.
Data help make the case
Dinah Applewhite, MD, a primary care physician and addiction medicine specialist at Massachusetts General Hospital in Boston, who was not part of the study, said clinicians there have seen the benefits of integrating various aspects of addiction medicine into primary care but these data on outcomes and cost-effectiveness can help make the case to hospital leaders, legislators, and grant providers.
The primary care setting also provides a chance to engage patients around their injection practice and explore ways to minimize risk, she said.
“By offering them these kits, it lets them know your priority is their safety and well-being,” Dr. Applewhite said.
She noted that the linkage to primary care was low for patients who inject drugs, which speaks to the need for models in addition to this one, such as bringing primary care clinicians into syringe service programs.
“The medical establishment has a lot to learn from these programs,” she said.
Practices need support
She said it’s important to note that primary care practices need support from administrative leaders, philanthropists, and grant providers to help cover the costs.
“It’s one of the barriers to doing this,” she said. “There isn’t a mechanism to pay for this.”
Sarah Bagley, MD, a primary care physician at Boston Medical Center and medical director of BMC’s Center for Addiction Treatment for Adolescents/Young Adults Who Use Substances told this publication she was excited to see that the addition of harm reduction kits to buprenorphine seemed to have the optimal effect in improving outcomes. People with substance abuse disorders should feel they are welcome in primary care even if they are not yet ready to stop drug use, she said.
She said she was also glad to see increased life expectancy with these interventions. The news of overdose deaths contributing to a decrease in life expectancy can be overwhelming, she said.
But this study, she says, offers a road map for addressing the overdose crisis “by including harm reduction in the substance abuse care we provide.”
She pointed out that the study showed that costs increase per patient with both interventions, compared with the status quo. The study found that health care costs per person during a lifetime increased, compared with the status quo, by 69.1% for BUP and 74.3% for BUP plus HR.
But it’s important to understand the reason for that, she said: “The cost was higher because people were staying alive.”
She said it may help to compare giving optimal care to people who have substance abuse disorders with giving optimal care to people with other chronic conditions, such as diabetes, who may not always adhere to recommended diets or treatment regimens.
“We still invite those patients in and work with them based on where they are,” she said.
Growing epidemic
The researchers point to the urgent need for solutions given the U.S. opioid epidemic, which has led to increasing numbers of overdoses and injection drug use–related infections, such as infective endocarditis, and severe skin and soft tissue infections.
They point out that primary care providers are the largest clinical workforce in the United States, but few of their practices offer comprehensive addiction care onsite.
“Primary care practices are a practical place to integrate addiction services, where PCPs can prescribe buprenorphine and deliver harm reduction kits,” they write.
Coauthor Dr. Kimmel reports personal fees from Massachusetts Department of Public Health, Bureau of Substance Addiction Services Overdose Education and Prevention Program, and American Academy of Addiction Psychiatry, Opioid Response Network for harm reduction education outside the submitted work and previous consulting with Abt Associates on a Massachusetts Department of Public Health–funded project to improve access to medications for opioid use disorder treatment. Dr. Applewhite and Dr. Bagley report no relevant financial relationships.
Integrating buprenorphine and harm eduction tools into primary care may improve clinical outcomes, increase costs only modestly, and be cost effective in health systems, authors conclude in an original investigation in JAMA Network Open.
A team led by Raagini Jawa, MD, MPH, with the Center for Research on Healthcare, University of Pittsburgh, set out to analyze costs of the interventions versus increased benefit in extending life expectancy.
Their analysis found that, compared with the status quo, integrating buprenorphine and harm reduction kits (syringes, wound care supplies, etc.) reduced drug use–related deaths by 33% and was cost effective.
“Our results suggest that integrated addiction care in primary care has the potential to save lives and increase nonemergency health care use, which is consistent with prior literature,” the authors write. “Colocated addiction services within primary care is pragmatic and effective and has comparable quality to specialty care. We found that onsite BUP [buprenorphine prescribing] plus HR [harm reduction] provides better outcomes than BUP alone at a lower cost.”
Three strategies compared
Using a microsimulation model of 2.25 million people in the United States who inject opioids, with an average age of 44 (69% of them male), the researchers tested three strategies:
- Status quo. PCP refers to addiction care.
- BUP. PCP services plus onsite buprenorphine prescribing with referral to off-site harm reduction kits.
- BUP plus HR. PCP services plus on-site buprenorphine prescribing and harm reduction kits.
The model is the Reducing Infections Related to Drug Use Cost-Effectiveness (REDUCE) microsimulation model, which tracks serious injection-related infections, overdose, hospitalization, and death.
The status quo (referral for treatment) resulted in 1,162 overdose deaths per 10,000 people (95% credible interval, 1,144-2,303), whereas both BUP and BUP plus HR resulted in about 160 fewer deaths per 10,000 people (95% Crl for BUP, 802-1718; 95% CrI for BUP plus HR, 692-1,810).
Compared with the status quo strategy, life expectancy was lengthened with the BUP strategy by 2.65 years and BUP plus HR by 2.71 years.
Researchers found the average discounted lifetime cost per person of both the BUP strategy and the BUP plus HR strategy were higher than the average status quo.
“The dominating strategy was BUP plus HR,” the authors write. “Compared with status quo, BUP plus HR was cost effective (incremental cost-effectiveness ratio [ICER], $34,400 per life year).”
Cost for primary care practices
Comparatively, over a 5-year period, BUP plus HR was found to cost an individual PCP practice approximately $13,000.
That cost includes direct costs for resources and opportunity costs, the authors write. These costs could be offset by health care system savings.
“These costs included those for X-waiver training, which has been eliminated; thus, we expect this to cost less. Put another way, our findings inform ways to reinvest health care dollars as financial incentives for PCPs to adopt this new paradigm. Public health departments could provide grants or harm reduction kit supplies directly to PCPs to offset these costs as they do in some places with syringe service programs and/or increase Medicaid reimbursements for providing addiction care in primary care,” they write.
Data help make the case
Dinah Applewhite, MD, a primary care physician and addiction medicine specialist at Massachusetts General Hospital in Boston, who was not part of the study, said clinicians there have seen the benefits of integrating various aspects of addiction medicine into primary care but these data on outcomes and cost-effectiveness can help make the case to hospital leaders, legislators, and grant providers.
The primary care setting also provides a chance to engage patients around their injection practice and explore ways to minimize risk, she said.
“By offering them these kits, it lets them know your priority is their safety and well-being,” Dr. Applewhite said.
She noted that the linkage to primary care was low for patients who inject drugs, which speaks to the need for models in addition to this one, such as bringing primary care clinicians into syringe service programs.
“The medical establishment has a lot to learn from these programs,” she said.
Practices need support
She said it’s important to note that primary care practices need support from administrative leaders, philanthropists, and grant providers to help cover the costs.
“It’s one of the barriers to doing this,” she said. “There isn’t a mechanism to pay for this.”
Sarah Bagley, MD, a primary care physician at Boston Medical Center and medical director of BMC’s Center for Addiction Treatment for Adolescents/Young Adults Who Use Substances told this publication she was excited to see that the addition of harm reduction kits to buprenorphine seemed to have the optimal effect in improving outcomes. People with substance abuse disorders should feel they are welcome in primary care even if they are not yet ready to stop drug use, she said.
She said she was also glad to see increased life expectancy with these interventions. The news of overdose deaths contributing to a decrease in life expectancy can be overwhelming, she said.
But this study, she says, offers a road map for addressing the overdose crisis “by including harm reduction in the substance abuse care we provide.”
She pointed out that the study showed that costs increase per patient with both interventions, compared with the status quo. The study found that health care costs per person during a lifetime increased, compared with the status quo, by 69.1% for BUP and 74.3% for BUP plus HR.
But it’s important to understand the reason for that, she said: “The cost was higher because people were staying alive.”
She said it may help to compare giving optimal care to people who have substance abuse disorders with giving optimal care to people with other chronic conditions, such as diabetes, who may not always adhere to recommended diets or treatment regimens.
“We still invite those patients in and work with them based on where they are,” she said.
Growing epidemic
The researchers point to the urgent need for solutions given the U.S. opioid epidemic, which has led to increasing numbers of overdoses and injection drug use–related infections, such as infective endocarditis, and severe skin and soft tissue infections.
They point out that primary care providers are the largest clinical workforce in the United States, but few of their practices offer comprehensive addiction care onsite.
“Primary care practices are a practical place to integrate addiction services, where PCPs can prescribe buprenorphine and deliver harm reduction kits,” they write.
Coauthor Dr. Kimmel reports personal fees from Massachusetts Department of Public Health, Bureau of Substance Addiction Services Overdose Education and Prevention Program, and American Academy of Addiction Psychiatry, Opioid Response Network for harm reduction education outside the submitted work and previous consulting with Abt Associates on a Massachusetts Department of Public Health–funded project to improve access to medications for opioid use disorder treatment. Dr. Applewhite and Dr. Bagley report no relevant financial relationships.
Integrating buprenorphine and harm eduction tools into primary care may improve clinical outcomes, increase costs only modestly, and be cost effective in health systems, authors conclude in an original investigation in JAMA Network Open.
A team led by Raagini Jawa, MD, MPH, with the Center for Research on Healthcare, University of Pittsburgh, set out to analyze costs of the interventions versus increased benefit in extending life expectancy.
Their analysis found that, compared with the status quo, integrating buprenorphine and harm reduction kits (syringes, wound care supplies, etc.) reduced drug use–related deaths by 33% and was cost effective.
“Our results suggest that integrated addiction care in primary care has the potential to save lives and increase nonemergency health care use, which is consistent with prior literature,” the authors write. “Colocated addiction services within primary care is pragmatic and effective and has comparable quality to specialty care. We found that onsite BUP [buprenorphine prescribing] plus HR [harm reduction] provides better outcomes than BUP alone at a lower cost.”
Three strategies compared
Using a microsimulation model of 2.25 million people in the United States who inject opioids, with an average age of 44 (69% of them male), the researchers tested three strategies:
- Status quo. PCP refers to addiction care.
- BUP. PCP services plus onsite buprenorphine prescribing with referral to off-site harm reduction kits.
- BUP plus HR. PCP services plus on-site buprenorphine prescribing and harm reduction kits.
The model is the Reducing Infections Related to Drug Use Cost-Effectiveness (REDUCE) microsimulation model, which tracks serious injection-related infections, overdose, hospitalization, and death.
The status quo (referral for treatment) resulted in 1,162 overdose deaths per 10,000 people (95% credible interval, 1,144-2,303), whereas both BUP and BUP plus HR resulted in about 160 fewer deaths per 10,000 people (95% Crl for BUP, 802-1718; 95% CrI for BUP plus HR, 692-1,810).
Compared with the status quo strategy, life expectancy was lengthened with the BUP strategy by 2.65 years and BUP plus HR by 2.71 years.
Researchers found the average discounted lifetime cost per person of both the BUP strategy and the BUP plus HR strategy were higher than the average status quo.
“The dominating strategy was BUP plus HR,” the authors write. “Compared with status quo, BUP plus HR was cost effective (incremental cost-effectiveness ratio [ICER], $34,400 per life year).”
Cost for primary care practices
Comparatively, over a 5-year period, BUP plus HR was found to cost an individual PCP practice approximately $13,000.
That cost includes direct costs for resources and opportunity costs, the authors write. These costs could be offset by health care system savings.
“These costs included those for X-waiver training, which has been eliminated; thus, we expect this to cost less. Put another way, our findings inform ways to reinvest health care dollars as financial incentives for PCPs to adopt this new paradigm. Public health departments could provide grants or harm reduction kit supplies directly to PCPs to offset these costs as they do in some places with syringe service programs and/or increase Medicaid reimbursements for providing addiction care in primary care,” they write.
Data help make the case
Dinah Applewhite, MD, a primary care physician and addiction medicine specialist at Massachusetts General Hospital in Boston, who was not part of the study, said clinicians there have seen the benefits of integrating various aspects of addiction medicine into primary care but these data on outcomes and cost-effectiveness can help make the case to hospital leaders, legislators, and grant providers.
The primary care setting also provides a chance to engage patients around their injection practice and explore ways to minimize risk, she said.
“By offering them these kits, it lets them know your priority is their safety and well-being,” Dr. Applewhite said.
She noted that the linkage to primary care was low for patients who inject drugs, which speaks to the need for models in addition to this one, such as bringing primary care clinicians into syringe service programs.
“The medical establishment has a lot to learn from these programs,” she said.
Practices need support
She said it’s important to note that primary care practices need support from administrative leaders, philanthropists, and grant providers to help cover the costs.
“It’s one of the barriers to doing this,” she said. “There isn’t a mechanism to pay for this.”
Sarah Bagley, MD, a primary care physician at Boston Medical Center and medical director of BMC’s Center for Addiction Treatment for Adolescents/Young Adults Who Use Substances told this publication she was excited to see that the addition of harm reduction kits to buprenorphine seemed to have the optimal effect in improving outcomes. People with substance abuse disorders should feel they are welcome in primary care even if they are not yet ready to stop drug use, she said.
She said she was also glad to see increased life expectancy with these interventions. The news of overdose deaths contributing to a decrease in life expectancy can be overwhelming, she said.
But this study, she says, offers a road map for addressing the overdose crisis “by including harm reduction in the substance abuse care we provide.”
She pointed out that the study showed that costs increase per patient with both interventions, compared with the status quo. The study found that health care costs per person during a lifetime increased, compared with the status quo, by 69.1% for BUP and 74.3% for BUP plus HR.
But it’s important to understand the reason for that, she said: “The cost was higher because people were staying alive.”
She said it may help to compare giving optimal care to people who have substance abuse disorders with giving optimal care to people with other chronic conditions, such as diabetes, who may not always adhere to recommended diets or treatment regimens.
“We still invite those patients in and work with them based on where they are,” she said.
Growing epidemic
The researchers point to the urgent need for solutions given the U.S. opioid epidemic, which has led to increasing numbers of overdoses and injection drug use–related infections, such as infective endocarditis, and severe skin and soft tissue infections.
They point out that primary care providers are the largest clinical workforce in the United States, but few of their practices offer comprehensive addiction care onsite.
“Primary care practices are a practical place to integrate addiction services, where PCPs can prescribe buprenorphine and deliver harm reduction kits,” they write.
Coauthor Dr. Kimmel reports personal fees from Massachusetts Department of Public Health, Bureau of Substance Addiction Services Overdose Education and Prevention Program, and American Academy of Addiction Psychiatry, Opioid Response Network for harm reduction education outside the submitted work and previous consulting with Abt Associates on a Massachusetts Department of Public Health–funded project to improve access to medications for opioid use disorder treatment. Dr. Applewhite and Dr. Bagley report no relevant financial relationships.
JAMA NETWORK OPEN
Can asthma incidence be reduced by attention to sleep disorders?
Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.
The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.
Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.
The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.
Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.
Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.
In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.
Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.
“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.
Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.
Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.
The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
Complex and multifactorial
“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.
“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.
“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.
The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.
The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.
Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.
The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.
Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.
Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.
In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.
Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.
“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.
Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.
Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.
The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
Complex and multifactorial
“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.
“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.
“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.
The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.
The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.
Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.
The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.
Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.
Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.
In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.
Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.
“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.
Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.
Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.
The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
Complex and multifactorial
“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.
“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.
“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.
The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM BMJ OPEN RESPIRATORY RESEARCH
The essential care team
As you may have seen in the February issue, in my year serving as President of the American College of Chest Physicians, I will be periodically contributing to CHEST Physician with the latest updates and to serve as a touchpoint for what we are currently working on.
For this contribution, I want to share and reflect upon the recent Nurse Work Environment study published by the American Association of Critical-Care Nurses (AACN). Deployed in 2021, the now-published study concluded that there is serious need for “bold, intentional, and relentless” efforts to create and sustain healthy work environments that foster excellence in patient care and optimal outcomes for patients, nurses, and other members of the health care team.
To achieve this, AACN recommends adhering to the Healthy Work Environments (HWE) Standards created in 2005 but that are more pertinent than ever in 2023.
In a previous article for CHEST Physician, I spoke about my goals for 2023 and one of those goals was to focus on increasing the membership of a variety of providers who help care for patients, including advanced practice providers, respiratory therapists, registered nurses, and others. CHEST is already an inclusive organization to a variety of health care providers, but we can do more, and this is a great time to reemphasize the importance of the care team by showing our support of the AACN and the working conditions of nurses.
Beyond supporting other organizations, the CHEST Board of Regents will focus on new ways to make the organization a valuable resource to every member at every level of their career and with every designation.
The (HWE) Standards that I encourage all CHEST members to support include:
- Skilled communication and true collaboration between doctors, nurses and other clinicians.
- Effective decision-making that includes nurses in the process for input and expertise.
- Appropriate staffing that ensures an effective match between patient needs and the skills of the nurse.
- Meaningful recognition by rewarding and appreciating the value that everyone brings to the team.
- Authentic leadership that embraces a healthy work environment and is supportive of every member of the care team.
Let’s all make a dedicated effort to be intentional in our support of our care team colleagues to improve the working environment and overall patient care.
Think of one thing you can do at your own institution or in your practice to improve the work environment for all those on your team. And then make it happen!
Please reach out with ideas or questions.
As you may have seen in the February issue, in my year serving as President of the American College of Chest Physicians, I will be periodically contributing to CHEST Physician with the latest updates and to serve as a touchpoint for what we are currently working on.
For this contribution, I want to share and reflect upon the recent Nurse Work Environment study published by the American Association of Critical-Care Nurses (AACN). Deployed in 2021, the now-published study concluded that there is serious need for “bold, intentional, and relentless” efforts to create and sustain healthy work environments that foster excellence in patient care and optimal outcomes for patients, nurses, and other members of the health care team.
To achieve this, AACN recommends adhering to the Healthy Work Environments (HWE) Standards created in 2005 but that are more pertinent than ever in 2023.
In a previous article for CHEST Physician, I spoke about my goals for 2023 and one of those goals was to focus on increasing the membership of a variety of providers who help care for patients, including advanced practice providers, respiratory therapists, registered nurses, and others. CHEST is already an inclusive organization to a variety of health care providers, but we can do more, and this is a great time to reemphasize the importance of the care team by showing our support of the AACN and the working conditions of nurses.
Beyond supporting other organizations, the CHEST Board of Regents will focus on new ways to make the organization a valuable resource to every member at every level of their career and with every designation.
The (HWE) Standards that I encourage all CHEST members to support include:
- Skilled communication and true collaboration between doctors, nurses and other clinicians.
- Effective decision-making that includes nurses in the process for input and expertise.
- Appropriate staffing that ensures an effective match between patient needs and the skills of the nurse.
- Meaningful recognition by rewarding and appreciating the value that everyone brings to the team.
- Authentic leadership that embraces a healthy work environment and is supportive of every member of the care team.
Let’s all make a dedicated effort to be intentional in our support of our care team colleagues to improve the working environment and overall patient care.
Think of one thing you can do at your own institution or in your practice to improve the work environment for all those on your team. And then make it happen!
Please reach out with ideas or questions.
As you may have seen in the February issue, in my year serving as President of the American College of Chest Physicians, I will be periodically contributing to CHEST Physician with the latest updates and to serve as a touchpoint for what we are currently working on.
For this contribution, I want to share and reflect upon the recent Nurse Work Environment study published by the American Association of Critical-Care Nurses (AACN). Deployed in 2021, the now-published study concluded that there is serious need for “bold, intentional, and relentless” efforts to create and sustain healthy work environments that foster excellence in patient care and optimal outcomes for patients, nurses, and other members of the health care team.
To achieve this, AACN recommends adhering to the Healthy Work Environments (HWE) Standards created in 2005 but that are more pertinent than ever in 2023.
In a previous article for CHEST Physician, I spoke about my goals for 2023 and one of those goals was to focus on increasing the membership of a variety of providers who help care for patients, including advanced practice providers, respiratory therapists, registered nurses, and others. CHEST is already an inclusive organization to a variety of health care providers, but we can do more, and this is a great time to reemphasize the importance of the care team by showing our support of the AACN and the working conditions of nurses.
Beyond supporting other organizations, the CHEST Board of Regents will focus on new ways to make the organization a valuable resource to every member at every level of their career and with every designation.
The (HWE) Standards that I encourage all CHEST members to support include:
- Skilled communication and true collaboration between doctors, nurses and other clinicians.
- Effective decision-making that includes nurses in the process for input and expertise.
- Appropriate staffing that ensures an effective match between patient needs and the skills of the nurse.
- Meaningful recognition by rewarding and appreciating the value that everyone brings to the team.
- Authentic leadership that embraces a healthy work environment and is supportive of every member of the care team.
Let’s all make a dedicated effort to be intentional in our support of our care team colleagues to improve the working environment and overall patient care.
Think of one thing you can do at your own institution or in your practice to improve the work environment for all those on your team. And then make it happen!
Please reach out with ideas or questions.
FDA clears first patch to treat axillary hyperhidrosis
The Food and Drug Administration on April 13 cleared the first patch to reduce excessive underarm sweating for adults with primary axillary hyperhidrosis.
The single-use, disposable, prescription-only patch will be marketed as Brella. It consists of a sodium sheet with an adhesive overlay. A health care provider applies it to the patient’s underarm for up to 3 minutes and then repeats the process on the other underarm.
The developer, Candesant Biomedical, says the patch uses the company’s patented targeted alkali thermolysis (TAT) technology, which was built on the principle that heat is generated when sodium reacts with water in sweat. “The thermal energy created by the sodium sheet is precisely localized, microtargeting sweat glands to significantly reduce sweat production,” according to the company’s press release announcing the FDA decision.
FDA clearance was based on data from the pivotal randomized, double-blind, multicenter SAHARA study, which indicated that the product is effective and well tolerated.
Patients experienced a reduction in sweat that was maintained for 3 months or longer, according to trial results.
The SAHARA trial results were reported in a late-breaking abstract at the annual meeting of the American Academy of Dermatology in March.
The trial enrolled 110 individuals with Hyperhidrosis Disease Severity Scale (HDSS) scores of 3 or 4 (indicating frequent sweating or sweating that always interferes with daily activities). Trial participants were randomly assigned to receive either an active TAT or a sham patch, which was applied for up to 3 minutes.
At the meeting, lead investigator David M. Pariser, MD, a dermatologist practicing in Norfolk, Va., reported that at 4 weeks, 63.6% of patients in the active patch group achieved an HDSS score of 1 or 2, compared with 44.2% of those in the sham treatment group (P = .0332). Also, 43.2% of those in the active-patch group achieved an improvement of 2 points or greater on the HDSS, as compared with 16.3% of those in the sham treatment group (P = .0107) .
In addition, 9.1% of those in the active-patch group achieved a 3-point improvement on the HDSS, compared with none in the sham group. “That’s an amazing improvement; you’re basically going from moderate or severe to none,” Dr. Pariser said at the meeting.
As for adverse events (AEs), 13 patients in the active-patch group experienced AEs at the treatment site. Six patients experienced erythema; four experienced erosion; two experienced burning, itching, or stinging; and one had underarm odor.
“The two procedure-related AEs in the TAT-treated group were compensatory sweating and irritant contact dermatitis due to the adhesive,” Dr. Pariser said. He noted that most AEs resolved in fewer than 2 weeks, and all AEs were mild to moderate.
According to the International Hyperhidrosis Society, about 1.3 million people in the United States have axillary hyperhidrosis, and about a third report that sweating is barely tolerable and frequently interferes with daily activities or is intolerable and always interferes with daily activities.
The patch will be available within months in select U.S. markets beginning in late summer. The company says the markets will be listed on its website.
A company representative told this news organization that because it is an in-office procedure, pricing will vary, depending on the practice. “With that said, Candesant expects doctors will charge about the same for one session of the Brella SweatControl Patch as they would for a high-end, in-office facial or chemical peel,” the representative said.
Dr. Pariser is a consultant or investigator for Bickel Biotechnology, Biofrontera AG, Bristol-Myers Squibb, the Celgene Corporation, Novartis Pharmaceuticals, Pfizer, Regeneron, and Sanofi.
A version of this article originally appeared on Medscape.com.
The Food and Drug Administration on April 13 cleared the first patch to reduce excessive underarm sweating for adults with primary axillary hyperhidrosis.
The single-use, disposable, prescription-only patch will be marketed as Brella. It consists of a sodium sheet with an adhesive overlay. A health care provider applies it to the patient’s underarm for up to 3 minutes and then repeats the process on the other underarm.
The developer, Candesant Biomedical, says the patch uses the company’s patented targeted alkali thermolysis (TAT) technology, which was built on the principle that heat is generated when sodium reacts with water in sweat. “The thermal energy created by the sodium sheet is precisely localized, microtargeting sweat glands to significantly reduce sweat production,” according to the company’s press release announcing the FDA decision.
FDA clearance was based on data from the pivotal randomized, double-blind, multicenter SAHARA study, which indicated that the product is effective and well tolerated.
Patients experienced a reduction in sweat that was maintained for 3 months or longer, according to trial results.
The SAHARA trial results were reported in a late-breaking abstract at the annual meeting of the American Academy of Dermatology in March.
The trial enrolled 110 individuals with Hyperhidrosis Disease Severity Scale (HDSS) scores of 3 or 4 (indicating frequent sweating or sweating that always interferes with daily activities). Trial participants were randomly assigned to receive either an active TAT or a sham patch, which was applied for up to 3 minutes.
At the meeting, lead investigator David M. Pariser, MD, a dermatologist practicing in Norfolk, Va., reported that at 4 weeks, 63.6% of patients in the active patch group achieved an HDSS score of 1 or 2, compared with 44.2% of those in the sham treatment group (P = .0332). Also, 43.2% of those in the active-patch group achieved an improvement of 2 points or greater on the HDSS, as compared with 16.3% of those in the sham treatment group (P = .0107) .
In addition, 9.1% of those in the active-patch group achieved a 3-point improvement on the HDSS, compared with none in the sham group. “That’s an amazing improvement; you’re basically going from moderate or severe to none,” Dr. Pariser said at the meeting.
As for adverse events (AEs), 13 patients in the active-patch group experienced AEs at the treatment site. Six patients experienced erythema; four experienced erosion; two experienced burning, itching, or stinging; and one had underarm odor.
“The two procedure-related AEs in the TAT-treated group were compensatory sweating and irritant contact dermatitis due to the adhesive,” Dr. Pariser said. He noted that most AEs resolved in fewer than 2 weeks, and all AEs were mild to moderate.
According to the International Hyperhidrosis Society, about 1.3 million people in the United States have axillary hyperhidrosis, and about a third report that sweating is barely tolerable and frequently interferes with daily activities or is intolerable and always interferes with daily activities.
The patch will be available within months in select U.S. markets beginning in late summer. The company says the markets will be listed on its website.
A company representative told this news organization that because it is an in-office procedure, pricing will vary, depending on the practice. “With that said, Candesant expects doctors will charge about the same for one session of the Brella SweatControl Patch as they would for a high-end, in-office facial or chemical peel,” the representative said.
Dr. Pariser is a consultant or investigator for Bickel Biotechnology, Biofrontera AG, Bristol-Myers Squibb, the Celgene Corporation, Novartis Pharmaceuticals, Pfizer, Regeneron, and Sanofi.
A version of this article originally appeared on Medscape.com.
The Food and Drug Administration on April 13 cleared the first patch to reduce excessive underarm sweating for adults with primary axillary hyperhidrosis.
The single-use, disposable, prescription-only patch will be marketed as Brella. It consists of a sodium sheet with an adhesive overlay. A health care provider applies it to the patient’s underarm for up to 3 minutes and then repeats the process on the other underarm.
The developer, Candesant Biomedical, says the patch uses the company’s patented targeted alkali thermolysis (TAT) technology, which was built on the principle that heat is generated when sodium reacts with water in sweat. “The thermal energy created by the sodium sheet is precisely localized, microtargeting sweat glands to significantly reduce sweat production,” according to the company’s press release announcing the FDA decision.
FDA clearance was based on data from the pivotal randomized, double-blind, multicenter SAHARA study, which indicated that the product is effective and well tolerated.
Patients experienced a reduction in sweat that was maintained for 3 months or longer, according to trial results.
The SAHARA trial results were reported in a late-breaking abstract at the annual meeting of the American Academy of Dermatology in March.
The trial enrolled 110 individuals with Hyperhidrosis Disease Severity Scale (HDSS) scores of 3 or 4 (indicating frequent sweating or sweating that always interferes with daily activities). Trial participants were randomly assigned to receive either an active TAT or a sham patch, which was applied for up to 3 minutes.
At the meeting, lead investigator David M. Pariser, MD, a dermatologist practicing in Norfolk, Va., reported that at 4 weeks, 63.6% of patients in the active patch group achieved an HDSS score of 1 or 2, compared with 44.2% of those in the sham treatment group (P = .0332). Also, 43.2% of those in the active-patch group achieved an improvement of 2 points or greater on the HDSS, as compared with 16.3% of those in the sham treatment group (P = .0107) .
In addition, 9.1% of those in the active-patch group achieved a 3-point improvement on the HDSS, compared with none in the sham group. “That’s an amazing improvement; you’re basically going from moderate or severe to none,” Dr. Pariser said at the meeting.
As for adverse events (AEs), 13 patients in the active-patch group experienced AEs at the treatment site. Six patients experienced erythema; four experienced erosion; two experienced burning, itching, or stinging; and one had underarm odor.
“The two procedure-related AEs in the TAT-treated group were compensatory sweating and irritant contact dermatitis due to the adhesive,” Dr. Pariser said. He noted that most AEs resolved in fewer than 2 weeks, and all AEs were mild to moderate.
According to the International Hyperhidrosis Society, about 1.3 million people in the United States have axillary hyperhidrosis, and about a third report that sweating is barely tolerable and frequently interferes with daily activities or is intolerable and always interferes with daily activities.
The patch will be available within months in select U.S. markets beginning in late summer. The company says the markets will be listed on its website.
A company representative told this news organization that because it is an in-office procedure, pricing will vary, depending on the practice. “With that said, Candesant expects doctors will charge about the same for one session of the Brella SweatControl Patch as they would for a high-end, in-office facial or chemical peel,” the representative said.
Dr. Pariser is a consultant or investigator for Bickel Biotechnology, Biofrontera AG, Bristol-Myers Squibb, the Celgene Corporation, Novartis Pharmaceuticals, Pfizer, Regeneron, and Sanofi.
A version of this article originally appeared on Medscape.com.
ECT vs. ketamine for major depressive disorder: New data
“Although ECT is superior to ketamine for patients with a major depressive episode, our findings suggest that the therapeutic advantage may be smaller than what was demonstrated in prior analyses,” first author Vikas Menon, MD, department of psychiatry, Jawaharlal Institute of Postgraduate Medical Education & Research, Puducherry, India, told this news organization.
“This supports a recommendation for a trial of ketamine before a trial of ECT for patients with MDE, though this recommendation is limited by the small size and number of existing trials,” Dr. Menon said.
The study was published online in JAMA Psychiatry.
Questions remain
The meta-analysis included five trials of 278 adults with MDE (141 treated with ketamine and 137 with ECT).
In the main analysis, posttreatment depression ratings showed a trend for lower scores with ECT, compared with ketamine (standardized mean difference, −0.39; 95% confidence interval, −0.81 to 0.02).
In a sensitivity analysis of the two methodologically stronger trials, ECT was superior to ketamine (pooled SMD, −0.45; 95% CI, −0.75 to −0.14).
ECT was also superior to ketamine in terms of response rates (risk ratio, 1.27; 95% CI, 1.06-1.53) and remission rates (RR, 1.43; 95% CI, 1.12-1.82).
There were no significant between-group differences for number of sessions to response and remission and for cognitive outcomes.
Key limitations of the analysis were the small number of studies with limited sample sizes and a high risk of bias in all trials.
“There is a need for more comparative studies with adequate sample size in non-inferiority designs, examining a wider range of benefits and side effects and followed up for longer durations to answer clinically relevant questions about the nature and durability of observed benefits with ketamine,” said Dr. Menon.
“In patients with MDE for whom the administration of ECT is limited by restricted availability of the treatment, concerns about its cognitive adverse effects, negative patient attitudes, and other issues, clinicians may consider a trial of ketamine,” he added.
‘Important research’
Several experts offered perspective on the analysis in a statement from the U.K.-based nonprofit Science Media Centre, which was not involved with the conduct of this study.
Rupert McShane, MD, psychiatrist at the University of Oxford (England), noted that ECT and ketamine are both “potent” treatments for depression, and this meta-analysis shows that they are, “broadly speaking, equally as good as each other with perhaps a slight advantage for ECT.”
“Whether or not there is a difference depends on exactly how you define it and how you cut the data. Despite the slight advantage for ECT in this analysis, the authors support using ketamine before ECT, especially in patients who are worried about the cognitive risks of ECT. This seems sensible,” Dr. McShane said.
Allan Young, MBChB, clinical psychiatrist at King’s College London, noted that both ketamine and ECT have been shown to help some patients with treatment-resistant depression.
“Clearly the relative benefits of these two treatments need to be understood better, but this review of the existing literature suggests that ECT may benefit some more than ketamine,” said Mr. Young.
“There is evidence that ketamine with ECT may add little extra benefit, but much more work needs to be done to fully understand how these treatments fit best into the treatment pathway for major depressive episodes. However, based on this evidence, ECT clearly still merits a place in the treatment pathway,” Mr. Young added.
George Kirov, PhD, clinical professor, division of psychological medicine and clinical neurosciences, Cardiff University (England), said while the study is conducted well, most of the evidence is coming from one large trial conducted in Sweden.
“The other studies add small numbers of patients and the authors even present a sensitivity analysis after removing studies of poor quality, thus leaving only two studies and exposing even further the dependence of the results on one single study,” Dr. Kirov noted.
“The small studies should not be blamed for their size, as this is very difficult research to perform. On the other hand, the trends were in the same direction,” he added.
With those caveats in mind, Dr. Kirov said he still thinks this is “important research. It establishes the superiority of ECT against an active comparator (ketamine) which is very popular now and accepted to be quite effective.”
The study had no specific funding. Dr. Menon reports no relevant financial relationships. Dr. McShane is former chair of the ECT and Related Treatments Committee, Royal College of Psychiatrists and runs a ketamine clinic and an ECT service. Mr. Young has received compensation for lectures and advisory boards for AstraZeneca, Eli Lilly, Lundbeck, Sunovion, Servier, Livanova, Janssen, Allergan, Bionomics, Sumitomo Dainippon Pharma, COMPASS, and Sage, and has served as principal investigator on a trial of intranasal esketamine in treatment-resistant depression. Dr. Kirov has no interest to declare other than running the ECT service in Cardiff.
A version of this article first appeared on Medscape.com.
“Although ECT is superior to ketamine for patients with a major depressive episode, our findings suggest that the therapeutic advantage may be smaller than what was demonstrated in prior analyses,” first author Vikas Menon, MD, department of psychiatry, Jawaharlal Institute of Postgraduate Medical Education & Research, Puducherry, India, told this news organization.
“This supports a recommendation for a trial of ketamine before a trial of ECT for patients with MDE, though this recommendation is limited by the small size and number of existing trials,” Dr. Menon said.
The study was published online in JAMA Psychiatry.
Questions remain
The meta-analysis included five trials of 278 adults with MDE (141 treated with ketamine and 137 with ECT).
In the main analysis, posttreatment depression ratings showed a trend for lower scores with ECT, compared with ketamine (standardized mean difference, −0.39; 95% confidence interval, −0.81 to 0.02).
In a sensitivity analysis of the two methodologically stronger trials, ECT was superior to ketamine (pooled SMD, −0.45; 95% CI, −0.75 to −0.14).
ECT was also superior to ketamine in terms of response rates (risk ratio, 1.27; 95% CI, 1.06-1.53) and remission rates (RR, 1.43; 95% CI, 1.12-1.82).
There were no significant between-group differences for number of sessions to response and remission and for cognitive outcomes.
Key limitations of the analysis were the small number of studies with limited sample sizes and a high risk of bias in all trials.
“There is a need for more comparative studies with adequate sample size in non-inferiority designs, examining a wider range of benefits and side effects and followed up for longer durations to answer clinically relevant questions about the nature and durability of observed benefits with ketamine,” said Dr. Menon.
“In patients with MDE for whom the administration of ECT is limited by restricted availability of the treatment, concerns about its cognitive adverse effects, negative patient attitudes, and other issues, clinicians may consider a trial of ketamine,” he added.
‘Important research’
Several experts offered perspective on the analysis in a statement from the U.K.-based nonprofit Science Media Centre, which was not involved with the conduct of this study.
Rupert McShane, MD, psychiatrist at the University of Oxford (England), noted that ECT and ketamine are both “potent” treatments for depression, and this meta-analysis shows that they are, “broadly speaking, equally as good as each other with perhaps a slight advantage for ECT.”
“Whether or not there is a difference depends on exactly how you define it and how you cut the data. Despite the slight advantage for ECT in this analysis, the authors support using ketamine before ECT, especially in patients who are worried about the cognitive risks of ECT. This seems sensible,” Dr. McShane said.
Allan Young, MBChB, clinical psychiatrist at King’s College London, noted that both ketamine and ECT have been shown to help some patients with treatment-resistant depression.
“Clearly the relative benefits of these two treatments need to be understood better, but this review of the existing literature suggests that ECT may benefit some more than ketamine,” said Mr. Young.
“There is evidence that ketamine with ECT may add little extra benefit, but much more work needs to be done to fully understand how these treatments fit best into the treatment pathway for major depressive episodes. However, based on this evidence, ECT clearly still merits a place in the treatment pathway,” Mr. Young added.
George Kirov, PhD, clinical professor, division of psychological medicine and clinical neurosciences, Cardiff University (England), said while the study is conducted well, most of the evidence is coming from one large trial conducted in Sweden.
“The other studies add small numbers of patients and the authors even present a sensitivity analysis after removing studies of poor quality, thus leaving only two studies and exposing even further the dependence of the results on one single study,” Dr. Kirov noted.
“The small studies should not be blamed for their size, as this is very difficult research to perform. On the other hand, the trends were in the same direction,” he added.
With those caveats in mind, Dr. Kirov said he still thinks this is “important research. It establishes the superiority of ECT against an active comparator (ketamine) which is very popular now and accepted to be quite effective.”
The study had no specific funding. Dr. Menon reports no relevant financial relationships. Dr. McShane is former chair of the ECT and Related Treatments Committee, Royal College of Psychiatrists and runs a ketamine clinic and an ECT service. Mr. Young has received compensation for lectures and advisory boards for AstraZeneca, Eli Lilly, Lundbeck, Sunovion, Servier, Livanova, Janssen, Allergan, Bionomics, Sumitomo Dainippon Pharma, COMPASS, and Sage, and has served as principal investigator on a trial of intranasal esketamine in treatment-resistant depression. Dr. Kirov has no interest to declare other than running the ECT service in Cardiff.
A version of this article first appeared on Medscape.com.
“Although ECT is superior to ketamine for patients with a major depressive episode, our findings suggest that the therapeutic advantage may be smaller than what was demonstrated in prior analyses,” first author Vikas Menon, MD, department of psychiatry, Jawaharlal Institute of Postgraduate Medical Education & Research, Puducherry, India, told this news organization.
“This supports a recommendation for a trial of ketamine before a trial of ECT for patients with MDE, though this recommendation is limited by the small size and number of existing trials,” Dr. Menon said.
The study was published online in JAMA Psychiatry.
Questions remain
The meta-analysis included five trials of 278 adults with MDE (141 treated with ketamine and 137 with ECT).
In the main analysis, posttreatment depression ratings showed a trend for lower scores with ECT, compared with ketamine (standardized mean difference, −0.39; 95% confidence interval, −0.81 to 0.02).
In a sensitivity analysis of the two methodologically stronger trials, ECT was superior to ketamine (pooled SMD, −0.45; 95% CI, −0.75 to −0.14).
ECT was also superior to ketamine in terms of response rates (risk ratio, 1.27; 95% CI, 1.06-1.53) and remission rates (RR, 1.43; 95% CI, 1.12-1.82).
There were no significant between-group differences for number of sessions to response and remission and for cognitive outcomes.
Key limitations of the analysis were the small number of studies with limited sample sizes and a high risk of bias in all trials.
“There is a need for more comparative studies with adequate sample size in non-inferiority designs, examining a wider range of benefits and side effects and followed up for longer durations to answer clinically relevant questions about the nature and durability of observed benefits with ketamine,” said Dr. Menon.
“In patients with MDE for whom the administration of ECT is limited by restricted availability of the treatment, concerns about its cognitive adverse effects, negative patient attitudes, and other issues, clinicians may consider a trial of ketamine,” he added.
‘Important research’
Several experts offered perspective on the analysis in a statement from the U.K.-based nonprofit Science Media Centre, which was not involved with the conduct of this study.
Rupert McShane, MD, psychiatrist at the University of Oxford (England), noted that ECT and ketamine are both “potent” treatments for depression, and this meta-analysis shows that they are, “broadly speaking, equally as good as each other with perhaps a slight advantage for ECT.”
“Whether or not there is a difference depends on exactly how you define it and how you cut the data. Despite the slight advantage for ECT in this analysis, the authors support using ketamine before ECT, especially in patients who are worried about the cognitive risks of ECT. This seems sensible,” Dr. McShane said.
Allan Young, MBChB, clinical psychiatrist at King’s College London, noted that both ketamine and ECT have been shown to help some patients with treatment-resistant depression.
“Clearly the relative benefits of these two treatments need to be understood better, but this review of the existing literature suggests that ECT may benefit some more than ketamine,” said Mr. Young.
“There is evidence that ketamine with ECT may add little extra benefit, but much more work needs to be done to fully understand how these treatments fit best into the treatment pathway for major depressive episodes. However, based on this evidence, ECT clearly still merits a place in the treatment pathway,” Mr. Young added.
George Kirov, PhD, clinical professor, division of psychological medicine and clinical neurosciences, Cardiff University (England), said while the study is conducted well, most of the evidence is coming from one large trial conducted in Sweden.
“The other studies add small numbers of patients and the authors even present a sensitivity analysis after removing studies of poor quality, thus leaving only two studies and exposing even further the dependence of the results on one single study,” Dr. Kirov noted.
“The small studies should not be blamed for their size, as this is very difficult research to perform. On the other hand, the trends were in the same direction,” he added.
With those caveats in mind, Dr. Kirov said he still thinks this is “important research. It establishes the superiority of ECT against an active comparator (ketamine) which is very popular now and accepted to be quite effective.”
The study had no specific funding. Dr. Menon reports no relevant financial relationships. Dr. McShane is former chair of the ECT and Related Treatments Committee, Royal College of Psychiatrists and runs a ketamine clinic and an ECT service. Mr. Young has received compensation for lectures and advisory boards for AstraZeneca, Eli Lilly, Lundbeck, Sunovion, Servier, Livanova, Janssen, Allergan, Bionomics, Sumitomo Dainippon Pharma, COMPASS, and Sage, and has served as principal investigator on a trial of intranasal esketamine in treatment-resistant depression. Dr. Kirov has no interest to declare other than running the ECT service in Cardiff.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
LGBTQ+ Youth Consult Questions remain over use of sex hormone therapy
“They Paused Puberty but Is There a Cost?”
“Bone Health: Puberty Blockers Not Fully Reversible.”
Headlines such as these from major national news outlets have begun to cast doubt on one of the medications used in treating gender-diverse adolescents and young adults. GnRH agonists, such as leuprorelin and triptorelin, were first approved by the Food and Drug Administration in the 1980s and have been used since then for a variety of medical indications. In the decades since, these medications have been successfully used with a generally favorable side effect profile.
GnRH agonists and puberty
In the treatment of precocious puberty, GnRH agonists are often started prior to the age of 7, depending on the age at which the affected patient begins showing signs of central puberty. These include breast development, scrotal enlargement, and so on. GnRH agonists typically are continued until age 10-12, depending on the patient and an informed discussion with the patient’s parents about optimal outcomes.1 Therefore, it is not uncommon to see these medications used for anywhere from 1 to 4 years, depending on the age at which precocious puberty started.
GnRH agonists are used in two populations of transgender individuals. The first group is those youths who have just started their natal, or biological, puberty. The medication is not started until the patient has biochemical or physical exam evidence that puberty has started. The medication is then continued until hormones are started. This is usually 2-3 years on average, depending on the age at which the medication was started. This is essentially comparable with cisgender youths who have taken these medications for precocious puberty. The second population of individuals who use GnRH agonists is transgender women who are also on estrogen therapy. In these women, the GnRH agonist is used for androgen (testosterone) suppression.
Concerns over bone health
One of the main concerns recently expressed about long-term use of GnRH agonists is their effect on bone density. Adolescence is a critical time for bone mineral density (BMD) accrual and this is driven by sex hormones. When GnRH agonists are used to delay puberty in transgender adolescents, this then delays the maturation of the adult skeleton until the GnRH agonist is stopped (and natal puberty resumes) or cross-sex hormones are started. In a recent multicenter study2 looking at baseline BMD of transgender youth at the time of GnRH agonist initiation, 30% of those assigned male at birth and 13% of those assigned female at birth had low bone mineral density for age (defined as a BMD z score of <–2). For those with low BMD, their physical activity scores were significantly lower than those with normal BMD. Thus, these adolescents require close follow-up, just like their cisgender peers.
There are currently no long-term data on the risk of developing fractures or osteoporosis in those individuals who were treated with GnRH agonists and then went on to start cross-sex hormone therapy. Some studies suggest that there is a risk that BMD does not recover after being on cross-sex hormones,3 while another study suggested that transgender men recover their BMD after being on testosterone.4 It is still unclear in that study why transgender women did not recover their BMD or why they were low at baseline. Interestingly, a 2012 study5 from Brazil showed that there was no difference in BMD for cisgender girls who had been off their GnRH agonist therapy for at least 3 years, as compared with their age-matched controls who had never been on GnRH agonist therapy. These conflicting data highlight the importance of long-term follow-up, as well as the need to include age-matched, cisgender control subjects, to better understand if there is truly a difference in transgender individuals or if today’s adolescents, in general, have low BMD.
Lingering questions
In summary, the use of GnRH agonists in transgender adolescents remains controversial because of the potential long-term effects on bone mineral density. However, this risk must be balanced against the risks of allowing natal puberty to progress in certain transgender individuals with the development of undesired secondary sex characteristics. More longitudinal studies are needed to better understand the long-term risks of osteoporosis and fractures in those who have undergone GnRH agonist therapy as part of their gender-affirming medical care, as well as any clinical interventions that might help mitigate this risk.
Dr. Cooper is assistant professor of pediatrics at UT Southwestern, Dallas, and an adolescent medicine specialist at Children’s Medical Center Dallas.
References
1. Harrington J et al. Treatment of precocious puberty. UpToDate. www.uptodate.com/contents/treatment-of-precocious-puberty.
2. Lee JY et al. J Endocr Soc. 2020;4(9):bvaa065. doi: 10.1210/jendso/bvaa065.
3. Klink D et al. J Clin Endocrinol Metab. 2015;100(2):E270-5. doi: 10.1210/jc.2014-2439.
4. Schagen SEE et al. J Clin Endocrinol Metab. 2020;105(12):e4252-e4263. doi: 10.1210/clinem/dgaa604.
5. Alessandri SB et al. Clinics (Sao Paulo). 2012;67(6):591-6. doi: 10.6061/clinics/2012(06)08.
“They Paused Puberty but Is There a Cost?”
“Bone Health: Puberty Blockers Not Fully Reversible.”
Headlines such as these from major national news outlets have begun to cast doubt on one of the medications used in treating gender-diverse adolescents and young adults. GnRH agonists, such as leuprorelin and triptorelin, were first approved by the Food and Drug Administration in the 1980s and have been used since then for a variety of medical indications. In the decades since, these medications have been successfully used with a generally favorable side effect profile.
GnRH agonists and puberty
In the treatment of precocious puberty, GnRH agonists are often started prior to the age of 7, depending on the age at which the affected patient begins showing signs of central puberty. These include breast development, scrotal enlargement, and so on. GnRH agonists typically are continued until age 10-12, depending on the patient and an informed discussion with the patient’s parents about optimal outcomes.1 Therefore, it is not uncommon to see these medications used for anywhere from 1 to 4 years, depending on the age at which precocious puberty started.
GnRH agonists are used in two populations of transgender individuals. The first group is those youths who have just started their natal, or biological, puberty. The medication is not started until the patient has biochemical or physical exam evidence that puberty has started. The medication is then continued until hormones are started. This is usually 2-3 years on average, depending on the age at which the medication was started. This is essentially comparable with cisgender youths who have taken these medications for precocious puberty. The second population of individuals who use GnRH agonists is transgender women who are also on estrogen therapy. In these women, the GnRH agonist is used for androgen (testosterone) suppression.
Concerns over bone health
One of the main concerns recently expressed about long-term use of GnRH agonists is their effect on bone density. Adolescence is a critical time for bone mineral density (BMD) accrual and this is driven by sex hormones. When GnRH agonists are used to delay puberty in transgender adolescents, this then delays the maturation of the adult skeleton until the GnRH agonist is stopped (and natal puberty resumes) or cross-sex hormones are started. In a recent multicenter study2 looking at baseline BMD of transgender youth at the time of GnRH agonist initiation, 30% of those assigned male at birth and 13% of those assigned female at birth had low bone mineral density for age (defined as a BMD z score of <–2). For those with low BMD, their physical activity scores were significantly lower than those with normal BMD. Thus, these adolescents require close follow-up, just like their cisgender peers.
There are currently no long-term data on the risk of developing fractures or osteoporosis in those individuals who were treated with GnRH agonists and then went on to start cross-sex hormone therapy. Some studies suggest that there is a risk that BMD does not recover after being on cross-sex hormones,3 while another study suggested that transgender men recover their BMD after being on testosterone.4 It is still unclear in that study why transgender women did not recover their BMD or why they were low at baseline. Interestingly, a 2012 study5 from Brazil showed that there was no difference in BMD for cisgender girls who had been off their GnRH agonist therapy for at least 3 years, as compared with their age-matched controls who had never been on GnRH agonist therapy. These conflicting data highlight the importance of long-term follow-up, as well as the need to include age-matched, cisgender control subjects, to better understand if there is truly a difference in transgender individuals or if today’s adolescents, in general, have low BMD.
Lingering questions
In summary, the use of GnRH agonists in transgender adolescents remains controversial because of the potential long-term effects on bone mineral density. However, this risk must be balanced against the risks of allowing natal puberty to progress in certain transgender individuals with the development of undesired secondary sex characteristics. More longitudinal studies are needed to better understand the long-term risks of osteoporosis and fractures in those who have undergone GnRH agonist therapy as part of their gender-affirming medical care, as well as any clinical interventions that might help mitigate this risk.
Dr. Cooper is assistant professor of pediatrics at UT Southwestern, Dallas, and an adolescent medicine specialist at Children’s Medical Center Dallas.
References
1. Harrington J et al. Treatment of precocious puberty. UpToDate. www.uptodate.com/contents/treatment-of-precocious-puberty.
2. Lee JY et al. J Endocr Soc. 2020;4(9):bvaa065. doi: 10.1210/jendso/bvaa065.
3. Klink D et al. J Clin Endocrinol Metab. 2015;100(2):E270-5. doi: 10.1210/jc.2014-2439.
4. Schagen SEE et al. J Clin Endocrinol Metab. 2020;105(12):e4252-e4263. doi: 10.1210/clinem/dgaa604.
5. Alessandri SB et al. Clinics (Sao Paulo). 2012;67(6):591-6. doi: 10.6061/clinics/2012(06)08.
“They Paused Puberty but Is There a Cost?”
“Bone Health: Puberty Blockers Not Fully Reversible.”
Headlines such as these from major national news outlets have begun to cast doubt on one of the medications used in treating gender-diverse adolescents and young adults. GnRH agonists, such as leuprorelin and triptorelin, were first approved by the Food and Drug Administration in the 1980s and have been used since then for a variety of medical indications. In the decades since, these medications have been successfully used with a generally favorable side effect profile.
GnRH agonists and puberty
In the treatment of precocious puberty, GnRH agonists are often started prior to the age of 7, depending on the age at which the affected patient begins showing signs of central puberty. These include breast development, scrotal enlargement, and so on. GnRH agonists typically are continued until age 10-12, depending on the patient and an informed discussion with the patient’s parents about optimal outcomes.1 Therefore, it is not uncommon to see these medications used for anywhere from 1 to 4 years, depending on the age at which precocious puberty started.
GnRH agonists are used in two populations of transgender individuals. The first group is those youths who have just started their natal, or biological, puberty. The medication is not started until the patient has biochemical or physical exam evidence that puberty has started. The medication is then continued until hormones are started. This is usually 2-3 years on average, depending on the age at which the medication was started. This is essentially comparable with cisgender youths who have taken these medications for precocious puberty. The second population of individuals who use GnRH agonists is transgender women who are also on estrogen therapy. In these women, the GnRH agonist is used for androgen (testosterone) suppression.
Concerns over bone health
One of the main concerns recently expressed about long-term use of GnRH agonists is their effect on bone density. Adolescence is a critical time for bone mineral density (BMD) accrual and this is driven by sex hormones. When GnRH agonists are used to delay puberty in transgender adolescents, this then delays the maturation of the adult skeleton until the GnRH agonist is stopped (and natal puberty resumes) or cross-sex hormones are started. In a recent multicenter study2 looking at baseline BMD of transgender youth at the time of GnRH agonist initiation, 30% of those assigned male at birth and 13% of those assigned female at birth had low bone mineral density for age (defined as a BMD z score of <–2). For those with low BMD, their physical activity scores were significantly lower than those with normal BMD. Thus, these adolescents require close follow-up, just like their cisgender peers.
There are currently no long-term data on the risk of developing fractures or osteoporosis in those individuals who were treated with GnRH agonists and then went on to start cross-sex hormone therapy. Some studies suggest that there is a risk that BMD does not recover after being on cross-sex hormones,3 while another study suggested that transgender men recover their BMD after being on testosterone.4 It is still unclear in that study why transgender women did not recover their BMD or why they were low at baseline. Interestingly, a 2012 study5 from Brazil showed that there was no difference in BMD for cisgender girls who had been off their GnRH agonist therapy for at least 3 years, as compared with their age-matched controls who had never been on GnRH agonist therapy. These conflicting data highlight the importance of long-term follow-up, as well as the need to include age-matched, cisgender control subjects, to better understand if there is truly a difference in transgender individuals or if today’s adolescents, in general, have low BMD.
Lingering questions
In summary, the use of GnRH agonists in transgender adolescents remains controversial because of the potential long-term effects on bone mineral density. However, this risk must be balanced against the risks of allowing natal puberty to progress in certain transgender individuals with the development of undesired secondary sex characteristics. More longitudinal studies are needed to better understand the long-term risks of osteoporosis and fractures in those who have undergone GnRH agonist therapy as part of their gender-affirming medical care, as well as any clinical interventions that might help mitigate this risk.
Dr. Cooper is assistant professor of pediatrics at UT Southwestern, Dallas, and an adolescent medicine specialist at Children’s Medical Center Dallas.
References
1. Harrington J et al. Treatment of precocious puberty. UpToDate. www.uptodate.com/contents/treatment-of-precocious-puberty.
2. Lee JY et al. J Endocr Soc. 2020;4(9):bvaa065. doi: 10.1210/jendso/bvaa065.
3. Klink D et al. J Clin Endocrinol Metab. 2015;100(2):E270-5. doi: 10.1210/jc.2014-2439.
4. Schagen SEE et al. J Clin Endocrinol Metab. 2020;105(12):e4252-e4263. doi: 10.1210/clinem/dgaa604.
5. Alessandri SB et al. Clinics (Sao Paulo). 2012;67(6):591-6. doi: 10.6061/clinics/2012(06)08.
Health care in America: Let that tapeworm grow
In my most recent column, “ ‘They All Laughed When I Spoke of Greedy Doctors,’ ” I attempted to provide a global understanding of some of the economic forces that have made American medicine what it is, how that happened, and why it is still happening.
I did not propose a fix. I have been proposing fixes for more than 30 years, on the pages of JAMA until 1999 and then for this news organization, most recently in 2019 with “Healthcare for All in a Land of Special Interests.”
Where you stand depends a lot on where you sit.
Is this good news or bad news? When William Hubbard was the dean of the University of Michigan School of Medicine in 1969, he said that “an academic medical center is the most efficient energy and resource trapping device that has ever been created” (personal communication, 1969).
To me as a faculty member of an academic medical center for many years, that was great news. We could grow faculty, erect buildings, take the best care of sick people, churn out research papers, mint new physicians and specialists, and get paid well in the process for doing “the Lord’s work.” What’s not to like? At that time, the proportion of the country’s gross national product expended for medical and health care was about 7%. And the predicted life span of an American at birth was 70.5 years.
Is this good news or bad news? In 2021, the proportion of our annual gross domestic product (GDP) consumed by health care was 18.3%, totaling $4.3 trillion, or $12,914 per person. For perspective, in 2021, the median income per capita was $37,638. Because quite a few Americans have very high incomes, the mean income per capita is much higher: $63,444. Predicted life span in 2021 was 76.4 years.
Thus, in a span of 53 years (1969-2022), only 5.9 years of life were gained per person born, for how many trillions of dollars expended? To me as a tax-paying citizen and payer of medical insurance premiums, that is bad news.
Is this good news or bad news? If we compare developed societies globally, our medical system does a whole lot of things very well indeed. But we spend a great deal more than any other country for health care and objectively achieve poorer outcomes. Thus, we are neither efficient nor effective. We keep a lot of workers very busy doing stuff, and they are generally well paid. As a worker, that’s good news; as a manager who values efficiency, it’s bad news indeed.
Is this good news or bad news? We’re the leader at finding money to pay people to do “health care work.” More Americans work in health care than any other field. In 2019, the United States employed some 21,000,000 people doing “health care and social assistance.” Among others, these occupations include physicians, dentists, dental hygienists and assistants, pharmacists, registered nurses, LVNs/LPNs, nursing aides, technologists and technicians, home health aides, respiratory therapists, occupational and speech therapists, social workers, childcare workers, and personal and home care aides. For a patient, parent, grandparent, and great-grandparent, it is good news to have all those folks available to take care of us when we need it.
So, while I have cringed at the frequent exposés from Roy Poses of what seem to me to be massive societal betrayals by American health care industry giants, it doesn’t have to be that way. Might it still be possible to do well while doing good?
A jobs program
Consider such common medical procedures as coronary artery stents or bypass grafts for stable angina (when optimal medical therapy is as good, or better than, and much less expensive); PSAs on asymptomatic men followed by unnecessary surgery for localized cancer; excess surgery for low back pain; and the jobs created by managing the people caught up in medical complications of the obesity epidemic.
Don’t forget the number of people employed simply to “follow the money” within our byzantine cockamamie medical billing system. In 2009, this prompted me to describe the bloated system as a “health care bubble” not unlike Enron, the submarket real estate financing debacle, or the dot-com boom and bust. I warned of the downside of bursting that bubble, particularly lost jobs.
The Affordable Care Act (ACA) provided health insurance to some 35 million Americans who had been uninsured. It retarded health care inflation. But it did nothing to trim administrative costs or very high pay for nonclinical executives, or shareholder profits in those companies that were for-profit, or drug and device prices. Without the support of all those groups, the ACA would never have passed Congress. The ACA has clearly been a mixed blessing.
If any large American constituency were ever serious about reducing the percentage of our GDP expended on health care, we have excellent ways to do that while improving the health and well-being of the American people. But remember, one person’s liability (unnecessary work) is another person’s asset (needed job).
The MBAization of medicine
Meanwhile, back at Dean Hubbard’s voracious academic medical center, the high intellect and driven nature of those who are attracted to medicine as a career has had other effects. The resulting organizations reflect not only the glorious calling of caring for the sick and the availability of lots of money to recruit and compensate leaders, but also the necessity to develop strong executive types who won’t be “eaten alive” by the high-powered workforce of demanding physicians and the surrounding environment.
Thus, it came as no great surprise that in its 2021 determination of America’s top 25 Best Large Employers, Forbes included five health care organizations and seven universities. Beating out such giants as NASA, Cisco, Microsoft, Netflix, and Google, the University of Alabama Birmingham Hospital was ranked first. Mayo Clinic and Yale University came in third and fifth, respectively, and at the other end of the list were Duke (23), MIT (24), and MD Anderson (25).
My goodness! Well done.
Yet, as a country attempting to be balanced, Warren Buffett’s descriptive entreaty on the 2021 failure of Haven, the Amazon-Chase-Berkshire Hathaway joint initiative, remains troubling. Calling upon Haven to change the U.S. health care system, Buffet said, “We learned a lot about the difficulty of changing around an industry that’s 17% of the GDP. We were fighting a tapeworm in the American economy, and the tapeworm won.” They had failed to tame the American health care cost beast.
I am on record as despising the “MBAization” of American medicine. Unfairly, I blamed a professional and technical discipline for what I considered misuse. I hereby repent and renounce my earlier condemnations.
Take it all over?
Here’s an idea: If you can’t beat them, join them.
Medical care is important, especially for acute illnesses and injuries, early cancer therapy, and many chronic conditions. But the real determinants of health writ large are social: wealth, education, housing, nutritious food, childcare, climate, clean air and water, meaningful employment, safety from violence, exercise schemes, vaccinations, and so on.
Why doesn’t the American medical-industrial complex simply bestow the label of “health care” on all health-related social determinants? Take it all over. Good “health care” jobs for everyone. Medical professionals will still be blamed for the low health quality and poor outcome scores, the main social determinants of health over which we have no control or influence.
Let that tapeworm grow to encompass all social determinants of health, and measure results by length and quality of life, national human happiness, and, of course, jobs. We can do it. Let that bubble glow. Party time.
And that’s the way it is. That’s my opinion.
George Lundberg, MD, is editor-in-chief at Cancer Commons, president of the Lundberg Institute, executive advisor at Cureus, and a clinical professor of pathology at Northwestern University. Previously, he served as editor-in-chief of JAMA (including 10 specialty journals), American Medical News, and Medscape.
A version of this article first appeared on Medscape.com.
In my most recent column, “ ‘They All Laughed When I Spoke of Greedy Doctors,’ ” I attempted to provide a global understanding of some of the economic forces that have made American medicine what it is, how that happened, and why it is still happening.
I did not propose a fix. I have been proposing fixes for more than 30 years, on the pages of JAMA until 1999 and then for this news organization, most recently in 2019 with “Healthcare for All in a Land of Special Interests.”
Where you stand depends a lot on where you sit.
Is this good news or bad news? When William Hubbard was the dean of the University of Michigan School of Medicine in 1969, he said that “an academic medical center is the most efficient energy and resource trapping device that has ever been created” (personal communication, 1969).
To me as a faculty member of an academic medical center for many years, that was great news. We could grow faculty, erect buildings, take the best care of sick people, churn out research papers, mint new physicians and specialists, and get paid well in the process for doing “the Lord’s work.” What’s not to like? At that time, the proportion of the country’s gross national product expended for medical and health care was about 7%. And the predicted life span of an American at birth was 70.5 years.
Is this good news or bad news? In 2021, the proportion of our annual gross domestic product (GDP) consumed by health care was 18.3%, totaling $4.3 trillion, or $12,914 per person. For perspective, in 2021, the median income per capita was $37,638. Because quite a few Americans have very high incomes, the mean income per capita is much higher: $63,444. Predicted life span in 2021 was 76.4 years.
Thus, in a span of 53 years (1969-2022), only 5.9 years of life were gained per person born, for how many trillions of dollars expended? To me as a tax-paying citizen and payer of medical insurance premiums, that is bad news.
Is this good news or bad news? If we compare developed societies globally, our medical system does a whole lot of things very well indeed. But we spend a great deal more than any other country for health care and objectively achieve poorer outcomes. Thus, we are neither efficient nor effective. We keep a lot of workers very busy doing stuff, and they are generally well paid. As a worker, that’s good news; as a manager who values efficiency, it’s bad news indeed.
Is this good news or bad news? We’re the leader at finding money to pay people to do “health care work.” More Americans work in health care than any other field. In 2019, the United States employed some 21,000,000 people doing “health care and social assistance.” Among others, these occupations include physicians, dentists, dental hygienists and assistants, pharmacists, registered nurses, LVNs/LPNs, nursing aides, technologists and technicians, home health aides, respiratory therapists, occupational and speech therapists, social workers, childcare workers, and personal and home care aides. For a patient, parent, grandparent, and great-grandparent, it is good news to have all those folks available to take care of us when we need it.
So, while I have cringed at the frequent exposés from Roy Poses of what seem to me to be massive societal betrayals by American health care industry giants, it doesn’t have to be that way. Might it still be possible to do well while doing good?
A jobs program
Consider such common medical procedures as coronary artery stents or bypass grafts for stable angina (when optimal medical therapy is as good, or better than, and much less expensive); PSAs on asymptomatic men followed by unnecessary surgery for localized cancer; excess surgery for low back pain; and the jobs created by managing the people caught up in medical complications of the obesity epidemic.
Don’t forget the number of people employed simply to “follow the money” within our byzantine cockamamie medical billing system. In 2009, this prompted me to describe the bloated system as a “health care bubble” not unlike Enron, the submarket real estate financing debacle, or the dot-com boom and bust. I warned of the downside of bursting that bubble, particularly lost jobs.
The Affordable Care Act (ACA) provided health insurance to some 35 million Americans who had been uninsured. It retarded health care inflation. But it did nothing to trim administrative costs or very high pay for nonclinical executives, or shareholder profits in those companies that were for-profit, or drug and device prices. Without the support of all those groups, the ACA would never have passed Congress. The ACA has clearly been a mixed blessing.
If any large American constituency were ever serious about reducing the percentage of our GDP expended on health care, we have excellent ways to do that while improving the health and well-being of the American people. But remember, one person’s liability (unnecessary work) is another person’s asset (needed job).
The MBAization of medicine
Meanwhile, back at Dean Hubbard’s voracious academic medical center, the high intellect and driven nature of those who are attracted to medicine as a career has had other effects. The resulting organizations reflect not only the glorious calling of caring for the sick and the availability of lots of money to recruit and compensate leaders, but also the necessity to develop strong executive types who won’t be “eaten alive” by the high-powered workforce of demanding physicians and the surrounding environment.
Thus, it came as no great surprise that in its 2021 determination of America’s top 25 Best Large Employers, Forbes included five health care organizations and seven universities. Beating out such giants as NASA, Cisco, Microsoft, Netflix, and Google, the University of Alabama Birmingham Hospital was ranked first. Mayo Clinic and Yale University came in third and fifth, respectively, and at the other end of the list were Duke (23), MIT (24), and MD Anderson (25).
My goodness! Well done.
Yet, as a country attempting to be balanced, Warren Buffett’s descriptive entreaty on the 2021 failure of Haven, the Amazon-Chase-Berkshire Hathaway joint initiative, remains troubling. Calling upon Haven to change the U.S. health care system, Buffet said, “We learned a lot about the difficulty of changing around an industry that’s 17% of the GDP. We were fighting a tapeworm in the American economy, and the tapeworm won.” They had failed to tame the American health care cost beast.
I am on record as despising the “MBAization” of American medicine. Unfairly, I blamed a professional and technical discipline for what I considered misuse. I hereby repent and renounce my earlier condemnations.
Take it all over?
Here’s an idea: If you can’t beat them, join them.
Medical care is important, especially for acute illnesses and injuries, early cancer therapy, and many chronic conditions. But the real determinants of health writ large are social: wealth, education, housing, nutritious food, childcare, climate, clean air and water, meaningful employment, safety from violence, exercise schemes, vaccinations, and so on.
Why doesn’t the American medical-industrial complex simply bestow the label of “health care” on all health-related social determinants? Take it all over. Good “health care” jobs for everyone. Medical professionals will still be blamed for the low health quality and poor outcome scores, the main social determinants of health over which we have no control or influence.
Let that tapeworm grow to encompass all social determinants of health, and measure results by length and quality of life, national human happiness, and, of course, jobs. We can do it. Let that bubble glow. Party time.
And that’s the way it is. That’s my opinion.
George Lundberg, MD, is editor-in-chief at Cancer Commons, president of the Lundberg Institute, executive advisor at Cureus, and a clinical professor of pathology at Northwestern University. Previously, he served as editor-in-chief of JAMA (including 10 specialty journals), American Medical News, and Medscape.
A version of this article first appeared on Medscape.com.
In my most recent column, “ ‘They All Laughed When I Spoke of Greedy Doctors,’ ” I attempted to provide a global understanding of some of the economic forces that have made American medicine what it is, how that happened, and why it is still happening.
I did not propose a fix. I have been proposing fixes for more than 30 years, on the pages of JAMA until 1999 and then for this news organization, most recently in 2019 with “Healthcare for All in a Land of Special Interests.”
Where you stand depends a lot on where you sit.
Is this good news or bad news? When William Hubbard was the dean of the University of Michigan School of Medicine in 1969, he said that “an academic medical center is the most efficient energy and resource trapping device that has ever been created” (personal communication, 1969).
To me as a faculty member of an academic medical center for many years, that was great news. We could grow faculty, erect buildings, take the best care of sick people, churn out research papers, mint new physicians and specialists, and get paid well in the process for doing “the Lord’s work.” What’s not to like? At that time, the proportion of the country’s gross national product expended for medical and health care was about 7%. And the predicted life span of an American at birth was 70.5 years.
Is this good news or bad news? In 2021, the proportion of our annual gross domestic product (GDP) consumed by health care was 18.3%, totaling $4.3 trillion, or $12,914 per person. For perspective, in 2021, the median income per capita was $37,638. Because quite a few Americans have very high incomes, the mean income per capita is much higher: $63,444. Predicted life span in 2021 was 76.4 years.
Thus, in a span of 53 years (1969-2022), only 5.9 years of life were gained per person born, for how many trillions of dollars expended? To me as a tax-paying citizen and payer of medical insurance premiums, that is bad news.
Is this good news or bad news? If we compare developed societies globally, our medical system does a whole lot of things very well indeed. But we spend a great deal more than any other country for health care and objectively achieve poorer outcomes. Thus, we are neither efficient nor effective. We keep a lot of workers very busy doing stuff, and they are generally well paid. As a worker, that’s good news; as a manager who values efficiency, it’s bad news indeed.
Is this good news or bad news? We’re the leader at finding money to pay people to do “health care work.” More Americans work in health care than any other field. In 2019, the United States employed some 21,000,000 people doing “health care and social assistance.” Among others, these occupations include physicians, dentists, dental hygienists and assistants, pharmacists, registered nurses, LVNs/LPNs, nursing aides, technologists and technicians, home health aides, respiratory therapists, occupational and speech therapists, social workers, childcare workers, and personal and home care aides. For a patient, parent, grandparent, and great-grandparent, it is good news to have all those folks available to take care of us when we need it.
So, while I have cringed at the frequent exposés from Roy Poses of what seem to me to be massive societal betrayals by American health care industry giants, it doesn’t have to be that way. Might it still be possible to do well while doing good?
A jobs program
Consider such common medical procedures as coronary artery stents or bypass grafts for stable angina (when optimal medical therapy is as good, or better than, and much less expensive); PSAs on asymptomatic men followed by unnecessary surgery for localized cancer; excess surgery for low back pain; and the jobs created by managing the people caught up in medical complications of the obesity epidemic.
Don’t forget the number of people employed simply to “follow the money” within our byzantine cockamamie medical billing system. In 2009, this prompted me to describe the bloated system as a “health care bubble” not unlike Enron, the submarket real estate financing debacle, or the dot-com boom and bust. I warned of the downside of bursting that bubble, particularly lost jobs.
The Affordable Care Act (ACA) provided health insurance to some 35 million Americans who had been uninsured. It retarded health care inflation. But it did nothing to trim administrative costs or very high pay for nonclinical executives, or shareholder profits in those companies that were for-profit, or drug and device prices. Without the support of all those groups, the ACA would never have passed Congress. The ACA has clearly been a mixed blessing.
If any large American constituency were ever serious about reducing the percentage of our GDP expended on health care, we have excellent ways to do that while improving the health and well-being of the American people. But remember, one person’s liability (unnecessary work) is another person’s asset (needed job).
The MBAization of medicine
Meanwhile, back at Dean Hubbard’s voracious academic medical center, the high intellect and driven nature of those who are attracted to medicine as a career has had other effects. The resulting organizations reflect not only the glorious calling of caring for the sick and the availability of lots of money to recruit and compensate leaders, but also the necessity to develop strong executive types who won’t be “eaten alive” by the high-powered workforce of demanding physicians and the surrounding environment.
Thus, it came as no great surprise that in its 2021 determination of America’s top 25 Best Large Employers, Forbes included five health care organizations and seven universities. Beating out such giants as NASA, Cisco, Microsoft, Netflix, and Google, the University of Alabama Birmingham Hospital was ranked first. Mayo Clinic and Yale University came in third and fifth, respectively, and at the other end of the list were Duke (23), MIT (24), and MD Anderson (25).
My goodness! Well done.
Yet, as a country attempting to be balanced, Warren Buffett’s descriptive entreaty on the 2021 failure of Haven, the Amazon-Chase-Berkshire Hathaway joint initiative, remains troubling. Calling upon Haven to change the U.S. health care system, Buffet said, “We learned a lot about the difficulty of changing around an industry that’s 17% of the GDP. We were fighting a tapeworm in the American economy, and the tapeworm won.” They had failed to tame the American health care cost beast.
I am on record as despising the “MBAization” of American medicine. Unfairly, I blamed a professional and technical discipline for what I considered misuse. I hereby repent and renounce my earlier condemnations.
Take it all over?
Here’s an idea: If you can’t beat them, join them.
Medical care is important, especially for acute illnesses and injuries, early cancer therapy, and many chronic conditions. But the real determinants of health writ large are social: wealth, education, housing, nutritious food, childcare, climate, clean air and water, meaningful employment, safety from violence, exercise schemes, vaccinations, and so on.
Why doesn’t the American medical-industrial complex simply bestow the label of “health care” on all health-related social determinants? Take it all over. Good “health care” jobs for everyone. Medical professionals will still be blamed for the low health quality and poor outcome scores, the main social determinants of health over which we have no control or influence.
Let that tapeworm grow to encompass all social determinants of health, and measure results by length and quality of life, national human happiness, and, of course, jobs. We can do it. Let that bubble glow. Party time.
And that’s the way it is. That’s my opinion.
George Lundberg, MD, is editor-in-chief at Cancer Commons, president of the Lundberg Institute, executive advisor at Cureus, and a clinical professor of pathology at Northwestern University. Previously, he served as editor-in-chief of JAMA (including 10 specialty journals), American Medical News, and Medscape.
A version of this article first appeared on Medscape.com.