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Does noninvasive brain stimulation augment CBT for depression?
Results of a multicenter, placebo-controlled randomized clinical trials showed adjunctive transcranial direct current stimulation (tDCS) was not superior to sham-tDCS plus CBT or CBT alone.
“Combining these interventions does not lead to added value. This is an example where negative findings guide the way of future studies. What we learned is that we might change things in a few dimensions,” study investigator Malek Bajbouj, MD, Charité University Hospital, Berlin, told this news organization.
The study was published online in JAMA Psychiatry.
Urgent need for better treatment
MDD affects 10% of the global population. However, up to 30% of patients have an inadequate response to standard treatment of CBT, pharmacotherapy, or a combination of the two, highlighting the need to develop more effective therapeutic strategies, the investigators note.
A noninvasive approach, tDCS, in healthy populations, has been shown to enhance cognitive function in brain regions that are also relevant for CBT. Specifically, the investigators point out that tDCS can “positively modulate neuronal activity in prefrontal structures central for affective and cognitive processes,” including emotion regulation, cognitive control working memory, and learning.
Based on this early data, the investigators conducted a randomized, placebo-controlled trial to determine whether tDCS combined with CBT might have clinically relevant synergistic effects.
The multicenter study included adults aged 20-65 years with a single or recurrent depressive episode who were either not receiving medication or receiving a stable regimen of selective serotonin reuptake inhibitors (SSRIs) or mirtazapine (Remeron).
A total of 148 participants (89 women, 59 men) with a mean age of 41 years were randomly assigned to receive CBT alone (n = 53), CBT+ tDCS (n = 48) or CBT + sham tDCS (n = 47).
Participants attended a 6-week group intervention of 12 sessions of CBT. If assigned, tDCS was applied simultaneously. Active tDCS included stimulation with an intensity of 2 milliamps for 30 minutes.
The study’s primary outcome was the change in Montgomery-Åsberg Depression Rating Scale (MADRS) from baseline to post treatment in the intention-to-treat sample. A total of 126 patients completed the study.
At baseline, the average MADRS score was 23.0. In each of the study groups, MADRS scores were reduced by a mean of 6.5 points (95% confidence interval, 3.82-9.14 points). The Cohen d value was -0.90 (95% CI, -1.43 to -0.50), indicating a significant effect over time, the researchers report. However, they add that “there was not significant effect of group and no significant interaction of group x time, indicating the estimated additive effects were not statistically significant.”
Results suggest that more research is needed to optimize treatment synchronization to achieve synergies between noninvasive brain stimulation and psychotherapeutic interventions.
Beauty and promise
Commenting on the findings, Mark George, MD, director of the Medical University of South Carolina Center for Advanced Imaging Research and the Brain Stimulation Laboratory, Charleston, described the study as “a really good effort by a great group of researchers.”
It’s unclear, he added, why tDCS failed to augment CBT. “It may be about the nongeneralizability of tDCS to complex functions, it may be that they didn’t get the dose right, or it might be due to a placebo response,” he speculated.
Furthermore, “tDCS is the most simple form of brain stimulation. The beauty and promise of tDCS is that it is so inexpensive and safe,” Dr. George added.
If proven effective, tDCS could potentially be used at home and rolled out as a frontline therapy for depression, he added. “Everybody wants the technology to work as an antidepressant, since it could have a very big positive public health impact,” said Dr. George.
Referring to previous research showing tDCS’ ability to improve specific brain functions in healthy controls, Dr. George noted that the potential of tDCS may be limited to augmenting specific brain functions such as memory but not more complex behaviors like depression.
However, Dr. George believes a more plausible explanation is that the optimal dose for tDCS has not yet been determined.
With other types of neuromodulation, such as electroconvulsive therapy, “we know that we’re in the brain with the right dose. But for tDCS, we don’t know that, and we’ve got to figure that out before it’s ever really going to make it [as a treatment],” he said.
“There have been great advances through the years in the field of brain stimulation and the treatment of depression. But rates of depression and suicide are continuing to grow, and we have not yet made a significant dent in treatment, in part because these technologies require equipment, [and] they’re expensive. So when we figure out tDCS, it will be a very important piece of our toolkit – a real game changer,” Dr. George added.
A version of this article first appeared on Medscape.com.
Results of a multicenter, placebo-controlled randomized clinical trials showed adjunctive transcranial direct current stimulation (tDCS) was not superior to sham-tDCS plus CBT or CBT alone.
“Combining these interventions does not lead to added value. This is an example where negative findings guide the way of future studies. What we learned is that we might change things in a few dimensions,” study investigator Malek Bajbouj, MD, Charité University Hospital, Berlin, told this news organization.
The study was published online in JAMA Psychiatry.
Urgent need for better treatment
MDD affects 10% of the global population. However, up to 30% of patients have an inadequate response to standard treatment of CBT, pharmacotherapy, or a combination of the two, highlighting the need to develop more effective therapeutic strategies, the investigators note.
A noninvasive approach, tDCS, in healthy populations, has been shown to enhance cognitive function in brain regions that are also relevant for CBT. Specifically, the investigators point out that tDCS can “positively modulate neuronal activity in prefrontal structures central for affective and cognitive processes,” including emotion regulation, cognitive control working memory, and learning.
Based on this early data, the investigators conducted a randomized, placebo-controlled trial to determine whether tDCS combined with CBT might have clinically relevant synergistic effects.
The multicenter study included adults aged 20-65 years with a single or recurrent depressive episode who were either not receiving medication or receiving a stable regimen of selective serotonin reuptake inhibitors (SSRIs) or mirtazapine (Remeron).
A total of 148 participants (89 women, 59 men) with a mean age of 41 years were randomly assigned to receive CBT alone (n = 53), CBT+ tDCS (n = 48) or CBT + sham tDCS (n = 47).
Participants attended a 6-week group intervention of 12 sessions of CBT. If assigned, tDCS was applied simultaneously. Active tDCS included stimulation with an intensity of 2 milliamps for 30 minutes.
The study’s primary outcome was the change in Montgomery-Åsberg Depression Rating Scale (MADRS) from baseline to post treatment in the intention-to-treat sample. A total of 126 patients completed the study.
At baseline, the average MADRS score was 23.0. In each of the study groups, MADRS scores were reduced by a mean of 6.5 points (95% confidence interval, 3.82-9.14 points). The Cohen d value was -0.90 (95% CI, -1.43 to -0.50), indicating a significant effect over time, the researchers report. However, they add that “there was not significant effect of group and no significant interaction of group x time, indicating the estimated additive effects were not statistically significant.”
Results suggest that more research is needed to optimize treatment synchronization to achieve synergies between noninvasive brain stimulation and psychotherapeutic interventions.
Beauty and promise
Commenting on the findings, Mark George, MD, director of the Medical University of South Carolina Center for Advanced Imaging Research and the Brain Stimulation Laboratory, Charleston, described the study as “a really good effort by a great group of researchers.”
It’s unclear, he added, why tDCS failed to augment CBT. “It may be about the nongeneralizability of tDCS to complex functions, it may be that they didn’t get the dose right, or it might be due to a placebo response,” he speculated.
Furthermore, “tDCS is the most simple form of brain stimulation. The beauty and promise of tDCS is that it is so inexpensive and safe,” Dr. George added.
If proven effective, tDCS could potentially be used at home and rolled out as a frontline therapy for depression, he added. “Everybody wants the technology to work as an antidepressant, since it could have a very big positive public health impact,” said Dr. George.
Referring to previous research showing tDCS’ ability to improve specific brain functions in healthy controls, Dr. George noted that the potential of tDCS may be limited to augmenting specific brain functions such as memory but not more complex behaviors like depression.
However, Dr. George believes a more plausible explanation is that the optimal dose for tDCS has not yet been determined.
With other types of neuromodulation, such as electroconvulsive therapy, “we know that we’re in the brain with the right dose. But for tDCS, we don’t know that, and we’ve got to figure that out before it’s ever really going to make it [as a treatment],” he said.
“There have been great advances through the years in the field of brain stimulation and the treatment of depression. But rates of depression and suicide are continuing to grow, and we have not yet made a significant dent in treatment, in part because these technologies require equipment, [and] they’re expensive. So when we figure out tDCS, it will be a very important piece of our toolkit – a real game changer,” Dr. George added.
A version of this article first appeared on Medscape.com.
Results of a multicenter, placebo-controlled randomized clinical trials showed adjunctive transcranial direct current stimulation (tDCS) was not superior to sham-tDCS plus CBT or CBT alone.
“Combining these interventions does not lead to added value. This is an example where negative findings guide the way of future studies. What we learned is that we might change things in a few dimensions,” study investigator Malek Bajbouj, MD, Charité University Hospital, Berlin, told this news organization.
The study was published online in JAMA Psychiatry.
Urgent need for better treatment
MDD affects 10% of the global population. However, up to 30% of patients have an inadequate response to standard treatment of CBT, pharmacotherapy, or a combination of the two, highlighting the need to develop more effective therapeutic strategies, the investigators note.
A noninvasive approach, tDCS, in healthy populations, has been shown to enhance cognitive function in brain regions that are also relevant for CBT. Specifically, the investigators point out that tDCS can “positively modulate neuronal activity in prefrontal structures central for affective and cognitive processes,” including emotion regulation, cognitive control working memory, and learning.
Based on this early data, the investigators conducted a randomized, placebo-controlled trial to determine whether tDCS combined with CBT might have clinically relevant synergistic effects.
The multicenter study included adults aged 20-65 years with a single or recurrent depressive episode who were either not receiving medication or receiving a stable regimen of selective serotonin reuptake inhibitors (SSRIs) or mirtazapine (Remeron).
A total of 148 participants (89 women, 59 men) with a mean age of 41 years were randomly assigned to receive CBT alone (n = 53), CBT+ tDCS (n = 48) or CBT + sham tDCS (n = 47).
Participants attended a 6-week group intervention of 12 sessions of CBT. If assigned, tDCS was applied simultaneously. Active tDCS included stimulation with an intensity of 2 milliamps for 30 minutes.
The study’s primary outcome was the change in Montgomery-Åsberg Depression Rating Scale (MADRS) from baseline to post treatment in the intention-to-treat sample. A total of 126 patients completed the study.
At baseline, the average MADRS score was 23.0. In each of the study groups, MADRS scores were reduced by a mean of 6.5 points (95% confidence interval, 3.82-9.14 points). The Cohen d value was -0.90 (95% CI, -1.43 to -0.50), indicating a significant effect over time, the researchers report. However, they add that “there was not significant effect of group and no significant interaction of group x time, indicating the estimated additive effects were not statistically significant.”
Results suggest that more research is needed to optimize treatment synchronization to achieve synergies between noninvasive brain stimulation and psychotherapeutic interventions.
Beauty and promise
Commenting on the findings, Mark George, MD, director of the Medical University of South Carolina Center for Advanced Imaging Research and the Brain Stimulation Laboratory, Charleston, described the study as “a really good effort by a great group of researchers.”
It’s unclear, he added, why tDCS failed to augment CBT. “It may be about the nongeneralizability of tDCS to complex functions, it may be that they didn’t get the dose right, or it might be due to a placebo response,” he speculated.
Furthermore, “tDCS is the most simple form of brain stimulation. The beauty and promise of tDCS is that it is so inexpensive and safe,” Dr. George added.
If proven effective, tDCS could potentially be used at home and rolled out as a frontline therapy for depression, he added. “Everybody wants the technology to work as an antidepressant, since it could have a very big positive public health impact,” said Dr. George.
Referring to previous research showing tDCS’ ability to improve specific brain functions in healthy controls, Dr. George noted that the potential of tDCS may be limited to augmenting specific brain functions such as memory but not more complex behaviors like depression.
However, Dr. George believes a more plausible explanation is that the optimal dose for tDCS has not yet been determined.
With other types of neuromodulation, such as electroconvulsive therapy, “we know that we’re in the brain with the right dose. But for tDCS, we don’t know that, and we’ve got to figure that out before it’s ever really going to make it [as a treatment],” he said.
“There have been great advances through the years in the field of brain stimulation and the treatment of depression. But rates of depression and suicide are continuing to grow, and we have not yet made a significant dent in treatment, in part because these technologies require equipment, [and] they’re expensive. So when we figure out tDCS, it will be a very important piece of our toolkit – a real game changer,” Dr. George added.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
Neurology, psychiatry studies overlook sex as a variable
A large percentage of studies in neurology and psychiatry over the past decade have failed to account for differences between the sexes, according to a team of Canadian researchers.
“Despite the fact there are papers that are using males and females in the studies, they’re not using the males and females in the way that would optimally find the possibility of sex differences,” lead author Liisa A.M. Galea, PhD, told this news organization. Dr. Galea is a professor and distinguished scholar at the Djavad Mowafaghian Center for Brain Health at the University of British Columbia in Vancouver.
The study was published online in Nature Communications.
Optimal design uncommon
Differences in how neurologic and psychiatric diseases affect men and women have been well documented. Women, for example, are more susceptible to severe stroke, and men are more prone to cognitive decline with schizophrenia. With Alzheimer’s disease, women typically have more severe cognitive defects.
The researchers surveyed 3,193 papers that included a multitude of studies. Although most of the papers reported studies that included both sexes, only 19% of surveyed studies used what Dr. Galea called an optimal design for the discovery of sex differences. “What I mean by ‘optimally’ is the design of the experiments and the analysis of sex as a variable,” she said. And in 2019, only 5% of the studies used sex as a variable for determining differences between the sexes, the study found.
In the current research, two authors read the methods and results of each study described in each paper, Dr. Galea said. The readers noted whether the paper reported the study sample size and whether the studies used a balanced design. The surveyed journals include Nature Neuroscience, Neuron, Journal of Neuroscience, Molecular Psychiatry, Biological Psychiatry, and Neuropsychopharmacology.
‘Not much is changing’
“I had a suspicion that this was happening,” Dr. Galea said. “I didn’t know that it’s so bad, to be fair.” The “good news story,” she said, is that more papers considered sex as a factor in the later years surveyed. In 2019, more than 95% of papers across both disciplines reported participants’ sex, compared with about 70% in 2009. However, less than 20% of the papers in all study years reported studies that used sex optimally to determine differences between the sexes.
“The other thing that shocked me,” Dr. Galea said, “was that even despite the fact that we saw this increase in the number of papers that were using males and females, we didn’t see the sort of corresponding increase in those that were using ‘optimal design’ or ‘optimal analysis,’ ” Dr. Galea said. In 2009, 14% of papers used optimal design and 2% used optimal analysis for determining sex differences. By 2019, those percentages were 19% and 5%, respectively.
But even the papers that used both sexes had shortcomings, the study found. Just over one-third of these papers (34.5%) didn’t use a balanced design. Just over one-quarter (25.9%) didn’t identify the sample size, a shortcoming that marked 18% of these studies in 2009 and 33% in 2019. Fifteen percent of papers examined included studies that used both sexes inconsistently.
“That matters, because other studies have found that about 20% of papers are doing some kind of analysis with sex, but we had a suspicion that a lot of studies would include sex as a covariate,” Dr. Galea said. “Essentially what that does is, you remove that variable from the data. So, any statistical variation due to sex is then gone.
“The problem with that,” she added, “is you’re not actually looking to see if there’s an influence of sex; you’re removing it.”
Dr. Galea noted that this study points to a need for funding agencies to demand that researchers meet their mandates on sex- and gender-based analysis. “Despite the mandates, not much is really changing as far as the analysis or design of experiments, and we need to figure out how to change that,” she said. “We need to figure out how to get researchers more interested to use the power of studying sex differences.”
‘Not surprising, but disappointing’
Vladimir Hachinski, MD, professor of neurology and epidemiology at Western University in London, Ont., and former editor in chief of Stroke, told this news organization that women have almost twice the life risk of developing dementia, are at higher risk of stroke below age 35 years, and have more severe strokes and higher rates of disability at any age.
Commenting on the current study, Dr. Hachinski said, “It’s not surprising, but it’s disappointing, because we’ve known the difference for a long time.” He added, “The paper is very important because we were not aware that it was that bad.”
Dr. Hachinski also stated, “This paper needs a lot of reading. It’s a great resource, and it should be highlighted as one of those things that needs to be addressed, because it matters.”
The study was funded by a Natural Sciences and Engineering Research Council of Canada grant and by the British Columbia Women’s Foundation. Dr. Galea and Hachinski had no relevant disclosures.
A version of this article first appeared on Medscape.com.
A large percentage of studies in neurology and psychiatry over the past decade have failed to account for differences between the sexes, according to a team of Canadian researchers.
“Despite the fact there are papers that are using males and females in the studies, they’re not using the males and females in the way that would optimally find the possibility of sex differences,” lead author Liisa A.M. Galea, PhD, told this news organization. Dr. Galea is a professor and distinguished scholar at the Djavad Mowafaghian Center for Brain Health at the University of British Columbia in Vancouver.
The study was published online in Nature Communications.
Optimal design uncommon
Differences in how neurologic and psychiatric diseases affect men and women have been well documented. Women, for example, are more susceptible to severe stroke, and men are more prone to cognitive decline with schizophrenia. With Alzheimer’s disease, women typically have more severe cognitive defects.
The researchers surveyed 3,193 papers that included a multitude of studies. Although most of the papers reported studies that included both sexes, only 19% of surveyed studies used what Dr. Galea called an optimal design for the discovery of sex differences. “What I mean by ‘optimally’ is the design of the experiments and the analysis of sex as a variable,” she said. And in 2019, only 5% of the studies used sex as a variable for determining differences between the sexes, the study found.
In the current research, two authors read the methods and results of each study described in each paper, Dr. Galea said. The readers noted whether the paper reported the study sample size and whether the studies used a balanced design. The surveyed journals include Nature Neuroscience, Neuron, Journal of Neuroscience, Molecular Psychiatry, Biological Psychiatry, and Neuropsychopharmacology.
‘Not much is changing’
“I had a suspicion that this was happening,” Dr. Galea said. “I didn’t know that it’s so bad, to be fair.” The “good news story,” she said, is that more papers considered sex as a factor in the later years surveyed. In 2019, more than 95% of papers across both disciplines reported participants’ sex, compared with about 70% in 2009. However, less than 20% of the papers in all study years reported studies that used sex optimally to determine differences between the sexes.
“The other thing that shocked me,” Dr. Galea said, “was that even despite the fact that we saw this increase in the number of papers that were using males and females, we didn’t see the sort of corresponding increase in those that were using ‘optimal design’ or ‘optimal analysis,’ ” Dr. Galea said. In 2009, 14% of papers used optimal design and 2% used optimal analysis for determining sex differences. By 2019, those percentages were 19% and 5%, respectively.
But even the papers that used both sexes had shortcomings, the study found. Just over one-third of these papers (34.5%) didn’t use a balanced design. Just over one-quarter (25.9%) didn’t identify the sample size, a shortcoming that marked 18% of these studies in 2009 and 33% in 2019. Fifteen percent of papers examined included studies that used both sexes inconsistently.
“That matters, because other studies have found that about 20% of papers are doing some kind of analysis with sex, but we had a suspicion that a lot of studies would include sex as a covariate,” Dr. Galea said. “Essentially what that does is, you remove that variable from the data. So, any statistical variation due to sex is then gone.
“The problem with that,” she added, “is you’re not actually looking to see if there’s an influence of sex; you’re removing it.”
Dr. Galea noted that this study points to a need for funding agencies to demand that researchers meet their mandates on sex- and gender-based analysis. “Despite the mandates, not much is really changing as far as the analysis or design of experiments, and we need to figure out how to change that,” she said. “We need to figure out how to get researchers more interested to use the power of studying sex differences.”
‘Not surprising, but disappointing’
Vladimir Hachinski, MD, professor of neurology and epidemiology at Western University in London, Ont., and former editor in chief of Stroke, told this news organization that women have almost twice the life risk of developing dementia, are at higher risk of stroke below age 35 years, and have more severe strokes and higher rates of disability at any age.
Commenting on the current study, Dr. Hachinski said, “It’s not surprising, but it’s disappointing, because we’ve known the difference for a long time.” He added, “The paper is very important because we were not aware that it was that bad.”
Dr. Hachinski also stated, “This paper needs a lot of reading. It’s a great resource, and it should be highlighted as one of those things that needs to be addressed, because it matters.”
The study was funded by a Natural Sciences and Engineering Research Council of Canada grant and by the British Columbia Women’s Foundation. Dr. Galea and Hachinski had no relevant disclosures.
A version of this article first appeared on Medscape.com.
A large percentage of studies in neurology and psychiatry over the past decade have failed to account for differences between the sexes, according to a team of Canadian researchers.
“Despite the fact there are papers that are using males and females in the studies, they’re not using the males and females in the way that would optimally find the possibility of sex differences,” lead author Liisa A.M. Galea, PhD, told this news organization. Dr. Galea is a professor and distinguished scholar at the Djavad Mowafaghian Center for Brain Health at the University of British Columbia in Vancouver.
The study was published online in Nature Communications.
Optimal design uncommon
Differences in how neurologic and psychiatric diseases affect men and women have been well documented. Women, for example, are more susceptible to severe stroke, and men are more prone to cognitive decline with schizophrenia. With Alzheimer’s disease, women typically have more severe cognitive defects.
The researchers surveyed 3,193 papers that included a multitude of studies. Although most of the papers reported studies that included both sexes, only 19% of surveyed studies used what Dr. Galea called an optimal design for the discovery of sex differences. “What I mean by ‘optimally’ is the design of the experiments and the analysis of sex as a variable,” she said. And in 2019, only 5% of the studies used sex as a variable for determining differences between the sexes, the study found.
In the current research, two authors read the methods and results of each study described in each paper, Dr. Galea said. The readers noted whether the paper reported the study sample size and whether the studies used a balanced design. The surveyed journals include Nature Neuroscience, Neuron, Journal of Neuroscience, Molecular Psychiatry, Biological Psychiatry, and Neuropsychopharmacology.
‘Not much is changing’
“I had a suspicion that this was happening,” Dr. Galea said. “I didn’t know that it’s so bad, to be fair.” The “good news story,” she said, is that more papers considered sex as a factor in the later years surveyed. In 2019, more than 95% of papers across both disciplines reported participants’ sex, compared with about 70% in 2009. However, less than 20% of the papers in all study years reported studies that used sex optimally to determine differences between the sexes.
“The other thing that shocked me,” Dr. Galea said, “was that even despite the fact that we saw this increase in the number of papers that were using males and females, we didn’t see the sort of corresponding increase in those that were using ‘optimal design’ or ‘optimal analysis,’ ” Dr. Galea said. In 2009, 14% of papers used optimal design and 2% used optimal analysis for determining sex differences. By 2019, those percentages were 19% and 5%, respectively.
But even the papers that used both sexes had shortcomings, the study found. Just over one-third of these papers (34.5%) didn’t use a balanced design. Just over one-quarter (25.9%) didn’t identify the sample size, a shortcoming that marked 18% of these studies in 2009 and 33% in 2019. Fifteen percent of papers examined included studies that used both sexes inconsistently.
“That matters, because other studies have found that about 20% of papers are doing some kind of analysis with sex, but we had a suspicion that a lot of studies would include sex as a covariate,” Dr. Galea said. “Essentially what that does is, you remove that variable from the data. So, any statistical variation due to sex is then gone.
“The problem with that,” she added, “is you’re not actually looking to see if there’s an influence of sex; you’re removing it.”
Dr. Galea noted that this study points to a need for funding agencies to demand that researchers meet their mandates on sex- and gender-based analysis. “Despite the mandates, not much is really changing as far as the analysis or design of experiments, and we need to figure out how to change that,” she said. “We need to figure out how to get researchers more interested to use the power of studying sex differences.”
‘Not surprising, but disappointing’
Vladimir Hachinski, MD, professor of neurology and epidemiology at Western University in London, Ont., and former editor in chief of Stroke, told this news organization that women have almost twice the life risk of developing dementia, are at higher risk of stroke below age 35 years, and have more severe strokes and higher rates of disability at any age.
Commenting on the current study, Dr. Hachinski said, “It’s not surprising, but it’s disappointing, because we’ve known the difference for a long time.” He added, “The paper is very important because we were not aware that it was that bad.”
Dr. Hachinski also stated, “This paper needs a lot of reading. It’s a great resource, and it should be highlighted as one of those things that needs to be addressed, because it matters.”
The study was funded by a Natural Sciences and Engineering Research Council of Canada grant and by the British Columbia Women’s Foundation. Dr. Galea and Hachinski had no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM NATURE COMMUNICATIONS
Do psychotropic meds raise or lower COVID risk in psych patients?
Investigators found that second-generation antipsychotics were associated with a 48% lower risk of COVID-19, while valproic acid was associated with a 39% increased risk of the disease.
“Exposures to several psychotropic medications were associated with risk of COVID-19 infection among inpatients with serious mental illness; decreased risk was observed with the use of second generation antipsychotics, with paliperidone use associated with the largest effect size. Valproic acid use was associated with an increased risk of infection,” the investigators, led by Katlyn Nemani, MD, at NYU Langone Medical Center, New York, write.
The study was published online in JAMA Network Open.
Vulnerable population
Patients with serious mental illness are particularly vulnerable to COVID-19. Several psychotropic medications have been identified as potential therapeutic agents to prevent or treat COVID-19, but they have not been systematically studied in this patient population.
The researchers analyzed data from 1,958 adults who were continuously hospitalized with serious mental illness from March 8 to July 1, 2020. The mean age was 51.4 years, and 1,442 (74%) were men.
A total of 969 patients (49.5%) had laboratory-confirmed COVID-19 while hospitalized, and 38 (3.9%) died – a mortality rate four times higher than estimates from the general population in New York during the same time frame, the researchers note.
“This finding is consistent with prior studies that have found increased rates of infection in congregate settings and increased mortality after infection among patients with serious mental illness,” the investigators write.
The use of second-generation antipsychotic medications, as a class, was associated with a lower likelihood of COVID-19 (odds ratio, 0.62; 95% confidence interval, 0.45-0.86), while the use of mood stabilizers was associated with increased likelihood of infection (OR, 1.23; 95% CI, 1.03-1.47).
In a multivariable model of individual medications, use of the long-acting atypical antipsychotic paliperidone was associated with a lower odds of infection (OR, 0.59; 95% CI, 0.41-0.84), and use of valproic acid was associated with increased odds of infection (OR, 1.39; 95% CI, 1.10-1.76).
Valproic acid downregulates angiotensin-converting enzyme 2 in endothelial cells, which may impair immune function and contribute to poor outcomes for patients with COVID-19, the researchers say.
The use of clozapine was associated with reduced odds of COVID-related death (unadjusted OR, 0.25; 95% CI, 0.10-0.62; fully adjusted OR, 0.43; 95% CI, 0.17-1.12).
“Although there have been concerns about clozapine use during the pandemic as a risk factor for pneumonia and potential toxic effects during acute infection, clozapine use was not associated with an increased risk of COVID-19 infection or death in the present study. In fact, unadjusted estimates suggested a significant protective association,” the investigators write.
However, they note, data on clozapine and COVID-19 have been mixed.
Two prior studies of health record data showed an increased risk of COVID-19 associated with clozapine treatment, while a study that was limited to inpatients found a lower risk of infection and a lower risk of symptomatic disease in association with clozapine use.
The researchers also found a lower mortality risk in patients taking antidepressants; there were no COVID-related deaths among patients taking escitalopram, venlafaxine, bupropion, or fluvoxamine.
Although the association was not statistically significant, this observation is in line with larger studies that showed reduced risk of adverse outcomes associated with antidepressant use, the researchers note.
A matter of debate
In an accompanying commentary, Benedetta Vai, PhD, and Mario Gennaro Mazza, MD, with IRCCS San Raffaele Scientific Institute, Milan, point out that the link between psychopharmacologic compounds, in particular antipsychotics, and severe COVID-19 outcomes remains “a matter of debate, with inconsistent findings between studies.”
They note further research is needed to determine whether the protective role of second-generation antipsychotics on risk of COVID-19 is mediated by an immune effect or by the direct antiviral properties of these molecules.
The study had no specific funding. Dr. Nemani, Dr. Vai, and Dr. Mazza have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Investigators found that second-generation antipsychotics were associated with a 48% lower risk of COVID-19, while valproic acid was associated with a 39% increased risk of the disease.
“Exposures to several psychotropic medications were associated with risk of COVID-19 infection among inpatients with serious mental illness; decreased risk was observed with the use of second generation antipsychotics, with paliperidone use associated with the largest effect size. Valproic acid use was associated with an increased risk of infection,” the investigators, led by Katlyn Nemani, MD, at NYU Langone Medical Center, New York, write.
The study was published online in JAMA Network Open.
Vulnerable population
Patients with serious mental illness are particularly vulnerable to COVID-19. Several psychotropic medications have been identified as potential therapeutic agents to prevent or treat COVID-19, but they have not been systematically studied in this patient population.
The researchers analyzed data from 1,958 adults who were continuously hospitalized with serious mental illness from March 8 to July 1, 2020. The mean age was 51.4 years, and 1,442 (74%) were men.
A total of 969 patients (49.5%) had laboratory-confirmed COVID-19 while hospitalized, and 38 (3.9%) died – a mortality rate four times higher than estimates from the general population in New York during the same time frame, the researchers note.
“This finding is consistent with prior studies that have found increased rates of infection in congregate settings and increased mortality after infection among patients with serious mental illness,” the investigators write.
The use of second-generation antipsychotic medications, as a class, was associated with a lower likelihood of COVID-19 (odds ratio, 0.62; 95% confidence interval, 0.45-0.86), while the use of mood stabilizers was associated with increased likelihood of infection (OR, 1.23; 95% CI, 1.03-1.47).
In a multivariable model of individual medications, use of the long-acting atypical antipsychotic paliperidone was associated with a lower odds of infection (OR, 0.59; 95% CI, 0.41-0.84), and use of valproic acid was associated with increased odds of infection (OR, 1.39; 95% CI, 1.10-1.76).
Valproic acid downregulates angiotensin-converting enzyme 2 in endothelial cells, which may impair immune function and contribute to poor outcomes for patients with COVID-19, the researchers say.
The use of clozapine was associated with reduced odds of COVID-related death (unadjusted OR, 0.25; 95% CI, 0.10-0.62; fully adjusted OR, 0.43; 95% CI, 0.17-1.12).
“Although there have been concerns about clozapine use during the pandemic as a risk factor for pneumonia and potential toxic effects during acute infection, clozapine use was not associated with an increased risk of COVID-19 infection or death in the present study. In fact, unadjusted estimates suggested a significant protective association,” the investigators write.
However, they note, data on clozapine and COVID-19 have been mixed.
Two prior studies of health record data showed an increased risk of COVID-19 associated with clozapine treatment, while a study that was limited to inpatients found a lower risk of infection and a lower risk of symptomatic disease in association with clozapine use.
The researchers also found a lower mortality risk in patients taking antidepressants; there were no COVID-related deaths among patients taking escitalopram, venlafaxine, bupropion, or fluvoxamine.
Although the association was not statistically significant, this observation is in line with larger studies that showed reduced risk of adverse outcomes associated with antidepressant use, the researchers note.
A matter of debate
In an accompanying commentary, Benedetta Vai, PhD, and Mario Gennaro Mazza, MD, with IRCCS San Raffaele Scientific Institute, Milan, point out that the link between psychopharmacologic compounds, in particular antipsychotics, and severe COVID-19 outcomes remains “a matter of debate, with inconsistent findings between studies.”
They note further research is needed to determine whether the protective role of second-generation antipsychotics on risk of COVID-19 is mediated by an immune effect or by the direct antiviral properties of these molecules.
The study had no specific funding. Dr. Nemani, Dr. Vai, and Dr. Mazza have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Investigators found that second-generation antipsychotics were associated with a 48% lower risk of COVID-19, while valproic acid was associated with a 39% increased risk of the disease.
“Exposures to several psychotropic medications were associated with risk of COVID-19 infection among inpatients with serious mental illness; decreased risk was observed with the use of second generation antipsychotics, with paliperidone use associated with the largest effect size. Valproic acid use was associated with an increased risk of infection,” the investigators, led by Katlyn Nemani, MD, at NYU Langone Medical Center, New York, write.
The study was published online in JAMA Network Open.
Vulnerable population
Patients with serious mental illness are particularly vulnerable to COVID-19. Several psychotropic medications have been identified as potential therapeutic agents to prevent or treat COVID-19, but they have not been systematically studied in this patient population.
The researchers analyzed data from 1,958 adults who were continuously hospitalized with serious mental illness from March 8 to July 1, 2020. The mean age was 51.4 years, and 1,442 (74%) were men.
A total of 969 patients (49.5%) had laboratory-confirmed COVID-19 while hospitalized, and 38 (3.9%) died – a mortality rate four times higher than estimates from the general population in New York during the same time frame, the researchers note.
“This finding is consistent with prior studies that have found increased rates of infection in congregate settings and increased mortality after infection among patients with serious mental illness,” the investigators write.
The use of second-generation antipsychotic medications, as a class, was associated with a lower likelihood of COVID-19 (odds ratio, 0.62; 95% confidence interval, 0.45-0.86), while the use of mood stabilizers was associated with increased likelihood of infection (OR, 1.23; 95% CI, 1.03-1.47).
In a multivariable model of individual medications, use of the long-acting atypical antipsychotic paliperidone was associated with a lower odds of infection (OR, 0.59; 95% CI, 0.41-0.84), and use of valproic acid was associated with increased odds of infection (OR, 1.39; 95% CI, 1.10-1.76).
Valproic acid downregulates angiotensin-converting enzyme 2 in endothelial cells, which may impair immune function and contribute to poor outcomes for patients with COVID-19, the researchers say.
The use of clozapine was associated with reduced odds of COVID-related death (unadjusted OR, 0.25; 95% CI, 0.10-0.62; fully adjusted OR, 0.43; 95% CI, 0.17-1.12).
“Although there have been concerns about clozapine use during the pandemic as a risk factor for pneumonia and potential toxic effects during acute infection, clozapine use was not associated with an increased risk of COVID-19 infection or death in the present study. In fact, unadjusted estimates suggested a significant protective association,” the investigators write.
However, they note, data on clozapine and COVID-19 have been mixed.
Two prior studies of health record data showed an increased risk of COVID-19 associated with clozapine treatment, while a study that was limited to inpatients found a lower risk of infection and a lower risk of symptomatic disease in association with clozapine use.
The researchers also found a lower mortality risk in patients taking antidepressants; there were no COVID-related deaths among patients taking escitalopram, venlafaxine, bupropion, or fluvoxamine.
Although the association was not statistically significant, this observation is in line with larger studies that showed reduced risk of adverse outcomes associated with antidepressant use, the researchers note.
A matter of debate
In an accompanying commentary, Benedetta Vai, PhD, and Mario Gennaro Mazza, MD, with IRCCS San Raffaele Scientific Institute, Milan, point out that the link between psychopharmacologic compounds, in particular antipsychotics, and severe COVID-19 outcomes remains “a matter of debate, with inconsistent findings between studies.”
They note further research is needed to determine whether the protective role of second-generation antipsychotics on risk of COVID-19 is mediated by an immune effect or by the direct antiviral properties of these molecules.
The study had no specific funding. Dr. Nemani, Dr. Vai, and Dr. Mazza have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
TikTok challenge hits Taco Bell right in its ‘Stuft Nacho’
Losing weight for TikTok: Taco Bell edition
There are many reasons why a person would want to lose weight. Too numerous to list. Losing weight to improve your health, however, doesn’t bring in a few hundred thousand TikTok subscribers. Losing weight to convince Taco Bell to bring back an obscure menu item, on the other hand ...
Chris Sandberg, a 37-year-old man from San Francisco, has struggled with his weight for years, losing and gaining hundreds of pounds in an endless cycle of feast and famine. In an unrelated development, at the start of the pandemic he also started making videos on TikTok. As the pandemic wore on, he realized that his excess weight put him at increased risk for severe COVID, as well as other chronic diseases, and he resolved to lose weight. He decided to turn his weight-loss journey into a TikTok challenge but, as we said, losing weight for its own sake isn’t enough for the almighty algorithm. He needed a different goal, preferably something offbeat and a little silly.
Back in 2013, Taco Bell introduced the Grilled Stuft Nacho, “a flour tortilla, shaped like a nacho, stuffed with beef, cheesy jalapeño sauce, sour cream and crunchy red strips,” according to its website. Mr. Sandberg discovered the item in 2015 and instantly fell in love, purchasing one every day for a week. After that first week, however, he discovered, to his horror, that the Grilled Stuft Nacho had been discontinued.
That loss haunted him for years, until inspiration struck in 2021. He pledged to work out every day on TikTok until Taco Bell brought back the Grilled Stuft Nacho. A bit incongruous, exercising for notoriously unhealthy fast food, but that’s kind of the point. He began the challenge on Jan. 4, 2021, and has continued it every day since, nearly 500 days. Over that time, he’s lost 87 pounds (from 275 at the start to under 190) and currently has 450,000 TikTok subscribers.
A year into the challenge, a local Taco Bell made Mr. Sandberg his beloved Grilled Stuft Nacho, but since the challenge was to exercise until Taco Bell brings the item back to all its restaurants, not just for him, the great journey continues. And we admire him for it. In fact, he’s inspired us: We will write a LOTME every week until it receives a Pulitzer Prize. This is important journalism we do here. Don’t deny it!
Episode XIX: COVID strikes back
So what’s next for COVID? Is Disney going to turn it into a series? Can it support a spin-off? Did James Cameron really buy the movie rights? Can it compete against the NFL in the all-important 18-34 demographic? When are Star Wars characters going to get involved?
COVID’s motivations and negotiations are pretty much a mystery to us, but we can answer that last question. They already are involved. Well, one of them anyway.
The Chinese government has been enforcing a COVID lockdown in Shanghai for over a month now, but authorities had started letting people out of their homes for short periods of time. A recent push to bring down transmission, however, has made residents increasingly frustrated and argumentative, according to Reuters.
A now-unavailable video, which Reuters could not verify, surfaced on Chinese social media showing police in hazmat suits arguing with people who were being told that they were going to be quarantined because a neighbor had tested positive.
That’s when the Force kicks in, and this next bit comes directly from the Reuters report: “This is so that we can thoroughly remove any positive cases,” one of the officers is heard saying. “Stop asking me why, there is no why.”
There is no why? Does that remind you of someone? Someone short and green, with an odd syntax? That’s right. Clearly, Yoda it is. Yoda is alive and working for the Chinese government in Shanghai. You read it here first.
Your coffee may be guilty of sexual discrimination
How do you take your coffee? Espresso, drip, instant, or brewed from a regular old coffee machine? Well, a recent study published in Open Heart suggests that gender and brewing method can alter your coffee’s effect on cholesterol levels.
Besides caffeine, coffee beans have naturally occurring chemicals such as diterpenes, cafestol, and kahweol that raise cholesterol levels in the blood. And then there are the various brewing methods, which are going to release different amounts of chemicals from the beans. According to Consumer Reports, an ounce of espresso has 63 mg of caffeine and an ounce of regular coffee has 12-16 mg. That’s a bit deceiving, though, since no one ever drinks an ounce of regular coffee, so figure 96-128 mg of caffeine for an 8-ounce cup. That’s enough to make anyone’s heart race.
Data from 21,083 participants in the seventh survey of the Tromsø Study who were aged 40 and older showed that women drank a mean of 3.8 cups per day while men drank 4.9 cups. Drinking six or more cups of plunger-brewed coffee was associated with increased cholesterol in both genders, but drinking three to five cups of espresso was significantly associated with high cholesterol in men only. Having six or more cups of filtered coffee daily raised cholesterol in women, but instant coffee increased cholesterol levels in both genders, regardless of how many cups they drank.
People all over the planet drink coffee, some of us like our lives depend on it. Since “coffee is the most frequently consumed central stimulant worldwide,” the investigators said, “even small health effects can have considerable health consequences.”
We’ll drink to that.
Have you ever dreamed of having a clone?
When will science grace us with the ability to clone ourselves? It sounds like a dream come true. Our clones can do the stuff that we don’t want to do, like sit in on that 3-hour meeting or do our grocery shopping – really just all the boring stuff we don’t want to do.
In 1996, when a sheep named Dolly became the first mammal cloned successfully, people thought it was the start of an amazing cloning era, but, alas, we haven’t made it to cloning humans yet, as LiveScience discovered when it took a look at the subject.
The idea of cloning was quite exciting for science, as people looked forward to eradicating genetic diseases and birth defects. Research done in 1999, however, countered those hopes by suggesting that cloning might increase birth defects.
So why do you think we haven’t advanced to truly cloning humans? Ethics? Time and effort? Technological barriers? “Human cloning is a particularly dramatic action, and was one of the topics that helped launch American bioethics,” Hank Greely, professor of law and genetics at Stanford (Calif.) University, told LiveScience.
What if the clones turned evil and were bent on destroying the world?
We might imagine a clone of ourselves being completely identical to us in our thoughts, actions, and physical looks. However, that’s not necessarily true; a clone would be its own person even if it looks exactly like you.
So what do the professionals think? Is it worth giving human cloning a shot? Are there benefits? Mr. Greely said that “there are none that we should be willing to consider.”
The dream of having a clone to help your son with his math homework may have gone down the drain, but maybe it’s best not to open doors that could lead to drastic changes in our world.
Losing weight for TikTok: Taco Bell edition
There are many reasons why a person would want to lose weight. Too numerous to list. Losing weight to improve your health, however, doesn’t bring in a few hundred thousand TikTok subscribers. Losing weight to convince Taco Bell to bring back an obscure menu item, on the other hand ...
Chris Sandberg, a 37-year-old man from San Francisco, has struggled with his weight for years, losing and gaining hundreds of pounds in an endless cycle of feast and famine. In an unrelated development, at the start of the pandemic he also started making videos on TikTok. As the pandemic wore on, he realized that his excess weight put him at increased risk for severe COVID, as well as other chronic diseases, and he resolved to lose weight. He decided to turn his weight-loss journey into a TikTok challenge but, as we said, losing weight for its own sake isn’t enough for the almighty algorithm. He needed a different goal, preferably something offbeat and a little silly.
Back in 2013, Taco Bell introduced the Grilled Stuft Nacho, “a flour tortilla, shaped like a nacho, stuffed with beef, cheesy jalapeño sauce, sour cream and crunchy red strips,” according to its website. Mr. Sandberg discovered the item in 2015 and instantly fell in love, purchasing one every day for a week. After that first week, however, he discovered, to his horror, that the Grilled Stuft Nacho had been discontinued.
That loss haunted him for years, until inspiration struck in 2021. He pledged to work out every day on TikTok until Taco Bell brought back the Grilled Stuft Nacho. A bit incongruous, exercising for notoriously unhealthy fast food, but that’s kind of the point. He began the challenge on Jan. 4, 2021, and has continued it every day since, nearly 500 days. Over that time, he’s lost 87 pounds (from 275 at the start to under 190) and currently has 450,000 TikTok subscribers.
A year into the challenge, a local Taco Bell made Mr. Sandberg his beloved Grilled Stuft Nacho, but since the challenge was to exercise until Taco Bell brings the item back to all its restaurants, not just for him, the great journey continues. And we admire him for it. In fact, he’s inspired us: We will write a LOTME every week until it receives a Pulitzer Prize. This is important journalism we do here. Don’t deny it!
Episode XIX: COVID strikes back
So what’s next for COVID? Is Disney going to turn it into a series? Can it support a spin-off? Did James Cameron really buy the movie rights? Can it compete against the NFL in the all-important 18-34 demographic? When are Star Wars characters going to get involved?
COVID’s motivations and negotiations are pretty much a mystery to us, but we can answer that last question. They already are involved. Well, one of them anyway.
The Chinese government has been enforcing a COVID lockdown in Shanghai for over a month now, but authorities had started letting people out of their homes for short periods of time. A recent push to bring down transmission, however, has made residents increasingly frustrated and argumentative, according to Reuters.
A now-unavailable video, which Reuters could not verify, surfaced on Chinese social media showing police in hazmat suits arguing with people who were being told that they were going to be quarantined because a neighbor had tested positive.
That’s when the Force kicks in, and this next bit comes directly from the Reuters report: “This is so that we can thoroughly remove any positive cases,” one of the officers is heard saying. “Stop asking me why, there is no why.”
There is no why? Does that remind you of someone? Someone short and green, with an odd syntax? That’s right. Clearly, Yoda it is. Yoda is alive and working for the Chinese government in Shanghai. You read it here first.
Your coffee may be guilty of sexual discrimination
How do you take your coffee? Espresso, drip, instant, or brewed from a regular old coffee machine? Well, a recent study published in Open Heart suggests that gender and brewing method can alter your coffee’s effect on cholesterol levels.
Besides caffeine, coffee beans have naturally occurring chemicals such as diterpenes, cafestol, and kahweol that raise cholesterol levels in the blood. And then there are the various brewing methods, which are going to release different amounts of chemicals from the beans. According to Consumer Reports, an ounce of espresso has 63 mg of caffeine and an ounce of regular coffee has 12-16 mg. That’s a bit deceiving, though, since no one ever drinks an ounce of regular coffee, so figure 96-128 mg of caffeine for an 8-ounce cup. That’s enough to make anyone’s heart race.
Data from 21,083 participants in the seventh survey of the Tromsø Study who were aged 40 and older showed that women drank a mean of 3.8 cups per day while men drank 4.9 cups. Drinking six or more cups of plunger-brewed coffee was associated with increased cholesterol in both genders, but drinking three to five cups of espresso was significantly associated with high cholesterol in men only. Having six or more cups of filtered coffee daily raised cholesterol in women, but instant coffee increased cholesterol levels in both genders, regardless of how many cups they drank.
People all over the planet drink coffee, some of us like our lives depend on it. Since “coffee is the most frequently consumed central stimulant worldwide,” the investigators said, “even small health effects can have considerable health consequences.”
We’ll drink to that.
Have you ever dreamed of having a clone?
When will science grace us with the ability to clone ourselves? It sounds like a dream come true. Our clones can do the stuff that we don’t want to do, like sit in on that 3-hour meeting or do our grocery shopping – really just all the boring stuff we don’t want to do.
In 1996, when a sheep named Dolly became the first mammal cloned successfully, people thought it was the start of an amazing cloning era, but, alas, we haven’t made it to cloning humans yet, as LiveScience discovered when it took a look at the subject.
The idea of cloning was quite exciting for science, as people looked forward to eradicating genetic diseases and birth defects. Research done in 1999, however, countered those hopes by suggesting that cloning might increase birth defects.
So why do you think we haven’t advanced to truly cloning humans? Ethics? Time and effort? Technological barriers? “Human cloning is a particularly dramatic action, and was one of the topics that helped launch American bioethics,” Hank Greely, professor of law and genetics at Stanford (Calif.) University, told LiveScience.
What if the clones turned evil and were bent on destroying the world?
We might imagine a clone of ourselves being completely identical to us in our thoughts, actions, and physical looks. However, that’s not necessarily true; a clone would be its own person even if it looks exactly like you.
So what do the professionals think? Is it worth giving human cloning a shot? Are there benefits? Mr. Greely said that “there are none that we should be willing to consider.”
The dream of having a clone to help your son with his math homework may have gone down the drain, but maybe it’s best not to open doors that could lead to drastic changes in our world.
Losing weight for TikTok: Taco Bell edition
There are many reasons why a person would want to lose weight. Too numerous to list. Losing weight to improve your health, however, doesn’t bring in a few hundred thousand TikTok subscribers. Losing weight to convince Taco Bell to bring back an obscure menu item, on the other hand ...
Chris Sandberg, a 37-year-old man from San Francisco, has struggled with his weight for years, losing and gaining hundreds of pounds in an endless cycle of feast and famine. In an unrelated development, at the start of the pandemic he also started making videos on TikTok. As the pandemic wore on, he realized that his excess weight put him at increased risk for severe COVID, as well as other chronic diseases, and he resolved to lose weight. He decided to turn his weight-loss journey into a TikTok challenge but, as we said, losing weight for its own sake isn’t enough for the almighty algorithm. He needed a different goal, preferably something offbeat and a little silly.
Back in 2013, Taco Bell introduced the Grilled Stuft Nacho, “a flour tortilla, shaped like a nacho, stuffed with beef, cheesy jalapeño sauce, sour cream and crunchy red strips,” according to its website. Mr. Sandberg discovered the item in 2015 and instantly fell in love, purchasing one every day for a week. After that first week, however, he discovered, to his horror, that the Grilled Stuft Nacho had been discontinued.
That loss haunted him for years, until inspiration struck in 2021. He pledged to work out every day on TikTok until Taco Bell brought back the Grilled Stuft Nacho. A bit incongruous, exercising for notoriously unhealthy fast food, but that’s kind of the point. He began the challenge on Jan. 4, 2021, and has continued it every day since, nearly 500 days. Over that time, he’s lost 87 pounds (from 275 at the start to under 190) and currently has 450,000 TikTok subscribers.
A year into the challenge, a local Taco Bell made Mr. Sandberg his beloved Grilled Stuft Nacho, but since the challenge was to exercise until Taco Bell brings the item back to all its restaurants, not just for him, the great journey continues. And we admire him for it. In fact, he’s inspired us: We will write a LOTME every week until it receives a Pulitzer Prize. This is important journalism we do here. Don’t deny it!
Episode XIX: COVID strikes back
So what’s next for COVID? Is Disney going to turn it into a series? Can it support a spin-off? Did James Cameron really buy the movie rights? Can it compete against the NFL in the all-important 18-34 demographic? When are Star Wars characters going to get involved?
COVID’s motivations and negotiations are pretty much a mystery to us, but we can answer that last question. They already are involved. Well, one of them anyway.
The Chinese government has been enforcing a COVID lockdown in Shanghai for over a month now, but authorities had started letting people out of their homes for short periods of time. A recent push to bring down transmission, however, has made residents increasingly frustrated and argumentative, according to Reuters.
A now-unavailable video, which Reuters could not verify, surfaced on Chinese social media showing police in hazmat suits arguing with people who were being told that they were going to be quarantined because a neighbor had tested positive.
That’s when the Force kicks in, and this next bit comes directly from the Reuters report: “This is so that we can thoroughly remove any positive cases,” one of the officers is heard saying. “Stop asking me why, there is no why.”
There is no why? Does that remind you of someone? Someone short and green, with an odd syntax? That’s right. Clearly, Yoda it is. Yoda is alive and working for the Chinese government in Shanghai. You read it here first.
Your coffee may be guilty of sexual discrimination
How do you take your coffee? Espresso, drip, instant, or brewed from a regular old coffee machine? Well, a recent study published in Open Heart suggests that gender and brewing method can alter your coffee’s effect on cholesterol levels.
Besides caffeine, coffee beans have naturally occurring chemicals such as diterpenes, cafestol, and kahweol that raise cholesterol levels in the blood. And then there are the various brewing methods, which are going to release different amounts of chemicals from the beans. According to Consumer Reports, an ounce of espresso has 63 mg of caffeine and an ounce of regular coffee has 12-16 mg. That’s a bit deceiving, though, since no one ever drinks an ounce of regular coffee, so figure 96-128 mg of caffeine for an 8-ounce cup. That’s enough to make anyone’s heart race.
Data from 21,083 participants in the seventh survey of the Tromsø Study who were aged 40 and older showed that women drank a mean of 3.8 cups per day while men drank 4.9 cups. Drinking six or more cups of plunger-brewed coffee was associated with increased cholesterol in both genders, but drinking three to five cups of espresso was significantly associated with high cholesterol in men only. Having six or more cups of filtered coffee daily raised cholesterol in women, but instant coffee increased cholesterol levels in both genders, regardless of how many cups they drank.
People all over the planet drink coffee, some of us like our lives depend on it. Since “coffee is the most frequently consumed central stimulant worldwide,” the investigators said, “even small health effects can have considerable health consequences.”
We’ll drink to that.
Have you ever dreamed of having a clone?
When will science grace us with the ability to clone ourselves? It sounds like a dream come true. Our clones can do the stuff that we don’t want to do, like sit in on that 3-hour meeting or do our grocery shopping – really just all the boring stuff we don’t want to do.
In 1996, when a sheep named Dolly became the first mammal cloned successfully, people thought it was the start of an amazing cloning era, but, alas, we haven’t made it to cloning humans yet, as LiveScience discovered when it took a look at the subject.
The idea of cloning was quite exciting for science, as people looked forward to eradicating genetic diseases and birth defects. Research done in 1999, however, countered those hopes by suggesting that cloning might increase birth defects.
So why do you think we haven’t advanced to truly cloning humans? Ethics? Time and effort? Technological barriers? “Human cloning is a particularly dramatic action, and was one of the topics that helped launch American bioethics,” Hank Greely, professor of law and genetics at Stanford (Calif.) University, told LiveScience.
What if the clones turned evil and were bent on destroying the world?
We might imagine a clone of ourselves being completely identical to us in our thoughts, actions, and physical looks. However, that’s not necessarily true; a clone would be its own person even if it looks exactly like you.
So what do the professionals think? Is it worth giving human cloning a shot? Are there benefits? Mr. Greely said that “there are none that we should be willing to consider.”
The dream of having a clone to help your son with his math homework may have gone down the drain, but maybe it’s best not to open doors that could lead to drastic changes in our world.
Study casts doubt on safety, efficacy of L-serine supplementation for AD
When given to patients with AD, L-serine supplements could be driving abnormally increased serine levels in the brain even higher, potentially accelerating neuronal death, according to study author Xu Chen, PhD, of the University of California, San Diego, and colleagues.
This conclusion conflicts with a 2020 study by Juliette Le Douce, PhD, and colleagues, who reported that oral L-serine supplementation may act as a “ready-to-use therapy” for AD, based on their findings that patients with AD had low levels of PHGDH, an enzyme necessary for synthesizing serine, and AD-like mice had low levels of serine.
Writing in Cell Metabolism, Dr. Chen and colleagues framed the present study, and their findings, in this context.
“In contrast to the work of Le Douce et al., here we report that PHGDH mRNA and protein levels are increased in the brains of two mouse models of AD and/or tauopathy, and are also progressively increased in human brains with no, early, and late AD pathology, as well as in people with no, asymptomatic, and symptomatic AD,” they wrote.
They suggested adjusting clinical recommendations for L-serine, the form of the amino acid commonly found in supplements. In the body, L-serine is converted to D-serine, which acts on the NMDA receptor (NMDAR).
‘Long-term use of D-serine contributes to neuronal death’ suggests research
“We feel oral L-serine as a ready-to-use therapy to AD warrants precaution,” Dr. Chen and colleagues wrote. “This is because despite being a cognitive enhancer, some [research] suggests that long-term use of D-serine contributes to neuronal death in AD through excitotoxicity. Furthermore, D-serine, as a co-agonist of NMDAR, would be expected to oppose NMDAR antagonists, which have proven clinical benefits in treating AD.”
According to principal author Sheng Zhong, PhD, of the University of California, San Diego, “Research is needed to test if targeting PHGDH can ameliorate cognitive decline in AD.”
Dr. Zhong also noted that the present findings support the “promise of using a specific RNA in blood as a biomarker for early detection of Alzheimer’s disease.” This approach is currently being validated at UCSD Shiley-Marcos Alzheimer’s Disease Research Center, he added.
Roles of PHGDH and serine in Alzheimer’s disease require further study
Commenting on both studies, Steve W. Barger, PhD, of the University of Arkansas for Medical Sciences, Little Rock, suggested that more work is needed to better understand the roles of PHGDH and serine in AD before clinical applications can be considered.
“In the end, these two studies fail to provide the clarity we need in designing evidence-based therapeutic hypotheses,” Dr. Barger said in an interview. “We still do not have a firm grasp on the role that D-serine plays in AD. Indeed, the evidence regarding even a single enzyme contributing to its levels is ambiguous.”
Dr. Barger, who has published extensively on the topic of neuronal death, with a particular focus on Alzheimer’s disease, noted that “determination of what happens to D-serine levels in AD has been of interest for decades,” but levels of the amino acid have been notoriously challenging to measure because “D-serine can disappear rapidly from the brain and its fluids after death.”
While Dr. Le Douce and colleagues did measure levels of serine in mice, Dr. Barger noted that the study by Dr. Chen and colleagues was conducted with more “quantitatively rigorous methods.” Even though Dr. Chen and colleagues “did not assay the levels of D-serine itself ... the implication of their findings is that PHGDH is poised to elevate this critical neurotransmitter,” leading to their conclusion that serine supplementation is “potentially dangerous.”
At this point, it may be too early to tell, according to Dr. Barger.
He suggested that conclusions drawn from PHGDH levels alone are “always limited,” and conclusions based on serine levels may be equally dubious, considering that the activities and effects of serine “are quite complex,” and may be influenced by other physiologic processes, including the effects of gut bacteria.
Instead, Dr. Barger suggested that changes in PHGDH and serine may be interpreted as signals coming from a more relevant process upstream: glucose metabolism.
“What we can say confidently is that the glucose metabolism that PHGDH connects to D-serine is most definitely a factor in AD,” he said. “Countless studies have documented what now appears to be a universal decline in glucose delivery to the cerebral cortex, even before frank dementia sets in.”
Dr. Barger noted that declining glucose delivery coincides with some of the earliest events in the development of AD, perhaps “linking accumulation of amyloid β-peptide to subsequent neurofibrillary tangles and tissue atrophy.”
Dr. Barger’s own work recently demonstrated that AD is associated with “an irregularity in the insertion of a specific glucose transporter (GLUT1) into the cell surface” of astrocytes.
“It could be more effective to direct therapeutic interventions at these events lying upstream of PHGDH or serine,” he concluded.
The study was partly supported by a Kreuger v. Wyeth research award. The investigators and Dr. Barger reported no conflicts of interest.
When given to patients with AD, L-serine supplements could be driving abnormally increased serine levels in the brain even higher, potentially accelerating neuronal death, according to study author Xu Chen, PhD, of the University of California, San Diego, and colleagues.
This conclusion conflicts with a 2020 study by Juliette Le Douce, PhD, and colleagues, who reported that oral L-serine supplementation may act as a “ready-to-use therapy” for AD, based on their findings that patients with AD had low levels of PHGDH, an enzyme necessary for synthesizing serine, and AD-like mice had low levels of serine.
Writing in Cell Metabolism, Dr. Chen and colleagues framed the present study, and their findings, in this context.
“In contrast to the work of Le Douce et al., here we report that PHGDH mRNA and protein levels are increased in the brains of two mouse models of AD and/or tauopathy, and are also progressively increased in human brains with no, early, and late AD pathology, as well as in people with no, asymptomatic, and symptomatic AD,” they wrote.
They suggested adjusting clinical recommendations for L-serine, the form of the amino acid commonly found in supplements. In the body, L-serine is converted to D-serine, which acts on the NMDA receptor (NMDAR).
‘Long-term use of D-serine contributes to neuronal death’ suggests research
“We feel oral L-serine as a ready-to-use therapy to AD warrants precaution,” Dr. Chen and colleagues wrote. “This is because despite being a cognitive enhancer, some [research] suggests that long-term use of D-serine contributes to neuronal death in AD through excitotoxicity. Furthermore, D-serine, as a co-agonist of NMDAR, would be expected to oppose NMDAR antagonists, which have proven clinical benefits in treating AD.”
According to principal author Sheng Zhong, PhD, of the University of California, San Diego, “Research is needed to test if targeting PHGDH can ameliorate cognitive decline in AD.”
Dr. Zhong also noted that the present findings support the “promise of using a specific RNA in blood as a biomarker for early detection of Alzheimer’s disease.” This approach is currently being validated at UCSD Shiley-Marcos Alzheimer’s Disease Research Center, he added.
Roles of PHGDH and serine in Alzheimer’s disease require further study
Commenting on both studies, Steve W. Barger, PhD, of the University of Arkansas for Medical Sciences, Little Rock, suggested that more work is needed to better understand the roles of PHGDH and serine in AD before clinical applications can be considered.
“In the end, these two studies fail to provide the clarity we need in designing evidence-based therapeutic hypotheses,” Dr. Barger said in an interview. “We still do not have a firm grasp on the role that D-serine plays in AD. Indeed, the evidence regarding even a single enzyme contributing to its levels is ambiguous.”
Dr. Barger, who has published extensively on the topic of neuronal death, with a particular focus on Alzheimer’s disease, noted that “determination of what happens to D-serine levels in AD has been of interest for decades,” but levels of the amino acid have been notoriously challenging to measure because “D-serine can disappear rapidly from the brain and its fluids after death.”
While Dr. Le Douce and colleagues did measure levels of serine in mice, Dr. Barger noted that the study by Dr. Chen and colleagues was conducted with more “quantitatively rigorous methods.” Even though Dr. Chen and colleagues “did not assay the levels of D-serine itself ... the implication of their findings is that PHGDH is poised to elevate this critical neurotransmitter,” leading to their conclusion that serine supplementation is “potentially dangerous.”
At this point, it may be too early to tell, according to Dr. Barger.
He suggested that conclusions drawn from PHGDH levels alone are “always limited,” and conclusions based on serine levels may be equally dubious, considering that the activities and effects of serine “are quite complex,” and may be influenced by other physiologic processes, including the effects of gut bacteria.
Instead, Dr. Barger suggested that changes in PHGDH and serine may be interpreted as signals coming from a more relevant process upstream: glucose metabolism.
“What we can say confidently is that the glucose metabolism that PHGDH connects to D-serine is most definitely a factor in AD,” he said. “Countless studies have documented what now appears to be a universal decline in glucose delivery to the cerebral cortex, even before frank dementia sets in.”
Dr. Barger noted that declining glucose delivery coincides with some of the earliest events in the development of AD, perhaps “linking accumulation of amyloid β-peptide to subsequent neurofibrillary tangles and tissue atrophy.”
Dr. Barger’s own work recently demonstrated that AD is associated with “an irregularity in the insertion of a specific glucose transporter (GLUT1) into the cell surface” of astrocytes.
“It could be more effective to direct therapeutic interventions at these events lying upstream of PHGDH or serine,” he concluded.
The study was partly supported by a Kreuger v. Wyeth research award. The investigators and Dr. Barger reported no conflicts of interest.
When given to patients with AD, L-serine supplements could be driving abnormally increased serine levels in the brain even higher, potentially accelerating neuronal death, according to study author Xu Chen, PhD, of the University of California, San Diego, and colleagues.
This conclusion conflicts with a 2020 study by Juliette Le Douce, PhD, and colleagues, who reported that oral L-serine supplementation may act as a “ready-to-use therapy” for AD, based on their findings that patients with AD had low levels of PHGDH, an enzyme necessary for synthesizing serine, and AD-like mice had low levels of serine.
Writing in Cell Metabolism, Dr. Chen and colleagues framed the present study, and their findings, in this context.
“In contrast to the work of Le Douce et al., here we report that PHGDH mRNA and protein levels are increased in the brains of two mouse models of AD and/or tauopathy, and are also progressively increased in human brains with no, early, and late AD pathology, as well as in people with no, asymptomatic, and symptomatic AD,” they wrote.
They suggested adjusting clinical recommendations for L-serine, the form of the amino acid commonly found in supplements. In the body, L-serine is converted to D-serine, which acts on the NMDA receptor (NMDAR).
‘Long-term use of D-serine contributes to neuronal death’ suggests research
“We feel oral L-serine as a ready-to-use therapy to AD warrants precaution,” Dr. Chen and colleagues wrote. “This is because despite being a cognitive enhancer, some [research] suggests that long-term use of D-serine contributes to neuronal death in AD through excitotoxicity. Furthermore, D-serine, as a co-agonist of NMDAR, would be expected to oppose NMDAR antagonists, which have proven clinical benefits in treating AD.”
According to principal author Sheng Zhong, PhD, of the University of California, San Diego, “Research is needed to test if targeting PHGDH can ameliorate cognitive decline in AD.”
Dr. Zhong also noted that the present findings support the “promise of using a specific RNA in blood as a biomarker for early detection of Alzheimer’s disease.” This approach is currently being validated at UCSD Shiley-Marcos Alzheimer’s Disease Research Center, he added.
Roles of PHGDH and serine in Alzheimer’s disease require further study
Commenting on both studies, Steve W. Barger, PhD, of the University of Arkansas for Medical Sciences, Little Rock, suggested that more work is needed to better understand the roles of PHGDH and serine in AD before clinical applications can be considered.
“In the end, these two studies fail to provide the clarity we need in designing evidence-based therapeutic hypotheses,” Dr. Barger said in an interview. “We still do not have a firm grasp on the role that D-serine plays in AD. Indeed, the evidence regarding even a single enzyme contributing to its levels is ambiguous.”
Dr. Barger, who has published extensively on the topic of neuronal death, with a particular focus on Alzheimer’s disease, noted that “determination of what happens to D-serine levels in AD has been of interest for decades,” but levels of the amino acid have been notoriously challenging to measure because “D-serine can disappear rapidly from the brain and its fluids after death.”
While Dr. Le Douce and colleagues did measure levels of serine in mice, Dr. Barger noted that the study by Dr. Chen and colleagues was conducted with more “quantitatively rigorous methods.” Even though Dr. Chen and colleagues “did not assay the levels of D-serine itself ... the implication of their findings is that PHGDH is poised to elevate this critical neurotransmitter,” leading to their conclusion that serine supplementation is “potentially dangerous.”
At this point, it may be too early to tell, according to Dr. Barger.
He suggested that conclusions drawn from PHGDH levels alone are “always limited,” and conclusions based on serine levels may be equally dubious, considering that the activities and effects of serine “are quite complex,” and may be influenced by other physiologic processes, including the effects of gut bacteria.
Instead, Dr. Barger suggested that changes in PHGDH and serine may be interpreted as signals coming from a more relevant process upstream: glucose metabolism.
“What we can say confidently is that the glucose metabolism that PHGDH connects to D-serine is most definitely a factor in AD,” he said. “Countless studies have documented what now appears to be a universal decline in glucose delivery to the cerebral cortex, even before frank dementia sets in.”
Dr. Barger noted that declining glucose delivery coincides with some of the earliest events in the development of AD, perhaps “linking accumulation of amyloid β-peptide to subsequent neurofibrillary tangles and tissue atrophy.”
Dr. Barger’s own work recently demonstrated that AD is associated with “an irregularity in the insertion of a specific glucose transporter (GLUT1) into the cell surface” of astrocytes.
“It could be more effective to direct therapeutic interventions at these events lying upstream of PHGDH or serine,” he concluded.
The study was partly supported by a Kreuger v. Wyeth research award. The investigators and Dr. Barger reported no conflicts of interest.
FROM CELL METABOLISM
Medical education programs tell how climate change affects health
Ms. Manivannan, copresident of Emory Medical Students for Climate Action, was in the first class of Emory’s medical students to experience the birth of a refined curriculum – lobbied for and partially created by students themselves. The new course of study addresses the myriad ways climate affects health: from air pollution and its effects on the lungs and cardiovascular system to heat-related kidney disease.
“We have known that climate has affected health for decades,” Ms. Manivannan said in a recent interview. “The narrative used to be that icebergs were melting and in 2050 polar bears would be extinct. The piece that’s different now is people are linking climate to increases in asthma and various diseases. We have a way to directly communicate that it’s not a far-off thing. It’s happening to your friends and family right now.”
Hospitals, medical schools, and public health programs are stepping up to educate the next generation of doctors as well as veteran medical workers on one of the most widespread, insidious health threats of our time – climate change – and specific ways it could affect their patients.
Although climate change may seem to many Americans like a distant threat, Marilyn Howarth, MD, a pediatrician in Philadelphia, is trying to make sure physicians are better prepared to treat a growing number of health problems associated with global warming.
“There isn’t a lot of education for pediatricians and internists on environmental health issues. It has not been a standard part of education in medical school or residency training,” Dr. Howarth, deputy director of the new Philadelphia Regional Center for Children’s Environmental Health, said. “With increasing attention on our climate, we really recognize there’s a real gap in physician knowledge, both in pediatric and adult care.”
Scientists have found that climate change can alter just about every system within the human body. Studies show that more extreme weather events, such as heat waves, thunderstorms, and floods, can worsen asthma and produce more pollen and mold, triggering debilitating respiratory problems.
According to the American Lung Association, ultrafine particles of air pollution can be inhaled and then travel throughout the bloodstream, wreaking havoc on organs and increasing risk of heart attack and stroke. Various types of air pollution also cause changes to the climate by trapping heat in the atmosphere, which leads to problems such as rising sea levels and extreme weather. Plus, in a new study published in Nature, scientists warn that warming climates are forcing animals to migrate to different areas, raising the risk that new infectious diseases will hop from animals – such as bats – to humans, a process called “zoonotic spillover” that many researchers believe is responsible for the COVID-19 pandemic.
The Philadelphia Regional Center for Children’s Environmental Health
One of the latest initiatives aimed at disseminating information about children’s health to health care providers is the Philadelphia Regional Center for Children’s Environmental Health, part of Children’s Hospital of Philadelphia and Penn Medicine. CHOP and Penn Medicine are jointly funding this center’s work, which will include educating health care providers on how to better screen for climate-caused health risks and treat related conditions, such as lead poisoning and asthma.
Outreach will focus on providers who treat patients with illnesses that researchers have linked to climate change, Dr. Howarth said. The center will offer clinicians access to seminars and webinars, along with online resources to help doctors treat environmental illnesses. For example, doctors at CHOP’s Poison Control Center are developing a toolkit for physicians to treat patients with elevated levels of lead in the blood. Scientists have linked extreme weather events related to climate change to flooding that pushes metals away from river banks where they were previously contained, allowing them to more easily contaminate homes, soils, and yards.
The initiative builds on CHOP’s Community Asthma Prevention Program (CAPP), which was launched in 1997 by Tyra Bryant-Stephens, MD, its current medical director. CAPP deploys community health workers into homes armed with supplies and tips for managing asthma. The new center will use similar tactics to provide education and resources to patients. The goal is to reach as many at-risk local children as possible.
Future generation of doctors fuel growth in climate change education
Lisa Doggett, MD, cofounder and president of the board of directors of Texas Physicians for Social Responsibility, announced in March that the University of Texas at Austin, Baylor College of Medicine, Houston, and the University of Texas Southwestern in Dallas have all decided to begin offering a course on environmental threats. Emory’s new curriculum has become more comprehensive every year since its start – thanks in part to the input of students like Ms. Manivannan. Faculty members tasked her with approving the new additions to the curriculum on how climate affects health, which in 2019 had consisted of a few slides about issues such as extreme heat exposure and air pollution and their effects on childbirth outcomes.
Material on climate change has now been woven into 13 courses. It is discussed at length in relation to pulmonology, cardiology, and gastropulmonology, for example, said Rebecca Philipsborn, MD, MPA, FAAP, faculty lead for the environmental and health curriculum at Emory.
The curriculum has only been incorporated into Emory’s program for the past 2 years. Dr. Philipsborn said the school plans to expand it to the clinical years to help trainees learn to treat conditions such as pediatric asthma.
“In the past few years, there has been so much momentum, and part of that is a testament to already seeing effects of climate change and how they affect delivery of health care,” she said.
At least one medical journal has recently ramped up its efforts to educate physicians on the links between health issues and climate change. Editors of Family Practice, from Oxford University Press, have announced that they plan to publish a special Climate Crisis and Primary Health Care issue in September.
Of course, not all climate initiatives in medicine are new. A select few have existed for decades.
But only now are physicians widely seeing the links between health and environment, according to Aaron Bernstein, MD, MPH, interim director of the Center for Climate, Health, and the Global Environment (C-CHANGE) at Harvard School of Public Health, Boston.
C-CHANGE, founded in 1996, was the first center in the world to focus on the health effects of environmental change.
“It’s taken 20 years, but what we’re seeing, I think, is the fruits of education,” Dr. Bernstein said. “There’s clearly a wave building here, and I think it really started with education and people younger than the people in charge calling them into account.”
Like the Philadelphia center, Harvard’s program conducts research on climate and health and educates people from high schoolers to health care veterans. Dr. Bernstein helps lead Climate MD, a program that aims to prepare health care workers for climate crises. The Climate MD team has published several articles in peer-reviewed journals on how to better treat patients struggling with environmental health problems. For example, an article on mapping patients in hurricane zones helped shed light on how systems can identify climate-vulnerable patients using public data.
They also developed a tool to help pediatricians provide “climate-informed primary care” – guidance on how to assess whether children are at risk of any harmful environmental exposures, a feature that is not part of standard pediatric visits.
Like the other programs, Climate MD uses community outreach to treat as many local patients as possible. Staff work with providers at more than 100 health clinics, particularly in areas where climate change disproportionately affects residents.
The next major step is to bring some of this into clinical practice, Dr. Bernstein said. In February 2020, C-CHANGE held its first symposium to address that issue.
“The key is to understand climate issues from a provider’s perspective,” he said. “Then those issues can really be brought to the bedside.”
A version of this article first appeared on Medscape.com.
Ms. Manivannan, copresident of Emory Medical Students for Climate Action, was in the first class of Emory’s medical students to experience the birth of a refined curriculum – lobbied for and partially created by students themselves. The new course of study addresses the myriad ways climate affects health: from air pollution and its effects on the lungs and cardiovascular system to heat-related kidney disease.
“We have known that climate has affected health for decades,” Ms. Manivannan said in a recent interview. “The narrative used to be that icebergs were melting and in 2050 polar bears would be extinct. The piece that’s different now is people are linking climate to increases in asthma and various diseases. We have a way to directly communicate that it’s not a far-off thing. It’s happening to your friends and family right now.”
Hospitals, medical schools, and public health programs are stepping up to educate the next generation of doctors as well as veteran medical workers on one of the most widespread, insidious health threats of our time – climate change – and specific ways it could affect their patients.
Although climate change may seem to many Americans like a distant threat, Marilyn Howarth, MD, a pediatrician in Philadelphia, is trying to make sure physicians are better prepared to treat a growing number of health problems associated with global warming.
“There isn’t a lot of education for pediatricians and internists on environmental health issues. It has not been a standard part of education in medical school or residency training,” Dr. Howarth, deputy director of the new Philadelphia Regional Center for Children’s Environmental Health, said. “With increasing attention on our climate, we really recognize there’s a real gap in physician knowledge, both in pediatric and adult care.”
Scientists have found that climate change can alter just about every system within the human body. Studies show that more extreme weather events, such as heat waves, thunderstorms, and floods, can worsen asthma and produce more pollen and mold, triggering debilitating respiratory problems.
According to the American Lung Association, ultrafine particles of air pollution can be inhaled and then travel throughout the bloodstream, wreaking havoc on organs and increasing risk of heart attack and stroke. Various types of air pollution also cause changes to the climate by trapping heat in the atmosphere, which leads to problems such as rising sea levels and extreme weather. Plus, in a new study published in Nature, scientists warn that warming climates are forcing animals to migrate to different areas, raising the risk that new infectious diseases will hop from animals – such as bats – to humans, a process called “zoonotic spillover” that many researchers believe is responsible for the COVID-19 pandemic.
The Philadelphia Regional Center for Children’s Environmental Health
One of the latest initiatives aimed at disseminating information about children’s health to health care providers is the Philadelphia Regional Center for Children’s Environmental Health, part of Children’s Hospital of Philadelphia and Penn Medicine. CHOP and Penn Medicine are jointly funding this center’s work, which will include educating health care providers on how to better screen for climate-caused health risks and treat related conditions, such as lead poisoning and asthma.
Outreach will focus on providers who treat patients with illnesses that researchers have linked to climate change, Dr. Howarth said. The center will offer clinicians access to seminars and webinars, along with online resources to help doctors treat environmental illnesses. For example, doctors at CHOP’s Poison Control Center are developing a toolkit for physicians to treat patients with elevated levels of lead in the blood. Scientists have linked extreme weather events related to climate change to flooding that pushes metals away from river banks where they were previously contained, allowing them to more easily contaminate homes, soils, and yards.
The initiative builds on CHOP’s Community Asthma Prevention Program (CAPP), which was launched in 1997 by Tyra Bryant-Stephens, MD, its current medical director. CAPP deploys community health workers into homes armed with supplies and tips for managing asthma. The new center will use similar tactics to provide education and resources to patients. The goal is to reach as many at-risk local children as possible.
Future generation of doctors fuel growth in climate change education
Lisa Doggett, MD, cofounder and president of the board of directors of Texas Physicians for Social Responsibility, announced in March that the University of Texas at Austin, Baylor College of Medicine, Houston, and the University of Texas Southwestern in Dallas have all decided to begin offering a course on environmental threats. Emory’s new curriculum has become more comprehensive every year since its start – thanks in part to the input of students like Ms. Manivannan. Faculty members tasked her with approving the new additions to the curriculum on how climate affects health, which in 2019 had consisted of a few slides about issues such as extreme heat exposure and air pollution and their effects on childbirth outcomes.
Material on climate change has now been woven into 13 courses. It is discussed at length in relation to pulmonology, cardiology, and gastropulmonology, for example, said Rebecca Philipsborn, MD, MPA, FAAP, faculty lead for the environmental and health curriculum at Emory.
The curriculum has only been incorporated into Emory’s program for the past 2 years. Dr. Philipsborn said the school plans to expand it to the clinical years to help trainees learn to treat conditions such as pediatric asthma.
“In the past few years, there has been so much momentum, and part of that is a testament to already seeing effects of climate change and how they affect delivery of health care,” she said.
At least one medical journal has recently ramped up its efforts to educate physicians on the links between health issues and climate change. Editors of Family Practice, from Oxford University Press, have announced that they plan to publish a special Climate Crisis and Primary Health Care issue in September.
Of course, not all climate initiatives in medicine are new. A select few have existed for decades.
But only now are physicians widely seeing the links between health and environment, according to Aaron Bernstein, MD, MPH, interim director of the Center for Climate, Health, and the Global Environment (C-CHANGE) at Harvard School of Public Health, Boston.
C-CHANGE, founded in 1996, was the first center in the world to focus on the health effects of environmental change.
“It’s taken 20 years, but what we’re seeing, I think, is the fruits of education,” Dr. Bernstein said. “There’s clearly a wave building here, and I think it really started with education and people younger than the people in charge calling them into account.”
Like the Philadelphia center, Harvard’s program conducts research on climate and health and educates people from high schoolers to health care veterans. Dr. Bernstein helps lead Climate MD, a program that aims to prepare health care workers for climate crises. The Climate MD team has published several articles in peer-reviewed journals on how to better treat patients struggling with environmental health problems. For example, an article on mapping patients in hurricane zones helped shed light on how systems can identify climate-vulnerable patients using public data.
They also developed a tool to help pediatricians provide “climate-informed primary care” – guidance on how to assess whether children are at risk of any harmful environmental exposures, a feature that is not part of standard pediatric visits.
Like the other programs, Climate MD uses community outreach to treat as many local patients as possible. Staff work with providers at more than 100 health clinics, particularly in areas where climate change disproportionately affects residents.
The next major step is to bring some of this into clinical practice, Dr. Bernstein said. In February 2020, C-CHANGE held its first symposium to address that issue.
“The key is to understand climate issues from a provider’s perspective,” he said. “Then those issues can really be brought to the bedside.”
A version of this article first appeared on Medscape.com.
Ms. Manivannan, copresident of Emory Medical Students for Climate Action, was in the first class of Emory’s medical students to experience the birth of a refined curriculum – lobbied for and partially created by students themselves. The new course of study addresses the myriad ways climate affects health: from air pollution and its effects on the lungs and cardiovascular system to heat-related kidney disease.
“We have known that climate has affected health for decades,” Ms. Manivannan said in a recent interview. “The narrative used to be that icebergs were melting and in 2050 polar bears would be extinct. The piece that’s different now is people are linking climate to increases in asthma and various diseases. We have a way to directly communicate that it’s not a far-off thing. It’s happening to your friends and family right now.”
Hospitals, medical schools, and public health programs are stepping up to educate the next generation of doctors as well as veteran medical workers on one of the most widespread, insidious health threats of our time – climate change – and specific ways it could affect their patients.
Although climate change may seem to many Americans like a distant threat, Marilyn Howarth, MD, a pediatrician in Philadelphia, is trying to make sure physicians are better prepared to treat a growing number of health problems associated with global warming.
“There isn’t a lot of education for pediatricians and internists on environmental health issues. It has not been a standard part of education in medical school or residency training,” Dr. Howarth, deputy director of the new Philadelphia Regional Center for Children’s Environmental Health, said. “With increasing attention on our climate, we really recognize there’s a real gap in physician knowledge, both in pediatric and adult care.”
Scientists have found that climate change can alter just about every system within the human body. Studies show that more extreme weather events, such as heat waves, thunderstorms, and floods, can worsen asthma and produce more pollen and mold, triggering debilitating respiratory problems.
According to the American Lung Association, ultrafine particles of air pollution can be inhaled and then travel throughout the bloodstream, wreaking havoc on organs and increasing risk of heart attack and stroke. Various types of air pollution also cause changes to the climate by trapping heat in the atmosphere, which leads to problems such as rising sea levels and extreme weather. Plus, in a new study published in Nature, scientists warn that warming climates are forcing animals to migrate to different areas, raising the risk that new infectious diseases will hop from animals – such as bats – to humans, a process called “zoonotic spillover” that many researchers believe is responsible for the COVID-19 pandemic.
The Philadelphia Regional Center for Children’s Environmental Health
One of the latest initiatives aimed at disseminating information about children’s health to health care providers is the Philadelphia Regional Center for Children’s Environmental Health, part of Children’s Hospital of Philadelphia and Penn Medicine. CHOP and Penn Medicine are jointly funding this center’s work, which will include educating health care providers on how to better screen for climate-caused health risks and treat related conditions, such as lead poisoning and asthma.
Outreach will focus on providers who treat patients with illnesses that researchers have linked to climate change, Dr. Howarth said. The center will offer clinicians access to seminars and webinars, along with online resources to help doctors treat environmental illnesses. For example, doctors at CHOP’s Poison Control Center are developing a toolkit for physicians to treat patients with elevated levels of lead in the blood. Scientists have linked extreme weather events related to climate change to flooding that pushes metals away from river banks where they were previously contained, allowing them to more easily contaminate homes, soils, and yards.
The initiative builds on CHOP’s Community Asthma Prevention Program (CAPP), which was launched in 1997 by Tyra Bryant-Stephens, MD, its current medical director. CAPP deploys community health workers into homes armed with supplies and tips for managing asthma. The new center will use similar tactics to provide education and resources to patients. The goal is to reach as many at-risk local children as possible.
Future generation of doctors fuel growth in climate change education
Lisa Doggett, MD, cofounder and president of the board of directors of Texas Physicians for Social Responsibility, announced in March that the University of Texas at Austin, Baylor College of Medicine, Houston, and the University of Texas Southwestern in Dallas have all decided to begin offering a course on environmental threats. Emory’s new curriculum has become more comprehensive every year since its start – thanks in part to the input of students like Ms. Manivannan. Faculty members tasked her with approving the new additions to the curriculum on how climate affects health, which in 2019 had consisted of a few slides about issues such as extreme heat exposure and air pollution and their effects on childbirth outcomes.
Material on climate change has now been woven into 13 courses. It is discussed at length in relation to pulmonology, cardiology, and gastropulmonology, for example, said Rebecca Philipsborn, MD, MPA, FAAP, faculty lead for the environmental and health curriculum at Emory.
The curriculum has only been incorporated into Emory’s program for the past 2 years. Dr. Philipsborn said the school plans to expand it to the clinical years to help trainees learn to treat conditions such as pediatric asthma.
“In the past few years, there has been so much momentum, and part of that is a testament to already seeing effects of climate change and how they affect delivery of health care,” she said.
At least one medical journal has recently ramped up its efforts to educate physicians on the links between health issues and climate change. Editors of Family Practice, from Oxford University Press, have announced that they plan to publish a special Climate Crisis and Primary Health Care issue in September.
Of course, not all climate initiatives in medicine are new. A select few have existed for decades.
But only now are physicians widely seeing the links between health and environment, according to Aaron Bernstein, MD, MPH, interim director of the Center for Climate, Health, and the Global Environment (C-CHANGE) at Harvard School of Public Health, Boston.
C-CHANGE, founded in 1996, was the first center in the world to focus on the health effects of environmental change.
“It’s taken 20 years, but what we’re seeing, I think, is the fruits of education,” Dr. Bernstein said. “There’s clearly a wave building here, and I think it really started with education and people younger than the people in charge calling them into account.”
Like the Philadelphia center, Harvard’s program conducts research on climate and health and educates people from high schoolers to health care veterans. Dr. Bernstein helps lead Climate MD, a program that aims to prepare health care workers for climate crises. The Climate MD team has published several articles in peer-reviewed journals on how to better treat patients struggling with environmental health problems. For example, an article on mapping patients in hurricane zones helped shed light on how systems can identify climate-vulnerable patients using public data.
They also developed a tool to help pediatricians provide “climate-informed primary care” – guidance on how to assess whether children are at risk of any harmful environmental exposures, a feature that is not part of standard pediatric visits.
Like the other programs, Climate MD uses community outreach to treat as many local patients as possible. Staff work with providers at more than 100 health clinics, particularly in areas where climate change disproportionately affects residents.
The next major step is to bring some of this into clinical practice, Dr. Bernstein said. In February 2020, C-CHANGE held its first symposium to address that issue.
“The key is to understand climate issues from a provider’s perspective,” he said. “Then those issues can really be brought to the bedside.”
A version of this article first appeared on Medscape.com.
Can sensitivity to common smells sniff out depression, anxiety?
Sensitivity to specific common odors correlates with symptoms of depression or anxiety, new research shows.
A study of more than 400 participants showed that symptoms of anxiety were associated with heightened awareness of floral scents or kitchen smells, while depression was linked to increased awareness of social odors including “good” and “bad” smells of other people.
“The assessment of meta-cognitive abilities may be a useful tool in assessing depressive, anxiety, and social anxiety symptoms,” study investigator Cinzia Cecchetto, PhD student, postdoctoral researcher, department of general psychology, University of Padua, Italy, told this news organization.
The findings were published online in the Journal of Affective Disorders.
Smell perception
Previous studies have shown a strong relationship between reduced odor detection and symptoms of depression, with less clear evidence of a link between olfactory perception and symptoms of anxiety, Dr. Cecchetto said.
However, few studies have investigated to what extent individuals with symptoms of anxiety or depression are aware of, or pay attention to, odors in their environment, she added.
The study included 429 healthy participants (76.9% women, aged 18-45 years) recruited through social media. The age cut-off was 45 because evidence shows that olfactory perceptions start to decline at that time of life, Dr. Cecchetto noted.
Participants completed psychological questionnaires, including the Beck Depression Inventory-II, the Beck Anxiety Inventory, and the Liebowitz Social Anxiety Scale.
They also completed olfactory questionnaires, including the Odor Awareness Scale for evaluating the degree to which an individual focuses on olfactory stimuli such as that from food; the Affective Impact of Odor scale for assessing how odors affect liking and memory for people, places, and things; the Vividness of Olfactory Imagery Questionnaire, which examines ability to form olfactory images such as fragrances from a garden; and the Social Odor Scale, which assesses awareness of social odors such as sweat in everyday interactions.
Results showed that general anxiety symptoms were a significant predictor of higher levels of awareness of common odors.
The investigators note that this finding is similar to that from previous research in which patients with panic disorder reported higher olfactory sensitivity, reactivity, and awareness of odors compared with a control group. It is also in line with clinical features of anxiety, in which individuals maintain heightened vigilance, hyperarousal, and action readiness to respond to sudden danger.
Individuals with social anxiety symptoms reported being less attentive toward social odors.
This finding is at odds with the tendency of individuals with social anxiety to continuously monitor the environment for signs of potential negative evaluations by others.
In addition, it contradicts findings from previous studies showing that social anxiety is associated with enhanced startle reactivity and faster processing of social odor anxiety signals, compared with healthy controls, the investigators note.
Clinical implications?
“A possible explanation for these conflicting findings could be that in our study we didn’t present real odors to participants, but asked them if they usually pay attention to these odors,” lead author Elisa Dal Bò, PhD student, Padova Neuroscience Center and department of general psychology, University of Padua, told this news organization.
“Indeed, other studies have shown individuals with social anxiety focus their attention more on themselves and avoid paying attention to other people during social interactions,” she added.
Depressive symptoms were a significant predictor of higher social odor awareness and lower affective responses to odors. Some past studies showed that “depression is characterized by an increased attention to social stimuli induced by the fear of social rejection,” Ms. Dal Bò noted.
The current findings showing that depression symptoms were associated with higher social odor awareness while social anxiety symptoms were associated with lower social odor awareness are at odds with what was hypothesized, Dr. Cecchetto said.
“Actually we were expecting the opposite pattern, and that’s why it’s important to investigate more deeply these meta-cognitive abilities,” she said.
Neither depressive nor anxiety symptoms were significant predictors of olfactory imagery.
Female respondents were more attentive to, and aware of, odors than men. This finding is “quite common in the literature,” Dr. Cecchetto noted.
Although preliminary, the results could eventually have clinical implications, the investigators note. Olfactory metacognitive abilities, obtained through questionnaires, could be used to assess potential olfactory impairment, which could signal future risk for psychiatric symptoms.
However, the relatively young age of participants in the study and the prevalence of women limits the generalization of the findings, the researchers note. In addition, clinical symptoms were self-reported and were not verified by health care professionals.
‘Not enough evidence’
Commenting for this news organization, Philip R. Muskin, MD, professor of clinical psychiatry, Columbia University Medical Center, New York, said he did not find the results surprising.
For example, that individuals with social anxiety are not particularly aware of others’ smell “makes perfect sense” because “people with social anxiety disorder are concerned with themselves,” he said.
Dr. Muskin, who has an interest in and has written about olfactory function, was not involved with the research.
He noted several study limitations. First, participants just reported on their smell awareness, but “having people actually smell stuff might have been more interesting.”
In addition, the study population was relatively young, mostly women, and women’s olfactory sensitivity changes throughout the menstrual cycle, Dr. Muskin said.
“We don’t know where these women are in their cycles when they’re reporting their awareness of odors,” he said. “It would be good to know if the women were all in the luteal phase or were premenstrual because that might correlate with their anxiety or depressive symptoms.”
Asking a patient about smell awareness may provide some insight when assessing for symptoms of depression, along with obtaining details on such things as sleep, Dr. Muskin noted.
However, he does not think the new findings are enough to include olfactory awareness in the interview process. “It’s not enough evidence to use as a clinical tool for diagnosis, and I don’t see this is clinically useful yet.”
The study was supported by the European Commission Horizon 2020 research and innovation program and the Austrian Science Fund. The investigators and Dr. Muskin have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Sensitivity to specific common odors correlates with symptoms of depression or anxiety, new research shows.
A study of more than 400 participants showed that symptoms of anxiety were associated with heightened awareness of floral scents or kitchen smells, while depression was linked to increased awareness of social odors including “good” and “bad” smells of other people.
“The assessment of meta-cognitive abilities may be a useful tool in assessing depressive, anxiety, and social anxiety symptoms,” study investigator Cinzia Cecchetto, PhD student, postdoctoral researcher, department of general psychology, University of Padua, Italy, told this news organization.
The findings were published online in the Journal of Affective Disorders.
Smell perception
Previous studies have shown a strong relationship between reduced odor detection and symptoms of depression, with less clear evidence of a link between olfactory perception and symptoms of anxiety, Dr. Cecchetto said.
However, few studies have investigated to what extent individuals with symptoms of anxiety or depression are aware of, or pay attention to, odors in their environment, she added.
The study included 429 healthy participants (76.9% women, aged 18-45 years) recruited through social media. The age cut-off was 45 because evidence shows that olfactory perceptions start to decline at that time of life, Dr. Cecchetto noted.
Participants completed psychological questionnaires, including the Beck Depression Inventory-II, the Beck Anxiety Inventory, and the Liebowitz Social Anxiety Scale.
They also completed olfactory questionnaires, including the Odor Awareness Scale for evaluating the degree to which an individual focuses on olfactory stimuli such as that from food; the Affective Impact of Odor scale for assessing how odors affect liking and memory for people, places, and things; the Vividness of Olfactory Imagery Questionnaire, which examines ability to form olfactory images such as fragrances from a garden; and the Social Odor Scale, which assesses awareness of social odors such as sweat in everyday interactions.
Results showed that general anxiety symptoms were a significant predictor of higher levels of awareness of common odors.
The investigators note that this finding is similar to that from previous research in which patients with panic disorder reported higher olfactory sensitivity, reactivity, and awareness of odors compared with a control group. It is also in line with clinical features of anxiety, in which individuals maintain heightened vigilance, hyperarousal, and action readiness to respond to sudden danger.
Individuals with social anxiety symptoms reported being less attentive toward social odors.
This finding is at odds with the tendency of individuals with social anxiety to continuously monitor the environment for signs of potential negative evaluations by others.
In addition, it contradicts findings from previous studies showing that social anxiety is associated with enhanced startle reactivity and faster processing of social odor anxiety signals, compared with healthy controls, the investigators note.
Clinical implications?
“A possible explanation for these conflicting findings could be that in our study we didn’t present real odors to participants, but asked them if they usually pay attention to these odors,” lead author Elisa Dal Bò, PhD student, Padova Neuroscience Center and department of general psychology, University of Padua, told this news organization.
“Indeed, other studies have shown individuals with social anxiety focus their attention more on themselves and avoid paying attention to other people during social interactions,” she added.
Depressive symptoms were a significant predictor of higher social odor awareness and lower affective responses to odors. Some past studies showed that “depression is characterized by an increased attention to social stimuli induced by the fear of social rejection,” Ms. Dal Bò noted.
The current findings showing that depression symptoms were associated with higher social odor awareness while social anxiety symptoms were associated with lower social odor awareness are at odds with what was hypothesized, Dr. Cecchetto said.
“Actually we were expecting the opposite pattern, and that’s why it’s important to investigate more deeply these meta-cognitive abilities,” she said.
Neither depressive nor anxiety symptoms were significant predictors of olfactory imagery.
Female respondents were more attentive to, and aware of, odors than men. This finding is “quite common in the literature,” Dr. Cecchetto noted.
Although preliminary, the results could eventually have clinical implications, the investigators note. Olfactory metacognitive abilities, obtained through questionnaires, could be used to assess potential olfactory impairment, which could signal future risk for psychiatric symptoms.
However, the relatively young age of participants in the study and the prevalence of women limits the generalization of the findings, the researchers note. In addition, clinical symptoms were self-reported and were not verified by health care professionals.
‘Not enough evidence’
Commenting for this news organization, Philip R. Muskin, MD, professor of clinical psychiatry, Columbia University Medical Center, New York, said he did not find the results surprising.
For example, that individuals with social anxiety are not particularly aware of others’ smell “makes perfect sense” because “people with social anxiety disorder are concerned with themselves,” he said.
Dr. Muskin, who has an interest in and has written about olfactory function, was not involved with the research.
He noted several study limitations. First, participants just reported on their smell awareness, but “having people actually smell stuff might have been more interesting.”
In addition, the study population was relatively young, mostly women, and women’s olfactory sensitivity changes throughout the menstrual cycle, Dr. Muskin said.
“We don’t know where these women are in their cycles when they’re reporting their awareness of odors,” he said. “It would be good to know if the women were all in the luteal phase or were premenstrual because that might correlate with their anxiety or depressive symptoms.”
Asking a patient about smell awareness may provide some insight when assessing for symptoms of depression, along with obtaining details on such things as sleep, Dr. Muskin noted.
However, he does not think the new findings are enough to include olfactory awareness in the interview process. “It’s not enough evidence to use as a clinical tool for diagnosis, and I don’t see this is clinically useful yet.”
The study was supported by the European Commission Horizon 2020 research and innovation program and the Austrian Science Fund. The investigators and Dr. Muskin have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Sensitivity to specific common odors correlates with symptoms of depression or anxiety, new research shows.
A study of more than 400 participants showed that symptoms of anxiety were associated with heightened awareness of floral scents or kitchen smells, while depression was linked to increased awareness of social odors including “good” and “bad” smells of other people.
“The assessment of meta-cognitive abilities may be a useful tool in assessing depressive, anxiety, and social anxiety symptoms,” study investigator Cinzia Cecchetto, PhD student, postdoctoral researcher, department of general psychology, University of Padua, Italy, told this news organization.
The findings were published online in the Journal of Affective Disorders.
Smell perception
Previous studies have shown a strong relationship between reduced odor detection and symptoms of depression, with less clear evidence of a link between olfactory perception and symptoms of anxiety, Dr. Cecchetto said.
However, few studies have investigated to what extent individuals with symptoms of anxiety or depression are aware of, or pay attention to, odors in their environment, she added.
The study included 429 healthy participants (76.9% women, aged 18-45 years) recruited through social media. The age cut-off was 45 because evidence shows that olfactory perceptions start to decline at that time of life, Dr. Cecchetto noted.
Participants completed psychological questionnaires, including the Beck Depression Inventory-II, the Beck Anxiety Inventory, and the Liebowitz Social Anxiety Scale.
They also completed olfactory questionnaires, including the Odor Awareness Scale for evaluating the degree to which an individual focuses on olfactory stimuli such as that from food; the Affective Impact of Odor scale for assessing how odors affect liking and memory for people, places, and things; the Vividness of Olfactory Imagery Questionnaire, which examines ability to form olfactory images such as fragrances from a garden; and the Social Odor Scale, which assesses awareness of social odors such as sweat in everyday interactions.
Results showed that general anxiety symptoms were a significant predictor of higher levels of awareness of common odors.
The investigators note that this finding is similar to that from previous research in which patients with panic disorder reported higher olfactory sensitivity, reactivity, and awareness of odors compared with a control group. It is also in line with clinical features of anxiety, in which individuals maintain heightened vigilance, hyperarousal, and action readiness to respond to sudden danger.
Individuals with social anxiety symptoms reported being less attentive toward social odors.
This finding is at odds with the tendency of individuals with social anxiety to continuously monitor the environment for signs of potential negative evaluations by others.
In addition, it contradicts findings from previous studies showing that social anxiety is associated with enhanced startle reactivity and faster processing of social odor anxiety signals, compared with healthy controls, the investigators note.
Clinical implications?
“A possible explanation for these conflicting findings could be that in our study we didn’t present real odors to participants, but asked them if they usually pay attention to these odors,” lead author Elisa Dal Bò, PhD student, Padova Neuroscience Center and department of general psychology, University of Padua, told this news organization.
“Indeed, other studies have shown individuals with social anxiety focus their attention more on themselves and avoid paying attention to other people during social interactions,” she added.
Depressive symptoms were a significant predictor of higher social odor awareness and lower affective responses to odors. Some past studies showed that “depression is characterized by an increased attention to social stimuli induced by the fear of social rejection,” Ms. Dal Bò noted.
The current findings showing that depression symptoms were associated with higher social odor awareness while social anxiety symptoms were associated with lower social odor awareness are at odds with what was hypothesized, Dr. Cecchetto said.
“Actually we were expecting the opposite pattern, and that’s why it’s important to investigate more deeply these meta-cognitive abilities,” she said.
Neither depressive nor anxiety symptoms were significant predictors of olfactory imagery.
Female respondents were more attentive to, and aware of, odors than men. This finding is “quite common in the literature,” Dr. Cecchetto noted.
Although preliminary, the results could eventually have clinical implications, the investigators note. Olfactory metacognitive abilities, obtained through questionnaires, could be used to assess potential olfactory impairment, which could signal future risk for psychiatric symptoms.
However, the relatively young age of participants in the study and the prevalence of women limits the generalization of the findings, the researchers note. In addition, clinical symptoms were self-reported and were not verified by health care professionals.
‘Not enough evidence’
Commenting for this news organization, Philip R. Muskin, MD, professor of clinical psychiatry, Columbia University Medical Center, New York, said he did not find the results surprising.
For example, that individuals with social anxiety are not particularly aware of others’ smell “makes perfect sense” because “people with social anxiety disorder are concerned with themselves,” he said.
Dr. Muskin, who has an interest in and has written about olfactory function, was not involved with the research.
He noted several study limitations. First, participants just reported on their smell awareness, but “having people actually smell stuff might have been more interesting.”
In addition, the study population was relatively young, mostly women, and women’s olfactory sensitivity changes throughout the menstrual cycle, Dr. Muskin said.
“We don’t know where these women are in their cycles when they’re reporting their awareness of odors,” he said. “It would be good to know if the women were all in the luteal phase or were premenstrual because that might correlate with their anxiety or depressive symptoms.”
Asking a patient about smell awareness may provide some insight when assessing for symptoms of depression, along with obtaining details on such things as sleep, Dr. Muskin noted.
However, he does not think the new findings are enough to include olfactory awareness in the interview process. “It’s not enough evidence to use as a clinical tool for diagnosis, and I don’t see this is clinically useful yet.”
The study was supported by the European Commission Horizon 2020 research and innovation program and the Austrian Science Fund. The investigators and Dr. Muskin have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
When coping skills and parenting behavioral interventions ‘don’t work’
You have an appointment with a 14-year-old youth you last saw for an annual camp physical. He had screened positive for depression, and you had referred him to a local therapist. He did not have an appointment until after camp, and you have only met a few times, but since you had spoken with him about his depression, he set up an appointment with you to ask about medications. When you meet him you ask about what he had been doing in therapy and he says, “I’m learning ‘coping skills,’ but they don’t work.”
From breathing exercises and sticker charts to mindfulness and grounding exercise, coping skills can be crucial for learning how to manage distress, regulate emotions, become more effective interpersonally, and function better. Similarly, parenting interventions, which change the way parents and youth interact, are a central family intervention for behavioral problems in youth.
It is very common, however, to hear that they “don’t work” or have a parent say, “We tried that, it doesn’t work.”
When kids and parents reject coping skills and behavioral interventions by saying they do not work, the consequences can be substantial. It can mean the rejection of coping skills and strategies that actually would have helped, given time and support; that kids and families bounce between services with increasing frustration; that they search for a magic bullet (which also won’t work); and, particularly concerning for physicians, a belief that the youth have not received the right medication, resulting in potentially unhelpful concoctions of medication.
One of the biggest challenges in helping youth and parents overcome their difficulties – whether these difficulties are depression and anxiety or being better parents to struggling kids – is helping them understand that despite the fact that coping skills and behavioral interventions do not seem to work, they work.
We just have to do a better job explaining what that “work” is.
There are five points you can make.
- First, the coping skill or behavioral intervention is not supposed to work if that means solving the underlying problem. Coping skills and behavioral interventions do not immediately cure anxiety, mend broken hearts, correct disruptive behaviors, disentangle power struggles, or alleviate depression. That is not what their job is. Coping skills and behavioral interventions are there to help us get better at handling complex situations and feelings. In particular, they are good at helping us manage our thoughts (“I can’t do it,” “He should behave better”) and our affect (anger, frustration, rage, anxiety, sadness), so that over time we get better at solving the problems, and break out of the patterns that perpetuate these problems.
- Second, kids and parents do not give skills credit for when they do work. That time you were spiraling out of control and told your mom you needed a break and watched some YouTube videos and then joined the family for dinner? Your coping skills worked, but nobody noticed because they worked. We need to help our young patients and families identify those times that coping skills and behavioral interventions worked.
- Third, let’s face it: Nothing works all the time. It is no wonder kids and families are disappointed by coping skills and behavioral interventions if they think they magically work once and forever. We need to manage expectations.
- Fourth, we know they are supposed to fail, and we should discuss this openly up front. This may sound surprising, but challenging behaviors often get worse when we begin to work on them. “Extinction bursts” is probably the easiest explanation, but for psychodynamically oriented youth and families we could talk about “resistance.” No matter what, things tend to get worse before they get better. We should let people know this ahead of time.
- Fifth, and this is the one that forces youth and parents to ask how hard they actually tried, these skills need to be practiced. You can’t be in the middle of a panic attack and for the first time start trying to pace your breathing with a technique a therapist told you about 3 weeks ago. This makes about as much sense as not training for a marathon. You need to practice and build up the skills, recognizing that as you become more familiar with them, they will help you manage during stressful situations. Every skill should be practiced, preferably several times or more in sessions, maybe every session, and definitely outside of sessions when not in distress.
We cannot blame children and parents for thinking that coping skills and behavioral interventions do not work. They are struggling, suffering, fighting, frightened, angry, anxious, frustrated, and often desperate for something to make everything better. Helping them recognize this desire for things to be better while managing expectations is an essential complement to supporting the use of coping skills and behavioral interventions, and a fairly easy conversation to have with youth.
So when you are talking about coping skills and parental behavioral interventions, it is important to be prepared for the “it didn’t work” conversation, and even to address these issues up front. After all, these strategies may not solve all the problems in the world, but can be lifelong ways of coping with life’s challenges.
Dr. Henderson is associate professor of clinical psychiatry at New York University and deputy director of child and adolescent psychiatry at Bellevue Hospital, New York.
You have an appointment with a 14-year-old youth you last saw for an annual camp physical. He had screened positive for depression, and you had referred him to a local therapist. He did not have an appointment until after camp, and you have only met a few times, but since you had spoken with him about his depression, he set up an appointment with you to ask about medications. When you meet him you ask about what he had been doing in therapy and he says, “I’m learning ‘coping skills,’ but they don’t work.”
From breathing exercises and sticker charts to mindfulness and grounding exercise, coping skills can be crucial for learning how to manage distress, regulate emotions, become more effective interpersonally, and function better. Similarly, parenting interventions, which change the way parents and youth interact, are a central family intervention for behavioral problems in youth.
It is very common, however, to hear that they “don’t work” or have a parent say, “We tried that, it doesn’t work.”
When kids and parents reject coping skills and behavioral interventions by saying they do not work, the consequences can be substantial. It can mean the rejection of coping skills and strategies that actually would have helped, given time and support; that kids and families bounce between services with increasing frustration; that they search for a magic bullet (which also won’t work); and, particularly concerning for physicians, a belief that the youth have not received the right medication, resulting in potentially unhelpful concoctions of medication.
One of the biggest challenges in helping youth and parents overcome their difficulties – whether these difficulties are depression and anxiety or being better parents to struggling kids – is helping them understand that despite the fact that coping skills and behavioral interventions do not seem to work, they work.
We just have to do a better job explaining what that “work” is.
There are five points you can make.
- First, the coping skill or behavioral intervention is not supposed to work if that means solving the underlying problem. Coping skills and behavioral interventions do not immediately cure anxiety, mend broken hearts, correct disruptive behaviors, disentangle power struggles, or alleviate depression. That is not what their job is. Coping skills and behavioral interventions are there to help us get better at handling complex situations and feelings. In particular, they are good at helping us manage our thoughts (“I can’t do it,” “He should behave better”) and our affect (anger, frustration, rage, anxiety, sadness), so that over time we get better at solving the problems, and break out of the patterns that perpetuate these problems.
- Second, kids and parents do not give skills credit for when they do work. That time you were spiraling out of control and told your mom you needed a break and watched some YouTube videos and then joined the family for dinner? Your coping skills worked, but nobody noticed because they worked. We need to help our young patients and families identify those times that coping skills and behavioral interventions worked.
- Third, let’s face it: Nothing works all the time. It is no wonder kids and families are disappointed by coping skills and behavioral interventions if they think they magically work once and forever. We need to manage expectations.
- Fourth, we know they are supposed to fail, and we should discuss this openly up front. This may sound surprising, but challenging behaviors often get worse when we begin to work on them. “Extinction bursts” is probably the easiest explanation, but for psychodynamically oriented youth and families we could talk about “resistance.” No matter what, things tend to get worse before they get better. We should let people know this ahead of time.
- Fifth, and this is the one that forces youth and parents to ask how hard they actually tried, these skills need to be practiced. You can’t be in the middle of a panic attack and for the first time start trying to pace your breathing with a technique a therapist told you about 3 weeks ago. This makes about as much sense as not training for a marathon. You need to practice and build up the skills, recognizing that as you become more familiar with them, they will help you manage during stressful situations. Every skill should be practiced, preferably several times or more in sessions, maybe every session, and definitely outside of sessions when not in distress.
We cannot blame children and parents for thinking that coping skills and behavioral interventions do not work. They are struggling, suffering, fighting, frightened, angry, anxious, frustrated, and often desperate for something to make everything better. Helping them recognize this desire for things to be better while managing expectations is an essential complement to supporting the use of coping skills and behavioral interventions, and a fairly easy conversation to have with youth.
So when you are talking about coping skills and parental behavioral interventions, it is important to be prepared for the “it didn’t work” conversation, and even to address these issues up front. After all, these strategies may not solve all the problems in the world, but can be lifelong ways of coping with life’s challenges.
Dr. Henderson is associate professor of clinical psychiatry at New York University and deputy director of child and adolescent psychiatry at Bellevue Hospital, New York.
You have an appointment with a 14-year-old youth you last saw for an annual camp physical. He had screened positive for depression, and you had referred him to a local therapist. He did not have an appointment until after camp, and you have only met a few times, but since you had spoken with him about his depression, he set up an appointment with you to ask about medications. When you meet him you ask about what he had been doing in therapy and he says, “I’m learning ‘coping skills,’ but they don’t work.”
From breathing exercises and sticker charts to mindfulness and grounding exercise, coping skills can be crucial for learning how to manage distress, regulate emotions, become more effective interpersonally, and function better. Similarly, parenting interventions, which change the way parents and youth interact, are a central family intervention for behavioral problems in youth.
It is very common, however, to hear that they “don’t work” or have a parent say, “We tried that, it doesn’t work.”
When kids and parents reject coping skills and behavioral interventions by saying they do not work, the consequences can be substantial. It can mean the rejection of coping skills and strategies that actually would have helped, given time and support; that kids and families bounce between services with increasing frustration; that they search for a magic bullet (which also won’t work); and, particularly concerning for physicians, a belief that the youth have not received the right medication, resulting in potentially unhelpful concoctions of medication.
One of the biggest challenges in helping youth and parents overcome their difficulties – whether these difficulties are depression and anxiety or being better parents to struggling kids – is helping them understand that despite the fact that coping skills and behavioral interventions do not seem to work, they work.
We just have to do a better job explaining what that “work” is.
There are five points you can make.
- First, the coping skill or behavioral intervention is not supposed to work if that means solving the underlying problem. Coping skills and behavioral interventions do not immediately cure anxiety, mend broken hearts, correct disruptive behaviors, disentangle power struggles, or alleviate depression. That is not what their job is. Coping skills and behavioral interventions are there to help us get better at handling complex situations and feelings. In particular, they are good at helping us manage our thoughts (“I can’t do it,” “He should behave better”) and our affect (anger, frustration, rage, anxiety, sadness), so that over time we get better at solving the problems, and break out of the patterns that perpetuate these problems.
- Second, kids and parents do not give skills credit for when they do work. That time you were spiraling out of control and told your mom you needed a break and watched some YouTube videos and then joined the family for dinner? Your coping skills worked, but nobody noticed because they worked. We need to help our young patients and families identify those times that coping skills and behavioral interventions worked.
- Third, let’s face it: Nothing works all the time. It is no wonder kids and families are disappointed by coping skills and behavioral interventions if they think they magically work once and forever. We need to manage expectations.
- Fourth, we know they are supposed to fail, and we should discuss this openly up front. This may sound surprising, but challenging behaviors often get worse when we begin to work on them. “Extinction bursts” is probably the easiest explanation, but for psychodynamically oriented youth and families we could talk about “resistance.” No matter what, things tend to get worse before they get better. We should let people know this ahead of time.
- Fifth, and this is the one that forces youth and parents to ask how hard they actually tried, these skills need to be practiced. You can’t be in the middle of a panic attack and for the first time start trying to pace your breathing with a technique a therapist told you about 3 weeks ago. This makes about as much sense as not training for a marathon. You need to practice and build up the skills, recognizing that as you become more familiar with them, they will help you manage during stressful situations. Every skill should be practiced, preferably several times or more in sessions, maybe every session, and definitely outside of sessions when not in distress.
We cannot blame children and parents for thinking that coping skills and behavioral interventions do not work. They are struggling, suffering, fighting, frightened, angry, anxious, frustrated, and often desperate for something to make everything better. Helping them recognize this desire for things to be better while managing expectations is an essential complement to supporting the use of coping skills and behavioral interventions, and a fairly easy conversation to have with youth.
So when you are talking about coping skills and parental behavioral interventions, it is important to be prepared for the “it didn’t work” conversation, and even to address these issues up front. After all, these strategies may not solve all the problems in the world, but can be lifelong ways of coping with life’s challenges.
Dr. Henderson is associate professor of clinical psychiatry at New York University and deputy director of child and adolescent psychiatry at Bellevue Hospital, New York.
Higher industriousness reduces risk of predementia syndrome in older adults
Higher industriousness was associated with a 25% reduced risk of concurrent motoric cognitive risk syndrome (MCR), based on data from approximately 6,000 individuals.
Previous research supports an association between conscientiousness and a lower risk of MCR, a form of predementia that involves slow gait speed and cognitive complaints, wrote Yannick Stephan, PhD, of the University of Montpellier (France), and colleagues. However, the specific facets of conscientiousness that impact MCR have not been examined.
In a study published in the Journal of Psychiatric Research, the authors reviewed data from 6,001 dementia-free adults aged 65-99 years who were enrolled in the Health and Retirement Study, a nationally representative longitudinal study of adults aged 50 years and older in the United States.
Baseline data were collected between 2008 and 2010, and participants were assessed for MCR at follow-up points during 2012-2014 and 2016-2018. Six facets of conscientiousness were assessed using a 24-item scale that has been used in previous studies. The six facets were industriousness, self-control, order, traditionalism, virtue, and responsibility. The researchers controlled for variables including demographic factors, cognition, physical activity, disease burden, depressive symptoms, and body mass index.
Overall, increased industriousness was significantly associated with a lower likelihood of concurrent MCR (odds ratio, 0.75) and a reduced risk of incident MCR (hazard ratio, 0.63,; P < .001 for both).
The conscientiousness facets of order, self-control, and responsibility also were associated with a lower likelihood of both concurrent and incident MCR, with ORs ranging from 0.82-0.88 for concurrent and HRs ranging from 0.72-0.82 for incident.
Traditionalism and virtue were significantly associated with a lower risk of incident MCR, but not concurrent MCR (HR, 0.84; P < .01 for both).
The mechanism of action for the association may be explained by several cognitive, health-related, behavioral, and psychological pathways, the researchers wrote. With regard to industriousness, the relationship could be partly explained by cognition, physical activity, disease burden, BMI, and depressive symptoms. However, industriousness also has been associated with a reduced risk of systemic inflammation, which may in turn reduce MCR risk. Also, data suggest that industriousness and MCR share a common genetic cause.
The study findings were limited by several factors including the observational design and the positive selection effect from patients with complete follow-up data, as these patients likely have higher levels of order, industriousness, and responsibility, the researchers noted. However, the results support those from previous studies and were strengthened by the large sample and examination of six facets of conscientiousness.
“This study thus provides a more detailed understanding of the specific components of conscientiousness that are associated with risk of MCR among older adults,” and the facets could be targeted in interventions to reduce both MCR and dementia, they concluded.
The Health and Retirement Study is supported by the National Institute on Aging and conducted by the University of Michigan. The current study was supported in part by the National Institutes of Health. The researchers had no financial conflicts to disclose.
Higher industriousness was associated with a 25% reduced risk of concurrent motoric cognitive risk syndrome (MCR), based on data from approximately 6,000 individuals.
Previous research supports an association between conscientiousness and a lower risk of MCR, a form of predementia that involves slow gait speed and cognitive complaints, wrote Yannick Stephan, PhD, of the University of Montpellier (France), and colleagues. However, the specific facets of conscientiousness that impact MCR have not been examined.
In a study published in the Journal of Psychiatric Research, the authors reviewed data from 6,001 dementia-free adults aged 65-99 years who were enrolled in the Health and Retirement Study, a nationally representative longitudinal study of adults aged 50 years and older in the United States.
Baseline data were collected between 2008 and 2010, and participants were assessed for MCR at follow-up points during 2012-2014 and 2016-2018. Six facets of conscientiousness were assessed using a 24-item scale that has been used in previous studies. The six facets were industriousness, self-control, order, traditionalism, virtue, and responsibility. The researchers controlled for variables including demographic factors, cognition, physical activity, disease burden, depressive symptoms, and body mass index.
Overall, increased industriousness was significantly associated with a lower likelihood of concurrent MCR (odds ratio, 0.75) and a reduced risk of incident MCR (hazard ratio, 0.63,; P < .001 for both).
The conscientiousness facets of order, self-control, and responsibility also were associated with a lower likelihood of both concurrent and incident MCR, with ORs ranging from 0.82-0.88 for concurrent and HRs ranging from 0.72-0.82 for incident.
Traditionalism and virtue were significantly associated with a lower risk of incident MCR, but not concurrent MCR (HR, 0.84; P < .01 for both).
The mechanism of action for the association may be explained by several cognitive, health-related, behavioral, and psychological pathways, the researchers wrote. With regard to industriousness, the relationship could be partly explained by cognition, physical activity, disease burden, BMI, and depressive symptoms. However, industriousness also has been associated with a reduced risk of systemic inflammation, which may in turn reduce MCR risk. Also, data suggest that industriousness and MCR share a common genetic cause.
The study findings were limited by several factors including the observational design and the positive selection effect from patients with complete follow-up data, as these patients likely have higher levels of order, industriousness, and responsibility, the researchers noted. However, the results support those from previous studies and were strengthened by the large sample and examination of six facets of conscientiousness.
“This study thus provides a more detailed understanding of the specific components of conscientiousness that are associated with risk of MCR among older adults,” and the facets could be targeted in interventions to reduce both MCR and dementia, they concluded.
The Health and Retirement Study is supported by the National Institute on Aging and conducted by the University of Michigan. The current study was supported in part by the National Institutes of Health. The researchers had no financial conflicts to disclose.
Higher industriousness was associated with a 25% reduced risk of concurrent motoric cognitive risk syndrome (MCR), based on data from approximately 6,000 individuals.
Previous research supports an association between conscientiousness and a lower risk of MCR, a form of predementia that involves slow gait speed and cognitive complaints, wrote Yannick Stephan, PhD, of the University of Montpellier (France), and colleagues. However, the specific facets of conscientiousness that impact MCR have not been examined.
In a study published in the Journal of Psychiatric Research, the authors reviewed data from 6,001 dementia-free adults aged 65-99 years who were enrolled in the Health and Retirement Study, a nationally representative longitudinal study of adults aged 50 years and older in the United States.
Baseline data were collected between 2008 and 2010, and participants were assessed for MCR at follow-up points during 2012-2014 and 2016-2018. Six facets of conscientiousness were assessed using a 24-item scale that has been used in previous studies. The six facets were industriousness, self-control, order, traditionalism, virtue, and responsibility. The researchers controlled for variables including demographic factors, cognition, physical activity, disease burden, depressive symptoms, and body mass index.
Overall, increased industriousness was significantly associated with a lower likelihood of concurrent MCR (odds ratio, 0.75) and a reduced risk of incident MCR (hazard ratio, 0.63,; P < .001 for both).
The conscientiousness facets of order, self-control, and responsibility also were associated with a lower likelihood of both concurrent and incident MCR, with ORs ranging from 0.82-0.88 for concurrent and HRs ranging from 0.72-0.82 for incident.
Traditionalism and virtue were significantly associated with a lower risk of incident MCR, but not concurrent MCR (HR, 0.84; P < .01 for both).
The mechanism of action for the association may be explained by several cognitive, health-related, behavioral, and psychological pathways, the researchers wrote. With regard to industriousness, the relationship could be partly explained by cognition, physical activity, disease burden, BMI, and depressive symptoms. However, industriousness also has been associated with a reduced risk of systemic inflammation, which may in turn reduce MCR risk. Also, data suggest that industriousness and MCR share a common genetic cause.
The study findings were limited by several factors including the observational design and the positive selection effect from patients with complete follow-up data, as these patients likely have higher levels of order, industriousness, and responsibility, the researchers noted. However, the results support those from previous studies and were strengthened by the large sample and examination of six facets of conscientiousness.
“This study thus provides a more detailed understanding of the specific components of conscientiousness that are associated with risk of MCR among older adults,” and the facets could be targeted in interventions to reduce both MCR and dementia, they concluded.
The Health and Retirement Study is supported by the National Institute on Aging and conducted by the University of Michigan. The current study was supported in part by the National Institutes of Health. The researchers had no financial conflicts to disclose.
FROM PSYCHIATRIC RESEARCH
Mechanical touch therapy device promising for anxiety
An at-home investigational device is a promising noninvasive therapeutic approach for anxiety disorders, results from an open-label pilot trial suggest.
The small study showed
“MATT is part of a large movement toward developing therapeutic devices that patients can self-administer at home,” study author Linda L. Carpenter, MD, professor of psychiatry at Brown University and director of the Neuromodulation & Neuroimaging Core at Butler Hospital, both in Providence, R.I., told this news organization, adding that the new study is a step in the right direction of improving the technology used to treat anxiety disorders.
The study was published online in Frontiers in Psychiatry.
Robust safety profile
Therapeutic noninvasive peripheral nerve stimulation is under investigation for anxiety as well as pain and depression. Nerve activation is achieved by delivering electrical or mechanical energy, although most devices to date have used electrical stimulation.
Although electrical stimulation is considered low risk, mechanical stimulation that activates somatosensory pathways has an even more robust safety profile, the investigators note.
The MATT device targets C-tactile fibers (CT) specialized unmyelinated Group C peripheral nerve fibers that fire when stroked at velocities perceived as pleasurable or comforting.
To use the device, participants wear a headset with a small vibrating piece that sits on the mastoid bone behind each ear. These pieces deliver gentle vibrations that can be adjusted by patients.
During development of the MATT stimulation, researchers noted that an isochronic 10 Hz wave, cycling 2 seconds on and 2 seconds off, induced a state of relaxation and increased occipital alpha oscillations in pilot study participants.
The current study was designed to confirm preliminary efficacy and feasibility signals. The sample included 22 patients (mean age 37.3 years, 72.7% female, 77.3% White). All study participants were diagnosed with an anxiety disorder and had at least moderately severe anxiety symptoms. Some also had symptoms of panic or depression.
Many participants were on medications that weren’t effective, and they wanted to find a nondrug method of relieving their symptoms, said Dr. Carpenter.
What’s the mechanism?
Participants learned how to administer the stimulation and adjust the intensity of vibrations to a level where it was consistently detectable but not uncomfortable. Then they received a MATT device to use at home at least twice daily for 20 minutes.
Patients kept daily diaries documenting device use, adverse effects, and technological problems. In-person assessments were held at 2 and 4 weeks.
Researchers collected resting EEG immediately before, and after, the second stimulation session and again following 4 weeks of MATT use.
At baseline and after 2 and 4 weeks, patients self-reported anxiety using the 7-item Generalized Anxiety Disorder (GAD-7) scale, depression with the Beck Depression Inventory (BDI), and stress using the Perceived Stress Scale (PSS). They also reported symptoms with the Depression, Anxiety, Stress Scale (DASS).
Researchers also investigated “interoceptive awareness” or being mindful of your body and internal feelings. For this, they had participants complete the 32-item Multidimensional Assessment of Interoceptive Awareness pre- and post treatment.
Interoceptive awareness “is a whole new area of interest in neuroscience and brain health,” said Dr. Carpenter. “The hypothesis was that one way this device might work is that vibrations would travel to the insular cortex, the part of the brain that involves mindfulness and self-awareness.”
Symptom reduction
In the completer sample of 17 participants, mean scores on anxiety and depression symptoms fell significantly from baseline to 4 weeks (all P < .01). For example, the GAD-7 mean score fell from 14.3 to 7.1 and the BDI mean score from 30.6 to 14.8.
The study also showed that mindfulness was enhanced. The MAIA total score increased from 83.1 to 93.5 (P = .014).
Device users had increased alpha and theta brainwave activity, findings that “go along with the concept of decreased anxiety,” said Dr. Carpenter. She noted a recent study of the same patient population showed the device enhanced functional brain connectivity.
This current study was too small to pick up signals showing the device was effective in any particular subpopulation, said Dr. Carpenter.
Unlike other stimulation interventions that require clinic visits, patients use the MATT in the comfort of their own home and at their own convenience.
However, there are still questions surrounding the use of the noninvasive device. For example, said Dr. Carpenter, it’s unclear if it would be more effective if combined with psychotherapy or whether patients can use it while sleeping and driving. A next step could be a sham-controlled trial, she said.
The study was supported by Affect Neuro, developer of MATT therapy, and the National Institute of General Medical Sciences. Dr. Carpenter reports receiving a consultancy fee from Affect Neuro.
A version of this article first appeared on Medscape.com.
An at-home investigational device is a promising noninvasive therapeutic approach for anxiety disorders, results from an open-label pilot trial suggest.
The small study showed
“MATT is part of a large movement toward developing therapeutic devices that patients can self-administer at home,” study author Linda L. Carpenter, MD, professor of psychiatry at Brown University and director of the Neuromodulation & Neuroimaging Core at Butler Hospital, both in Providence, R.I., told this news organization, adding that the new study is a step in the right direction of improving the technology used to treat anxiety disorders.
The study was published online in Frontiers in Psychiatry.
Robust safety profile
Therapeutic noninvasive peripheral nerve stimulation is under investigation for anxiety as well as pain and depression. Nerve activation is achieved by delivering electrical or mechanical energy, although most devices to date have used electrical stimulation.
Although electrical stimulation is considered low risk, mechanical stimulation that activates somatosensory pathways has an even more robust safety profile, the investigators note.
The MATT device targets C-tactile fibers (CT) specialized unmyelinated Group C peripheral nerve fibers that fire when stroked at velocities perceived as pleasurable or comforting.
To use the device, participants wear a headset with a small vibrating piece that sits on the mastoid bone behind each ear. These pieces deliver gentle vibrations that can be adjusted by patients.
During development of the MATT stimulation, researchers noted that an isochronic 10 Hz wave, cycling 2 seconds on and 2 seconds off, induced a state of relaxation and increased occipital alpha oscillations in pilot study participants.
The current study was designed to confirm preliminary efficacy and feasibility signals. The sample included 22 patients (mean age 37.3 years, 72.7% female, 77.3% White). All study participants were diagnosed with an anxiety disorder and had at least moderately severe anxiety symptoms. Some also had symptoms of panic or depression.
Many participants were on medications that weren’t effective, and they wanted to find a nondrug method of relieving their symptoms, said Dr. Carpenter.
What’s the mechanism?
Participants learned how to administer the stimulation and adjust the intensity of vibrations to a level where it was consistently detectable but not uncomfortable. Then they received a MATT device to use at home at least twice daily for 20 minutes.
Patients kept daily diaries documenting device use, adverse effects, and technological problems. In-person assessments were held at 2 and 4 weeks.
Researchers collected resting EEG immediately before, and after, the second stimulation session and again following 4 weeks of MATT use.
At baseline and after 2 and 4 weeks, patients self-reported anxiety using the 7-item Generalized Anxiety Disorder (GAD-7) scale, depression with the Beck Depression Inventory (BDI), and stress using the Perceived Stress Scale (PSS). They also reported symptoms with the Depression, Anxiety, Stress Scale (DASS).
Researchers also investigated “interoceptive awareness” or being mindful of your body and internal feelings. For this, they had participants complete the 32-item Multidimensional Assessment of Interoceptive Awareness pre- and post treatment.
Interoceptive awareness “is a whole new area of interest in neuroscience and brain health,” said Dr. Carpenter. “The hypothesis was that one way this device might work is that vibrations would travel to the insular cortex, the part of the brain that involves mindfulness and self-awareness.”
Symptom reduction
In the completer sample of 17 participants, mean scores on anxiety and depression symptoms fell significantly from baseline to 4 weeks (all P < .01). For example, the GAD-7 mean score fell from 14.3 to 7.1 and the BDI mean score from 30.6 to 14.8.
The study also showed that mindfulness was enhanced. The MAIA total score increased from 83.1 to 93.5 (P = .014).
Device users had increased alpha and theta brainwave activity, findings that “go along with the concept of decreased anxiety,” said Dr. Carpenter. She noted a recent study of the same patient population showed the device enhanced functional brain connectivity.
This current study was too small to pick up signals showing the device was effective in any particular subpopulation, said Dr. Carpenter.
Unlike other stimulation interventions that require clinic visits, patients use the MATT in the comfort of their own home and at their own convenience.
However, there are still questions surrounding the use of the noninvasive device. For example, said Dr. Carpenter, it’s unclear if it would be more effective if combined with psychotherapy or whether patients can use it while sleeping and driving. A next step could be a sham-controlled trial, she said.
The study was supported by Affect Neuro, developer of MATT therapy, and the National Institute of General Medical Sciences. Dr. Carpenter reports receiving a consultancy fee from Affect Neuro.
A version of this article first appeared on Medscape.com.
An at-home investigational device is a promising noninvasive therapeutic approach for anxiety disorders, results from an open-label pilot trial suggest.
The small study showed
“MATT is part of a large movement toward developing therapeutic devices that patients can self-administer at home,” study author Linda L. Carpenter, MD, professor of psychiatry at Brown University and director of the Neuromodulation & Neuroimaging Core at Butler Hospital, both in Providence, R.I., told this news organization, adding that the new study is a step in the right direction of improving the technology used to treat anxiety disorders.
The study was published online in Frontiers in Psychiatry.
Robust safety profile
Therapeutic noninvasive peripheral nerve stimulation is under investigation for anxiety as well as pain and depression. Nerve activation is achieved by delivering electrical or mechanical energy, although most devices to date have used electrical stimulation.
Although electrical stimulation is considered low risk, mechanical stimulation that activates somatosensory pathways has an even more robust safety profile, the investigators note.
The MATT device targets C-tactile fibers (CT) specialized unmyelinated Group C peripheral nerve fibers that fire when stroked at velocities perceived as pleasurable or comforting.
To use the device, participants wear a headset with a small vibrating piece that sits on the mastoid bone behind each ear. These pieces deliver gentle vibrations that can be adjusted by patients.
During development of the MATT stimulation, researchers noted that an isochronic 10 Hz wave, cycling 2 seconds on and 2 seconds off, induced a state of relaxation and increased occipital alpha oscillations in pilot study participants.
The current study was designed to confirm preliminary efficacy and feasibility signals. The sample included 22 patients (mean age 37.3 years, 72.7% female, 77.3% White). All study participants were diagnosed with an anxiety disorder and had at least moderately severe anxiety symptoms. Some also had symptoms of panic or depression.
Many participants were on medications that weren’t effective, and they wanted to find a nondrug method of relieving their symptoms, said Dr. Carpenter.
What’s the mechanism?
Participants learned how to administer the stimulation and adjust the intensity of vibrations to a level where it was consistently detectable but not uncomfortable. Then they received a MATT device to use at home at least twice daily for 20 minutes.
Patients kept daily diaries documenting device use, adverse effects, and technological problems. In-person assessments were held at 2 and 4 weeks.
Researchers collected resting EEG immediately before, and after, the second stimulation session and again following 4 weeks of MATT use.
At baseline and after 2 and 4 weeks, patients self-reported anxiety using the 7-item Generalized Anxiety Disorder (GAD-7) scale, depression with the Beck Depression Inventory (BDI), and stress using the Perceived Stress Scale (PSS). They also reported symptoms with the Depression, Anxiety, Stress Scale (DASS).
Researchers also investigated “interoceptive awareness” or being mindful of your body and internal feelings. For this, they had participants complete the 32-item Multidimensional Assessment of Interoceptive Awareness pre- and post treatment.
Interoceptive awareness “is a whole new area of interest in neuroscience and brain health,” said Dr. Carpenter. “The hypothesis was that one way this device might work is that vibrations would travel to the insular cortex, the part of the brain that involves mindfulness and self-awareness.”
Symptom reduction
In the completer sample of 17 participants, mean scores on anxiety and depression symptoms fell significantly from baseline to 4 weeks (all P < .01). For example, the GAD-7 mean score fell from 14.3 to 7.1 and the BDI mean score from 30.6 to 14.8.
The study also showed that mindfulness was enhanced. The MAIA total score increased from 83.1 to 93.5 (P = .014).
Device users had increased alpha and theta brainwave activity, findings that “go along with the concept of decreased anxiety,” said Dr. Carpenter. She noted a recent study of the same patient population showed the device enhanced functional brain connectivity.
This current study was too small to pick up signals showing the device was effective in any particular subpopulation, said Dr. Carpenter.
Unlike other stimulation interventions that require clinic visits, patients use the MATT in the comfort of their own home and at their own convenience.
However, there are still questions surrounding the use of the noninvasive device. For example, said Dr. Carpenter, it’s unclear if it would be more effective if combined with psychotherapy or whether patients can use it while sleeping and driving. A next step could be a sham-controlled trial, she said.
The study was supported by Affect Neuro, developer of MATT therapy, and the National Institute of General Medical Sciences. Dr. Carpenter reports receiving a consultancy fee from Affect Neuro.
A version of this article first appeared on Medscape.com.