Clinical Psychiatry News

Patients with persistent depressive or cognitive symptoms after mild to moderate COVID-19 (COVID-DC) may have gliosis and inflammation, data suggest.

In a case-control study of 40 patients who were treated at a tertiary care psychiatric hospital in Canada, the level of translocator protein total distribution volume (TSPO VT), a marker of gliosis, was 9.23 mL/cm³ among patients with COVID-DC and 7.72 mL/cm³ among control persons. Differences were particularly notable in the ventral striatum and dorsal putamen.

“Most theories assume there is inflammation in the brain [with] long COVID,” but that assumption had not been studied, author Jeffrey H. Meyer, MD, PhD, Canada Research Chair in Neurochemistry of Major Depressive Disorder at the University of Toronto, said in an interview. “Such information is pivotal to developing treatments.”

The study was published online in JAMA Psychiatry.
 

Quantifiable marker

The investigators sought to determine whether levels of TSPO VT, which are quantifiable with PET, are elevated in the dorsal putamen, ventral striatum, prefrontal cortex, anterior cingulate cortex, and hippocampus of patients with COVID-DC, compared with patients without this syndrome. These brain regions were chosen, according to the authors, “because injury in these regions, which can cause gliosis, also induces symptoms of COVID-DC.”

The study was conducted from April 2021 through June 30, 2022. The investigators compared levels of TSPO VT in the selected brain regions of 20 participants with COVID-DC (mean age, 32.7 years; 60% women) with that of 20 control persons (mean age, 33.3 years; 55% women). TSPO VT was measured with fluorine F18–labeled N-(2-(2-fluoroethoxy)benzyl)-N-(4-phenoxypyridin-3-yl)acetamide PET.

The difference in TSPO VT was most noticeable in the ventral striatum (mean difference, 1.97 mL/cm³) and dorsal putamen (mean difference, 1.70 mL/cm³). The study authors suggest that gliosis in these areas may explain some of the persistent symptoms reported in structured clinical interviews and assessed on neuropsychological and psychological testing.

For patients with COVID-DC, motor speed on the finger-tapping test was negatively associated with dorsal putamen TSPO VT (r, −0.53). The 10 participants with COVID-DC whose speed was lowest had higher mean dorsal putamen TSPO VT levels than those of control persons by 2.3 mL/cm³.

The investigators could not assess a possible association between the ventral striatum TSPO VT and anhedonia because all participants had these symptoms. No significant correlations were found between depression and TSPO VT in the prefrontal cortex or anterior cingulate cortex.

The authors acknowledged that the study was cross-sectional, and so the duration of persistently elevated TSPO VT is not yet known. In addition, elevation in TSPO VT is not completely specific to glial cells, and although correlations with finger-tapping test performance reflect associations between brain changes and symptoms, they do not prove cause and effect.

“Presently, clinicians can use treatments for symptoms in other illnesses that are [also] common with long COVID. We need better than this,” said Dr. Meyer. “Clients with long COVID should be able to state their symptoms, and the practitioner should have an evidence-based matching treatment to recommend.”

Research is ongoing. “We are acquiring more information regarding different types of inflammation in the brain, whether there is ongoing injury, and whether treatments that influence inflammation are helpful,” said Dr. Meyer.
 

Jigsaw puzzle

“While this is an important piece in the jigsaw puzzle of neuroinflammation in chronic neurological disease, it is important to keep in mind that we still lack understanding of the complex picture for several reasons,” Alexander Gerhard, MD, honorary senior lecturer in neuroscience at the University of Manchester, England, wrote in an accompanying editorial.

Among these reasons is that the PET technique used in the study is noisy and not restricted to glial cells, he wrote. TSPO expression is only one part of the brain’s neuroinflammatory response, but PET techniques “do not currently allow us to distinguish between different states of microglial activation.” In addition, “a much more detailed understanding of microglial activation at different time points” is needed before neuroinflammatory changes can be targeted therapeutically, Dr. Gerhard wrote.

In a comment, Vilma Gabbay, MD, professor of psychiatry and neuroscience and director of biomarkers and dimensional psychiatry in the Psychiatry Research Institute at Montefiore Einstein, Albert Einstein College of Medicine, New York, said that “this is an important initial step to better understand the neuropsychiatric consequences of COVID even in only a mild and moderate viral illness.” TSPO imaging through PET scanning has been used as an index for neuroinflammation and gliosis. Researchers have used it to study neurodegenerative diseases, but as the authors noted, the ligand is not specific for gliosis.

“Follow-up large cohort studies including other measures of neuroimaging modalities assessing circuitry and neurochemistry are needed,” she said. “Similarly, studying the blood-brain barrier will also allow us to better understand how the immune reaction in the blood transitions to the brain.”

This field of research is evolving, and clinical trials are ongoing, Dr. Gabbay added. Meanwhile, clinicians should monitor for, assess, and treat neuropsychiatric symptoms and “follow the literature for new research and management recommendations.”

The study was primarily funded by a Canadian Institutes of Health Research Project grant to the authors, with some funding from the Canadian Institute for Military and Veteran Health Research. Dr. Meyer received support from their Canada Research Chair awards and received grants and support from several pharmaceutical companies outside of the submitted work. Dr. Gerhard and Dr. Gabbay disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Patients with persistent depressive or cognitive symptoms after mild to moderate COVID-19 (COVID-DC) may have gliosis and inflammation, data suggest.

In a case-control study of 40 patients who were treated at a tertiary care psychiatric hospital in Canada, the level of translocator protein total distribution volume (TSPO VT), a marker of gliosis, was 9.23 mL/cm³ among patients with COVID-DC and 7.72 mL/cm³ among control persons. Differences were particularly notable in the ventral striatum and dorsal putamen.

“Most theories assume there is inflammation in the brain [with] long COVID,” but that assumption had not been studied, author Jeffrey H. Meyer, MD, PhD, Canada Research Chair in Neurochemistry of Major Depressive Disorder at the University of Toronto, said in an interview. “Such information is pivotal to developing treatments.”

The study was published online in JAMA Psychiatry.
 

Quantifiable marker

The investigators sought to determine whether levels of TSPO VT, which are quantifiable with PET, are elevated in the dorsal putamen, ventral striatum, prefrontal cortex, anterior cingulate cortex, and hippocampus of patients with COVID-DC, compared with patients without this syndrome. These brain regions were chosen, according to the authors, “because injury in these regions, which can cause gliosis, also induces symptoms of COVID-DC.”

The study was conducted from April 2021 through June 30, 2022. The investigators compared levels of TSPO VT in the selected brain regions of 20 participants with COVID-DC (mean age, 32.7 years; 60% women) with that of 20 control persons (mean age, 33.3 years; 55% women). TSPO VT was measured with fluorine F18–labeled N-(2-(2-fluoroethoxy)benzyl)-N-(4-phenoxypyridin-3-yl)acetamide PET.

The difference in TSPO VT was most noticeable in the ventral striatum (mean difference, 1.97 mL/cm³) and dorsal putamen (mean difference, 1.70 mL/cm³). The study authors suggest that gliosis in these areas may explain some of the persistent symptoms reported in structured clinical interviews and assessed on neuropsychological and psychological testing.

For patients with COVID-DC, motor speed on the finger-tapping test was negatively associated with dorsal putamen TSPO VT (r, −0.53). The 10 participants with COVID-DC whose speed was lowest had higher mean dorsal putamen TSPO VT levels than those of control persons by 2.3 mL/cm³.

The investigators could not assess a possible association between the ventral striatum TSPO VT and anhedonia because all participants had these symptoms. No significant correlations were found between depression and TSPO VT in the prefrontal cortex or anterior cingulate cortex.

The authors acknowledged that the study was cross-sectional, and so the duration of persistently elevated TSPO VT is not yet known. In addition, elevation in TSPO VT is not completely specific to glial cells, and although correlations with finger-tapping test performance reflect associations between brain changes and symptoms, they do not prove cause and effect.

“Presently, clinicians can use treatments for symptoms in other illnesses that are [also] common with long COVID. We need better than this,” said Dr. Meyer. “Clients with long COVID should be able to state their symptoms, and the practitioner should have an evidence-based matching treatment to recommend.”

Research is ongoing. “We are acquiring more information regarding different types of inflammation in the brain, whether there is ongoing injury, and whether treatments that influence inflammation are helpful,” said Dr. Meyer.
 

Jigsaw puzzle

“While this is an important piece in the jigsaw puzzle of neuroinflammation in chronic neurological disease, it is important to keep in mind that we still lack understanding of the complex picture for several reasons,” Alexander Gerhard, MD, honorary senior lecturer in neuroscience at the University of Manchester, England, wrote in an accompanying editorial.

Among these reasons is that the PET technique used in the study is noisy and not restricted to glial cells, he wrote. TSPO expression is only one part of the brain’s neuroinflammatory response, but PET techniques “do not currently allow us to distinguish between different states of microglial activation.” In addition, “a much more detailed understanding of microglial activation at different time points” is needed before neuroinflammatory changes can be targeted therapeutically, Dr. Gerhard wrote.

In a comment, Vilma Gabbay, MD, professor of psychiatry and neuroscience and director of biomarkers and dimensional psychiatry in the Psychiatry Research Institute at Montefiore Einstein, Albert Einstein College of Medicine, New York, said that “this is an important initial step to better understand the neuropsychiatric consequences of COVID even in only a mild and moderate viral illness.” TSPO imaging through PET scanning has been used as an index for neuroinflammation and gliosis. Researchers have used it to study neurodegenerative diseases, but as the authors noted, the ligand is not specific for gliosis.

“Follow-up large cohort studies including other measures of neuroimaging modalities assessing circuitry and neurochemistry are needed,” she said. “Similarly, studying the blood-brain barrier will also allow us to better understand how the immune reaction in the blood transitions to the brain.”

This field of research is evolving, and clinical trials are ongoing, Dr. Gabbay added. Meanwhile, clinicians should monitor for, assess, and treat neuropsychiatric symptoms and “follow the literature for new research and management recommendations.”

The study was primarily funded by a Canadian Institutes of Health Research Project grant to the authors, with some funding from the Canadian Institute for Military and Veteran Health Research. Dr. Meyer received support from their Canada Research Chair awards and received grants and support from several pharmaceutical companies outside of the submitted work. Dr. Gerhard and Dr. Gabbay disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Patients with persistent depressive or cognitive symptoms after mild to moderate COVID-19 (COVID-DC) may have gliosis and inflammation, data suggest.

In a case-control study of 40 patients who were treated at a tertiary care psychiatric hospital in Canada, the level of translocator protein total distribution volume (TSPO VT), a marker of gliosis, was 9.23 mL/cm³ among patients with COVID-DC and 7.72 mL/cm³ among control persons. Differences were particularly notable in the ventral striatum and dorsal putamen.

“Most theories assume there is inflammation in the brain [with] long COVID,” but that assumption had not been studied, author Jeffrey H. Meyer, MD, PhD, Canada Research Chair in Neurochemistry of Major Depressive Disorder at the University of Toronto, said in an interview. “Such information is pivotal to developing treatments.”

The study was published online in JAMA Psychiatry.
 

Quantifiable marker

The investigators sought to determine whether levels of TSPO VT, which are quantifiable with PET, are elevated in the dorsal putamen, ventral striatum, prefrontal cortex, anterior cingulate cortex, and hippocampus of patients with COVID-DC, compared with patients without this syndrome. These brain regions were chosen, according to the authors, “because injury in these regions, which can cause gliosis, also induces symptoms of COVID-DC.”

The study was conducted from April 2021 through June 30, 2022. The investigators compared levels of TSPO VT in the selected brain regions of 20 participants with COVID-DC (mean age, 32.7 years; 60% women) with that of 20 control persons (mean age, 33.3 years; 55% women). TSPO VT was measured with fluorine F18–labeled N-(2-(2-fluoroethoxy)benzyl)-N-(4-phenoxypyridin-3-yl)acetamide PET.

The difference in TSPO VT was most noticeable in the ventral striatum (mean difference, 1.97 mL/cm³) and dorsal putamen (mean difference, 1.70 mL/cm³). The study authors suggest that gliosis in these areas may explain some of the persistent symptoms reported in structured clinical interviews and assessed on neuropsychological and psychological testing.

For patients with COVID-DC, motor speed on the finger-tapping test was negatively associated with dorsal putamen TSPO VT (r, −0.53). The 10 participants with COVID-DC whose speed was lowest had higher mean dorsal putamen TSPO VT levels than those of control persons by 2.3 mL/cm³.

The investigators could not assess a possible association between the ventral striatum TSPO VT and anhedonia because all participants had these symptoms. No significant correlations were found between depression and TSPO VT in the prefrontal cortex or anterior cingulate cortex.

The authors acknowledged that the study was cross-sectional, and so the duration of persistently elevated TSPO VT is not yet known. In addition, elevation in TSPO VT is not completely specific to glial cells, and although correlations with finger-tapping test performance reflect associations between brain changes and symptoms, they do not prove cause and effect.

“Presently, clinicians can use treatments for symptoms in other illnesses that are [also] common with long COVID. We need better than this,” said Dr. Meyer. “Clients with long COVID should be able to state their symptoms, and the practitioner should have an evidence-based matching treatment to recommend.”

Research is ongoing. “We are acquiring more information regarding different types of inflammation in the brain, whether there is ongoing injury, and whether treatments that influence inflammation are helpful,” said Dr. Meyer.
 

Jigsaw puzzle

“While this is an important piece in the jigsaw puzzle of neuroinflammation in chronic neurological disease, it is important to keep in mind that we still lack understanding of the complex picture for several reasons,” Alexander Gerhard, MD, honorary senior lecturer in neuroscience at the University of Manchester, England, wrote in an accompanying editorial.

Among these reasons is that the PET technique used in the study is noisy and not restricted to glial cells, he wrote. TSPO expression is only one part of the brain’s neuroinflammatory response, but PET techniques “do not currently allow us to distinguish between different states of microglial activation.” In addition, “a much more detailed understanding of microglial activation at different time points” is needed before neuroinflammatory changes can be targeted therapeutically, Dr. Gerhard wrote.

In a comment, Vilma Gabbay, MD, professor of psychiatry and neuroscience and director of biomarkers and dimensional psychiatry in the Psychiatry Research Institute at Montefiore Einstein, Albert Einstein College of Medicine, New York, said that “this is an important initial step to better understand the neuropsychiatric consequences of COVID even in only a mild and moderate viral illness.” TSPO imaging through PET scanning has been used as an index for neuroinflammation and gliosis. Researchers have used it to study neurodegenerative diseases, but as the authors noted, the ligand is not specific for gliosis.

“Follow-up large cohort studies including other measures of neuroimaging modalities assessing circuitry and neurochemistry are needed,” she said. “Similarly, studying the blood-brain barrier will also allow us to better understand how the immune reaction in the blood transitions to the brain.”

This field of research is evolving, and clinical trials are ongoing, Dr. Gabbay added. Meanwhile, clinicians should monitor for, assess, and treat neuropsychiatric symptoms and “follow the literature for new research and management recommendations.”

The study was primarily funded by a Canadian Institutes of Health Research Project grant to the authors, with some funding from the Canadian Institute for Military and Veteran Health Research. Dr. Meyer received support from their Canada Research Chair awards and received grants and support from several pharmaceutical companies outside of the submitted work. Dr. Gerhard and Dr. Gabbay disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Baseline depression was significantly associated with recovered, incident, and persistent metabolic syndrome, based on data from more than 13,000 individuals.

Previous research has established a connection between metabolic syndrome and depression, but data on the increased risk for depressed individuals to develop metabolic syndrome (MetS) are lacking, wrote Lara Onofre Ferriani, PhD, of Federal University of Espírito Santo, Vitoria, Brazil, and colleagues.

“Individuals with MetS and depression have increased levels of inflammatory markers, and it is speculated that inflammation could mediate this comorbidity,” they said.

In a study published in the Journal of Psychiatric Research, the investigators reviewed data from 13,883 participants in the Brazilian Longitudinal Study of Adult Health; all were civil servants at universities in Brazil. The participants ranged from 35 to 74 years of age, with a mean age of 51.9 years; 54.3% were women; and 52.4% were white; the mean follow-up period was 3.8 years.

The primary outcome was the association between depression diagnosis and severity on components of MetS at baseline and over a 4-year period. Participants were classified by MetS trajectory as recovered, incident, or persistent, and classified by depression status as without depression or with a mild, moderate, or severe current depressive episode. Depression status was based on the Clinical Interview Schedule Revised. MetS components and diagnosis were based on the National Cholesterol Education Program Adult Treatment Panel III.

In a logistic regression analysis, baseline depression was positively associated with recovered, incident, and persistent MetS (odds ratios, 1.59, 1.45, and 1.70, respectively).

Depression at baseline also was significantly associated with separate components of MetS: large waist circumference, high triglycerides, low high-density lipoprotein cholesterol, and hyperglycemia, with odds ratios of 1.47, 1.23, 1.30, and 1.38, respectively.

Although not seen at baseline, a significant positive association between baseline depression and the presence of three or more MetS components was noted at follow-up, with a positive dose-response effect, the researchers wrote in their discussion.

Not all associations were statistically significant, but this was mainly because of the small number of cases of moderate and severe depression, they said. However, the magnitude of associations was greater in severe depression, when compared with moderate and mild, which suggests that the risk of MetS may be higher in this population, they added.

The study findings were limited by several factors including the possible misclassification of depression, inability to differentiate among depressive subtypes, and the potential lack of generalizability to other populations beyond Brazilian civil servants, the researchers noted.

However, the results were strengthened by the large sample size and support the role of depression as a risk factor for MetS, they said. More research is needed to determine a bidirectional relationship and to assess the trajectory of depression after MetS develops, but the findings “highlight the need to investigate and manage metabolic and cardiovascular alterations in the presence of depression in clinical settings,” they concluded.

The study was supported by the Brazilian Ministry of Health (Science and Technology Department) and the Brazilian Ministry of Science, Technology and Innovation FINEP and CNPq, and by the Coordenaçaõ de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES). The researchers had no financial conflicts to disclose.
 

Baseline depression was significantly associated with recovered, incident, and persistent metabolic syndrome, based on data from more than 13,000 individuals.

Previous research has established a connection between metabolic syndrome and depression, but data on the increased risk for depressed individuals to develop metabolic syndrome (MetS) are lacking, wrote Lara Onofre Ferriani, PhD, of Federal University of Espírito Santo, Vitoria, Brazil, and colleagues.

“Individuals with MetS and depression have increased levels of inflammatory markers, and it is speculated that inflammation could mediate this comorbidity,” they said.

In a study published in the Journal of Psychiatric Research, the investigators reviewed data from 13,883 participants in the Brazilian Longitudinal Study of Adult Health; all were civil servants at universities in Brazil. The participants ranged from 35 to 74 years of age, with a mean age of 51.9 years; 54.3% were women; and 52.4% were white; the mean follow-up period was 3.8 years.

The primary outcome was the association between depression diagnosis and severity on components of MetS at baseline and over a 4-year period. Participants were classified by MetS trajectory as recovered, incident, or persistent, and classified by depression status as without depression or with a mild, moderate, or severe current depressive episode. Depression status was based on the Clinical Interview Schedule Revised. MetS components and diagnosis were based on the National Cholesterol Education Program Adult Treatment Panel III.

In a logistic regression analysis, baseline depression was positively associated with recovered, incident, and persistent MetS (odds ratios, 1.59, 1.45, and 1.70, respectively).

Depression at baseline also was significantly associated with separate components of MetS: large waist circumference, high triglycerides, low high-density lipoprotein cholesterol, and hyperglycemia, with odds ratios of 1.47, 1.23, 1.30, and 1.38, respectively.

Although not seen at baseline, a significant positive association between baseline depression and the presence of three or more MetS components was noted at follow-up, with a positive dose-response effect, the researchers wrote in their discussion.

Not all associations were statistically significant, but this was mainly because of the small number of cases of moderate and severe depression, they said. However, the magnitude of associations was greater in severe depression, when compared with moderate and mild, which suggests that the risk of MetS may be higher in this population, they added.

The study findings were limited by several factors including the possible misclassification of depression, inability to differentiate among depressive subtypes, and the potential lack of generalizability to other populations beyond Brazilian civil servants, the researchers noted.

However, the results were strengthened by the large sample size and support the role of depression as a risk factor for MetS, they said. More research is needed to determine a bidirectional relationship and to assess the trajectory of depression after MetS develops, but the findings “highlight the need to investigate and manage metabolic and cardiovascular alterations in the presence of depression in clinical settings,” they concluded.

The study was supported by the Brazilian Ministry of Health (Science and Technology Department) and the Brazilian Ministry of Science, Technology and Innovation FINEP and CNPq, and by the Coordenaçaõ de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES). The researchers had no financial conflicts to disclose.
 

Baseline depression was significantly associated with recovered, incident, and persistent metabolic syndrome, based on data from more than 13,000 individuals.

Previous research has established a connection between metabolic syndrome and depression, but data on the increased risk for depressed individuals to develop metabolic syndrome (MetS) are lacking, wrote Lara Onofre Ferriani, PhD, of Federal University of Espírito Santo, Vitoria, Brazil, and colleagues.

“Individuals with MetS and depression have increased levels of inflammatory markers, and it is speculated that inflammation could mediate this comorbidity,” they said.

In a study published in the Journal of Psychiatric Research, the investigators reviewed data from 13,883 participants in the Brazilian Longitudinal Study of Adult Health; all were civil servants at universities in Brazil. The participants ranged from 35 to 74 years of age, with a mean age of 51.9 years; 54.3% were women; and 52.4% were white; the mean follow-up period was 3.8 years.

The primary outcome was the association between depression diagnosis and severity on components of MetS at baseline and over a 4-year period. Participants were classified by MetS trajectory as recovered, incident, or persistent, and classified by depression status as without depression or with a mild, moderate, or severe current depressive episode. Depression status was based on the Clinical Interview Schedule Revised. MetS components and diagnosis were based on the National Cholesterol Education Program Adult Treatment Panel III.

In a logistic regression analysis, baseline depression was positively associated with recovered, incident, and persistent MetS (odds ratios, 1.59, 1.45, and 1.70, respectively).

Depression at baseline also was significantly associated with separate components of MetS: large waist circumference, high triglycerides, low high-density lipoprotein cholesterol, and hyperglycemia, with odds ratios of 1.47, 1.23, 1.30, and 1.38, respectively.

Although not seen at baseline, a significant positive association between baseline depression and the presence of three or more MetS components was noted at follow-up, with a positive dose-response effect, the researchers wrote in their discussion.

Not all associations were statistically significant, but this was mainly because of the small number of cases of moderate and severe depression, they said. However, the magnitude of associations was greater in severe depression, when compared with moderate and mild, which suggests that the risk of MetS may be higher in this population, they added.

The study findings were limited by several factors including the possible misclassification of depression, inability to differentiate among depressive subtypes, and the potential lack of generalizability to other populations beyond Brazilian civil servants, the researchers noted.

However, the results were strengthened by the large sample size and support the role of depression as a risk factor for MetS, they said. More research is needed to determine a bidirectional relationship and to assess the trajectory of depression after MetS develops, but the findings “highlight the need to investigate and manage metabolic and cardiovascular alterations in the presence of depression in clinical settings,” they concluded.

The study was supported by the Brazilian Ministry of Health (Science and Technology Department) and the Brazilian Ministry of Science, Technology and Innovation FINEP and CNPq, and by the Coordenaçaõ de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES). The researchers had no financial conflicts to disclose.
 

With the exception of lysergic acid diethylamide, use of hallucinogens surged between 2018 and 2021 among adults younger than 30 years in the United States, new research shows.

In 2018, the prevalence of young adults’ past-year use of non-LSD hallucinogens was 3.4%. By 2021, it had jumped to 6.6%.

The increase in non-LSD hallucinogen use occurred while LSD use remained stable at around 4% in 2018 and 2021.

“While non-LSD hallucinogen use remains substantially less prevalent than use of substances such as alcohol and cannabis, a doubling of prevalence in just three years is a dramatic increase and raises possible public health concerns,” co-author Megan Patrick, PhD, with the University of Michigan Institute for Social Research, Ann Arbor, said in a news release.

The results were published online in the journal Addiction.
 

Health concerns

The estimates are derived from the Monitoring the Future study, which includes annual assessments of adolescent and adult health in the United States.

The analysis focused on 11,304 persons (52% female) aged 9-30 years from the U.S. general population who were interviewed between 2018 and 2021.

Participants were asked about past 12-month use of LSD, as well as use of non-LSD hallucinogens, such as psilocybin.

From 2018 to 2021, past 12-month use of LSD remained relatively stable; it was 3.7% in 2018 and 4.2% in 2021.

However, non-LSD hallucinogen use increased in prevalence from 3.4% to 6.6% from 2018 to 2021.

Across years, the odds of non-LSD use were higher among males, White people, and individuals from households with higher parental education – a proxy for higher socioeconomic status.

The most commonly used non-LSD hallucinogen was psilocybin.

The survey did not ask whether young adults used non-LSD hallucinogens for therapeutic or medical reasons.

“The use of psychedelic and hallucinogenic drugs for a range of therapeutic uses is increasing, given accumulating yet still preliminary data from randomized trials on clinical effectiveness,” lead author Katherine Keyes, PhD, with Columbia University Mailman School of Public Health, New York, said in the release.

“With increased visibility for medical and therapeutic use, however, potentially comes diversion and unregulated product availability, as well as a lack of understanding among the public of potential risks,” Dr. Keyes added.

“However, approved therapeutic use of psychedelics under a trained health professional’s care remains uncommon in the United States, thus the trends we observe here are undoubtedly in nonmedical and nontherapeutic use,” Dr. Keyes noted.

Dr. Patrick said the increased use of hallucinogens raises “concern for young adult health” and is not without risk. While hallucinogen dependence has historically been rare in the U.S. population, it could become more common as use increases, she noted.

The researchers will continue to track these trends to see whether the increases continue.

“We need additional research, including about the motives for hallucinogen use and how young adults are using these substances, in order to be able to mitigate the associated negative consequences,” Dr. Patrick said.

The study was funded by the National Institute on Drug Abuse, part of the National Institutes of Health. Dr. Keyes and Dr. Patrick have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

With the exception of lysergic acid diethylamide, use of hallucinogens surged between 2018 and 2021 among adults younger than 30 years in the United States, new research shows.

In 2018, the prevalence of young adults’ past-year use of non-LSD hallucinogens was 3.4%. By 2021, it had jumped to 6.6%.

The increase in non-LSD hallucinogen use occurred while LSD use remained stable at around 4% in 2018 and 2021.

“While non-LSD hallucinogen use remains substantially less prevalent than use of substances such as alcohol and cannabis, a doubling of prevalence in just three years is a dramatic increase and raises possible public health concerns,” co-author Megan Patrick, PhD, with the University of Michigan Institute for Social Research, Ann Arbor, said in a news release.

The results were published online in the journal Addiction.
 

Health concerns

The estimates are derived from the Monitoring the Future study, which includes annual assessments of adolescent and adult health in the United States.

The analysis focused on 11,304 persons (52% female) aged 9-30 years from the U.S. general population who were interviewed between 2018 and 2021.

Participants were asked about past 12-month use of LSD, as well as use of non-LSD hallucinogens, such as psilocybin.

From 2018 to 2021, past 12-month use of LSD remained relatively stable; it was 3.7% in 2018 and 4.2% in 2021.

However, non-LSD hallucinogen use increased in prevalence from 3.4% to 6.6% from 2018 to 2021.

Across years, the odds of non-LSD use were higher among males, White people, and individuals from households with higher parental education – a proxy for higher socioeconomic status.

The most commonly used non-LSD hallucinogen was psilocybin.

The survey did not ask whether young adults used non-LSD hallucinogens for therapeutic or medical reasons.

“The use of psychedelic and hallucinogenic drugs for a range of therapeutic uses is increasing, given accumulating yet still preliminary data from randomized trials on clinical effectiveness,” lead author Katherine Keyes, PhD, with Columbia University Mailman School of Public Health, New York, said in the release.

“With increased visibility for medical and therapeutic use, however, potentially comes diversion and unregulated product availability, as well as a lack of understanding among the public of potential risks,” Dr. Keyes added.

“However, approved therapeutic use of psychedelics under a trained health professional’s care remains uncommon in the United States, thus the trends we observe here are undoubtedly in nonmedical and nontherapeutic use,” Dr. Keyes noted.

Dr. Patrick said the increased use of hallucinogens raises “concern for young adult health” and is not without risk. While hallucinogen dependence has historically been rare in the U.S. population, it could become more common as use increases, she noted.

The researchers will continue to track these trends to see whether the increases continue.

“We need additional research, including about the motives for hallucinogen use and how young adults are using these substances, in order to be able to mitigate the associated negative consequences,” Dr. Patrick said.

The study was funded by the National Institute on Drug Abuse, part of the National Institutes of Health. Dr. Keyes and Dr. Patrick have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

With the exception of lysergic acid diethylamide, use of hallucinogens surged between 2018 and 2021 among adults younger than 30 years in the United States, new research shows.

In 2018, the prevalence of young adults’ past-year use of non-LSD hallucinogens was 3.4%. By 2021, it had jumped to 6.6%.

The increase in non-LSD hallucinogen use occurred while LSD use remained stable at around 4% in 2018 and 2021.

“While non-LSD hallucinogen use remains substantially less prevalent than use of substances such as alcohol and cannabis, a doubling of prevalence in just three years is a dramatic increase and raises possible public health concerns,” co-author Megan Patrick, PhD, with the University of Michigan Institute for Social Research, Ann Arbor, said in a news release.

The results were published online in the journal Addiction.
 

Health concerns

The estimates are derived from the Monitoring the Future study, which includes annual assessments of adolescent and adult health in the United States.

The analysis focused on 11,304 persons (52% female) aged 9-30 years from the U.S. general population who were interviewed between 2018 and 2021.

Participants were asked about past 12-month use of LSD, as well as use of non-LSD hallucinogens, such as psilocybin.

From 2018 to 2021, past 12-month use of LSD remained relatively stable; it was 3.7% in 2018 and 4.2% in 2021.

However, non-LSD hallucinogen use increased in prevalence from 3.4% to 6.6% from 2018 to 2021.

Across years, the odds of non-LSD use were higher among males, White people, and individuals from households with higher parental education – a proxy for higher socioeconomic status.

The most commonly used non-LSD hallucinogen was psilocybin.

The survey did not ask whether young adults used non-LSD hallucinogens for therapeutic or medical reasons.

“The use of psychedelic and hallucinogenic drugs for a range of therapeutic uses is increasing, given accumulating yet still preliminary data from randomized trials on clinical effectiveness,” lead author Katherine Keyes, PhD, with Columbia University Mailman School of Public Health, New York, said in the release.

“With increased visibility for medical and therapeutic use, however, potentially comes diversion and unregulated product availability, as well as a lack of understanding among the public of potential risks,” Dr. Keyes added.

“However, approved therapeutic use of psychedelics under a trained health professional’s care remains uncommon in the United States, thus the trends we observe here are undoubtedly in nonmedical and nontherapeutic use,” Dr. Keyes noted.

Dr. Patrick said the increased use of hallucinogens raises “concern for young adult health” and is not without risk. While hallucinogen dependence has historically been rare in the U.S. population, it could become more common as use increases, she noted.

The researchers will continue to track these trends to see whether the increases continue.

“We need additional research, including about the motives for hallucinogen use and how young adults are using these substances, in order to be able to mitigate the associated negative consequences,” Dr. Patrick said.

The study was funded by the National Institute on Drug Abuse, part of the National Institutes of Health. Dr. Keyes and Dr. Patrick have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

TOPLINE:

Prepandemic cortisol response to stress and amygdala emotion-evoked activation predicted persistent teen engagement in nonsuicidal self-injury (NSSI) among teensduring the COVID-19 pandemic.

METHODOLOGY:

The analysis included 64 mostly White and middle class or upper middle class female patients in Minneapolis, Minnesota (mean age, 16.2 years) who were part of a larger study of the neurobiology of NSSI.

Before the pandemic, researchers assessed the presence of NSSI and measured cortisol levels in saliva while the participant was experiencing stress, such as when giving a speech (less cortisol in response to stress is a sign of HPA axis hyporeactivity); adolescents were assessed for depression and underwent neuroimaging.

In the early stages of the pandemic, adolescents were assessed for recent engagement in NSSI.

Researchers classified adolescents into three NSSI groups: never (n = 17), desist (a history of NSSI but did not report it during the pandemic; n = 26), or persist (a history of NSSI and reported it during the pandemic; n = 21).
 

TAKEAWAY:

Lower prepandemic levels of under the curve ground (AUCg), an index of overall activation of cortisol levels (B = −0.250; standard error, 0.109; P = .022) and lower prepandemic amygdala activation (B = −0.789; SE = 0.352; P = .025) predicted desistance of NSSI, compared to persistence of NSSI, during the pandemic.

This remained significant after controlling for pandemic-related stressors that could exacerbate underlying risk factors

When depression was included as a covariate, decreased cortisol AUCg and amygdala activation remained significantly predictive of desistance. Decreased medial prefrontal cortex resting state functional connectivity and decreased depressive symptoms were also predictive of desistance of NSSI.
 

IN PRACTICE:

The results “may give insight into predictors of maladaptive patterns of coping with negative emotions” for those with a history of NSSI, the authors noted.

STUDY DETAILS:

The study was conducted by Katherine A. Carosella, department of psychology, University of Minnesota, Minneapolis, and colleagues. It was published online in Psychoneuroendocrinology.

LIMITATIONS:

The study was relatively small, and the investigators could not make causal inferences or rule out the possibility that different stages of development affected the data. Measures employed during COVID were not identical to those used in the prepandemic assessment.

DISCLOSURES:

The study received support from the National Institute of Mental Health and the University of Minnesota. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

TOPLINE:

Prepandemic cortisol response to stress and amygdala emotion-evoked activation predicted persistent teen engagement in nonsuicidal self-injury (NSSI) among teensduring the COVID-19 pandemic.

METHODOLOGY:

The analysis included 64 mostly White and middle class or upper middle class female patients in Minneapolis, Minnesota (mean age, 16.2 years) who were part of a larger study of the neurobiology of NSSI.

Before the pandemic, researchers assessed the presence of NSSI and measured cortisol levels in saliva while the participant was experiencing stress, such as when giving a speech (less cortisol in response to stress is a sign of HPA axis hyporeactivity); adolescents were assessed for depression and underwent neuroimaging.

In the early stages of the pandemic, adolescents were assessed for recent engagement in NSSI.

Researchers classified adolescents into three NSSI groups: never (n = 17), desist (a history of NSSI but did not report it during the pandemic; n = 26), or persist (a history of NSSI and reported it during the pandemic; n = 21).
 

TAKEAWAY:

Lower prepandemic levels of under the curve ground (AUCg), an index of overall activation of cortisol levels (B = −0.250; standard error, 0.109; P = .022) and lower prepandemic amygdala activation (B = −0.789; SE = 0.352; P = .025) predicted desistance of NSSI, compared to persistence of NSSI, during the pandemic.

This remained significant after controlling for pandemic-related stressors that could exacerbate underlying risk factors

When depression was included as a covariate, decreased cortisol AUCg and amygdala activation remained significantly predictive of desistance. Decreased medial prefrontal cortex resting state functional connectivity and decreased depressive symptoms were also predictive of desistance of NSSI.
 

IN PRACTICE:

The results “may give insight into predictors of maladaptive patterns of coping with negative emotions” for those with a history of NSSI, the authors noted.

STUDY DETAILS:

The study was conducted by Katherine A. Carosella, department of psychology, University of Minnesota, Minneapolis, and colleagues. It was published online in Psychoneuroendocrinology.

LIMITATIONS:

The study was relatively small, and the investigators could not make causal inferences or rule out the possibility that different stages of development affected the data. Measures employed during COVID were not identical to those used in the prepandemic assessment.

DISCLOSURES:

The study received support from the National Institute of Mental Health and the University of Minnesota. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

TOPLINE:

Prepandemic cortisol response to stress and amygdala emotion-evoked activation predicted persistent teen engagement in nonsuicidal self-injury (NSSI) among teensduring the COVID-19 pandemic.

METHODOLOGY:

The analysis included 64 mostly White and middle class or upper middle class female patients in Minneapolis, Minnesota (mean age, 16.2 years) who were part of a larger study of the neurobiology of NSSI.

Before the pandemic, researchers assessed the presence of NSSI and measured cortisol levels in saliva while the participant was experiencing stress, such as when giving a speech (less cortisol in response to stress is a sign of HPA axis hyporeactivity); adolescents were assessed for depression and underwent neuroimaging.

In the early stages of the pandemic, adolescents were assessed for recent engagement in NSSI.

Researchers classified adolescents into three NSSI groups: never (n = 17), desist (a history of NSSI but did not report it during the pandemic; n = 26), or persist (a history of NSSI and reported it during the pandemic; n = 21).
 

TAKEAWAY:

Lower prepandemic levels of under the curve ground (AUCg), an index of overall activation of cortisol levels (B = −0.250; standard error, 0.109; P = .022) and lower prepandemic amygdala activation (B = −0.789; SE = 0.352; P = .025) predicted desistance of NSSI, compared to persistence of NSSI, during the pandemic.

This remained significant after controlling for pandemic-related stressors that could exacerbate underlying risk factors

When depression was included as a covariate, decreased cortisol AUCg and amygdala activation remained significantly predictive of desistance. Decreased medial prefrontal cortex resting state functional connectivity and decreased depressive symptoms were also predictive of desistance of NSSI.
 

IN PRACTICE:

The results “may give insight into predictors of maladaptive patterns of coping with negative emotions” for those with a history of NSSI, the authors noted.

STUDY DETAILS:

The study was conducted by Katherine A. Carosella, department of psychology, University of Minnesota, Minneapolis, and colleagues. It was published online in Psychoneuroendocrinology.

LIMITATIONS:

The study was relatively small, and the investigators could not make causal inferences or rule out the possibility that different stages of development affected the data. Measures employed during COVID were not identical to those used in the prepandemic assessment.

DISCLOSURES:

The study received support from the National Institute of Mental Health and the University of Minnesota. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Three big bumps on the weight-loss journey

The search for the Holy Grail. The destruction of the One Ring. The never-ending struggle to Lose Weight.

Like most legendary quests, weight loss is a journey, and we need support to help us achieve our goal. Maybe it’s gaining a new workout partner or finding a similarly-goaled Facebook Group. For a lot of people, it’s as simple as your friends and family. A recent study, however, suggests that the people closest to you may be your worst weight-loss enemies, and they might not even know it.

Spencer Davis/Unsplash

Researchers at the University of Surrey reviewed the literature on the positives and negatives of social support when it comes to weight loss and identified three types of negative effects: acts of sabotage, feeding behavior, and collusion.

Let’s start with the softest of intentions and work our way up. Collusion is the least negative. Friends and family may just go with the flow, even if it doesn’t agree with the goals of the person who’s trying to lose weight. It can even happen when health care professionals try to help their patients navigate or avoid obesity, ultimately killing with kindness, so to speak.

Next up, feeding behavior. Maybe you know someone whose love language is cooking. There are also people who share food because they don’t want to waste it or because they’re trying to be polite. They act out of the goodness of their hearts, but they’re putting up roadblocks to someone’s goals. These types of acts are usually one-sided, the researchers found. Remember, it’s okay to say, “No thanks.”

The last method, sabotage, is the most sinister. The saboteur may discourage others from eating healthy, undermine their efforts to be physically active, or take jabs at their confidence or self-esteem. Something as simple as criticizing someone for eating a salad or refusing to go on a walk with them can cause a setback.

“We need to explore this area further to develop interventions which could target family and friends and help them be more supportive in helping those they are close to lose weight,” said lead author Jane Odgen, PhD, of the University of Surrey, Guildford, England.

Like we said before, weight loss is a journey. The right support can only improve the odds of success.
 

Robots vs. mosquitoes

If there’s one thing robots are bad at, it’s giving solid mental health advice to people in crisis. If there’s one thing robots are very, very good at, it’s causing apocalypses. And joyous day for humanity, this time we’re not the ones being apocalypsed.

Yet.

Liu et al., 2023, PLOS Neglected Tropical Diseases, CC-BY 4.0

Taiwan has a big mosquito problem. Not only do the mosquitoes in Taiwan carry dengue – among other dangerous diseases – but they’ve urbanized. Not urbanized in the sense that they’ve acquired a taste for organic coffee and avocado toast (that would be the millennial mosquito, a separate but even more terrifying creature), but more that they’ve adapted to reproduce literally anywhere and everywhere. Taiwanese mosquitoes like to breed in roadside sewer ditches, and this is where our genocidal robot comes in.

To combat the new, dangerous form of street-savvy mosquito, researchers built a robot armed with both insecticide and high-temperature, high-pressure water jets and sent it into the sewers of Kaohsiung City. The robot’s goal was simple: Whenever it came across signs of heavy mosquito breeding – eggs, larvae, pupae, and so on – the robot went to work. Utilizing both its primary weapons, the robot scrubbed numerous breeding sites across the city clean.

The researchers could just sit back and wait to see how effective their robot was. In the immediate aftermath, at various monitoring sites placed alongside the ditches, adult mosquito density fell by two-thirds in areas targeted by the robot. That’s nothing to sniff at, and it does make sense. After all, mosquitoes are quite difficult to kill in their adult stage, why not target them when they’re young and basically immobile?

The researchers saw promise with their mosquito-killing robot, but we’ve noticed a rather large issue. Killing two-thirds of mosquitoes is fine, but the third that’s left will be very angry. Very angry indeed. After all, we’re targeting the mosquito equivalent of children. Let’s hope our mosquito Terminator managed to kill mosquito Sarah Connor, or we’re going to have a big problem on our hands a bit later down the line.
 

This is knot what you were expecting

Physicians who aren’t surgeons probably don’t realize it, but the big thing that’s been getting between the knot-tying specialists and perfect suturing technique all these years is a lack of physics. Don’t believe us? Well, maybe you’ll believe plastic surgeon Samia Guerid, MD, of Lausanne, Switzerland: “The lack of physics-based analysis has been a limitation.” Nuff said.

Alain Herzog / EPFL

That’s not enough for you, is it? Fine, we were warned.

Any surgical knot, Dr. Guerid and associates explained in a written statement, involves the “complex interplay” between six key factors: topology, geometry, elasticity, contact, friction, and polymer plasticity of the suturing filament. The strength of a suture “depends on the tension applied during the tying of the knot, [which] permanently deforms, or stretches the filament, creating a holding force.” Not enough tension and the knot comes undone, while too much snaps the filament.

For the experiment, Dr. Guerid tied a few dozen surgical knots, which were then scanned using x-ray micro–computed tomography to facilitate finite element modeling with a “3D continuum-level constitutive model for elastic-viscoplastic mechanical behavior” – no, we have no idea what that means, either – developed by the research team.

That model, and a great deal of math – so much math – allowed the researchers to define a threshold between loose and tight knots and uncover “relationships between knot strength and pretension, friction, and number of throws,” they said.

But what about the big question? The one about the ideal amount of tension? You may want to sit down. The answer to the ultimate question of the relationship between knot pretension and strength is … Did we mention that the team had its own mathematician? Their predictive model for safe knot-tying is … You’re not going to like this. The best way to teach safe knot-tying to both trainees and robots is … not ready yet.

The secret to targeting the knot tension sweet spot, for now, anyway, is still intuition gained from years of experience. Nobody ever said science was perfect … or easy … or quick.

Three big bumps on the weight-loss journey

The search for the Holy Grail. The destruction of the One Ring. The never-ending struggle to Lose Weight.

Like most legendary quests, weight loss is a journey, and we need support to help us achieve our goal. Maybe it’s gaining a new workout partner or finding a similarly-goaled Facebook Group. For a lot of people, it’s as simple as your friends and family. A recent study, however, suggests that the people closest to you may be your worst weight-loss enemies, and they might not even know it.

Spencer Davis/Unsplash

Researchers at the University of Surrey reviewed the literature on the positives and negatives of social support when it comes to weight loss and identified three types of negative effects: acts of sabotage, feeding behavior, and collusion.

Let’s start with the softest of intentions and work our way up. Collusion is the least negative. Friends and family may just go with the flow, even if it doesn’t agree with the goals of the person who’s trying to lose weight. It can even happen when health care professionals try to help their patients navigate or avoid obesity, ultimately killing with kindness, so to speak.

Next up, feeding behavior. Maybe you know someone whose love language is cooking. There are also people who share food because they don’t want to waste it or because they’re trying to be polite. They act out of the goodness of their hearts, but they’re putting up roadblocks to someone’s goals. These types of acts are usually one-sided, the researchers found. Remember, it’s okay to say, “No thanks.”

The last method, sabotage, is the most sinister. The saboteur may discourage others from eating healthy, undermine their efforts to be physically active, or take jabs at their confidence or self-esteem. Something as simple as criticizing someone for eating a salad or refusing to go on a walk with them can cause a setback.

“We need to explore this area further to develop interventions which could target family and friends and help them be more supportive in helping those they are close to lose weight,” said lead author Jane Odgen, PhD, of the University of Surrey, Guildford, England.

Like we said before, weight loss is a journey. The right support can only improve the odds of success.
 

Robots vs. mosquitoes

If there’s one thing robots are bad at, it’s giving solid mental health advice to people in crisis. If there’s one thing robots are very, very good at, it’s causing apocalypses. And joyous day for humanity, this time we’re not the ones being apocalypsed.

Yet.

Liu et al., 2023, PLOS Neglected Tropical Diseases, CC-BY 4.0

Taiwan has a big mosquito problem. Not only do the mosquitoes in Taiwan carry dengue – among other dangerous diseases – but they’ve urbanized. Not urbanized in the sense that they’ve acquired a taste for organic coffee and avocado toast (that would be the millennial mosquito, a separate but even more terrifying creature), but more that they’ve adapted to reproduce literally anywhere and everywhere. Taiwanese mosquitoes like to breed in roadside sewer ditches, and this is where our genocidal robot comes in.

To combat the new, dangerous form of street-savvy mosquito, researchers built a robot armed with both insecticide and high-temperature, high-pressure water jets and sent it into the sewers of Kaohsiung City. The robot’s goal was simple: Whenever it came across signs of heavy mosquito breeding – eggs, larvae, pupae, and so on – the robot went to work. Utilizing both its primary weapons, the robot scrubbed numerous breeding sites across the city clean.

The researchers could just sit back and wait to see how effective their robot was. In the immediate aftermath, at various monitoring sites placed alongside the ditches, adult mosquito density fell by two-thirds in areas targeted by the robot. That’s nothing to sniff at, and it does make sense. After all, mosquitoes are quite difficult to kill in their adult stage, why not target them when they’re young and basically immobile?

The researchers saw promise with their mosquito-killing robot, but we’ve noticed a rather large issue. Killing two-thirds of mosquitoes is fine, but the third that’s left will be very angry. Very angry indeed. After all, we’re targeting the mosquito equivalent of children. Let’s hope our mosquito Terminator managed to kill mosquito Sarah Connor, or we’re going to have a big problem on our hands a bit later down the line.
 

This is knot what you were expecting

Physicians who aren’t surgeons probably don’t realize it, but the big thing that’s been getting between the knot-tying specialists and perfect suturing technique all these years is a lack of physics. Don’t believe us? Well, maybe you’ll believe plastic surgeon Samia Guerid, MD, of Lausanne, Switzerland: “The lack of physics-based analysis has been a limitation.” Nuff said.

Alain Herzog / EPFL

That’s not enough for you, is it? Fine, we were warned.

Any surgical knot, Dr. Guerid and associates explained in a written statement, involves the “complex interplay” between six key factors: topology, geometry, elasticity, contact, friction, and polymer plasticity of the suturing filament. The strength of a suture “depends on the tension applied during the tying of the knot, [which] permanently deforms, or stretches the filament, creating a holding force.” Not enough tension and the knot comes undone, while too much snaps the filament.

For the experiment, Dr. Guerid tied a few dozen surgical knots, which were then scanned using x-ray micro–computed tomography to facilitate finite element modeling with a “3D continuum-level constitutive model for elastic-viscoplastic mechanical behavior” – no, we have no idea what that means, either – developed by the research team.

That model, and a great deal of math – so much math – allowed the researchers to define a threshold between loose and tight knots and uncover “relationships between knot strength and pretension, friction, and number of throws,” they said.

But what about the big question? The one about the ideal amount of tension? You may want to sit down. The answer to the ultimate question of the relationship between knot pretension and strength is … Did we mention that the team had its own mathematician? Their predictive model for safe knot-tying is … You’re not going to like this. The best way to teach safe knot-tying to both trainees and robots is … not ready yet.

The secret to targeting the knot tension sweet spot, for now, anyway, is still intuition gained from years of experience. Nobody ever said science was perfect … or easy … or quick.

Three big bumps on the weight-loss journey

The search for the Holy Grail. The destruction of the One Ring. The never-ending struggle to Lose Weight.

Like most legendary quests, weight loss is a journey, and we need support to help us achieve our goal. Maybe it’s gaining a new workout partner or finding a similarly-goaled Facebook Group. For a lot of people, it’s as simple as your friends and family. A recent study, however, suggests that the people closest to you may be your worst weight-loss enemies, and they might not even know it.

Spencer Davis/Unsplash

Researchers at the University of Surrey reviewed the literature on the positives and negatives of social support when it comes to weight loss and identified three types of negative effects: acts of sabotage, feeding behavior, and collusion.

Let’s start with the softest of intentions and work our way up. Collusion is the least negative. Friends and family may just go with the flow, even if it doesn’t agree with the goals of the person who’s trying to lose weight. It can even happen when health care professionals try to help their patients navigate or avoid obesity, ultimately killing with kindness, so to speak.

Next up, feeding behavior. Maybe you know someone whose love language is cooking. There are also people who share food because they don’t want to waste it or because they’re trying to be polite. They act out of the goodness of their hearts, but they’re putting up roadblocks to someone’s goals. These types of acts are usually one-sided, the researchers found. Remember, it’s okay to say, “No thanks.”

The last method, sabotage, is the most sinister. The saboteur may discourage others from eating healthy, undermine their efforts to be physically active, or take jabs at their confidence or self-esteem. Something as simple as criticizing someone for eating a salad or refusing to go on a walk with them can cause a setback.

“We need to explore this area further to develop interventions which could target family and friends and help them be more supportive in helping those they are close to lose weight,” said lead author Jane Odgen, PhD, of the University of Surrey, Guildford, England.

Like we said before, weight loss is a journey. The right support can only improve the odds of success.
 

Robots vs. mosquitoes

If there’s one thing robots are bad at, it’s giving solid mental health advice to people in crisis. If there’s one thing robots are very, very good at, it’s causing apocalypses. And joyous day for humanity, this time we’re not the ones being apocalypsed.

Yet.

Liu et al., 2023, PLOS Neglected Tropical Diseases, CC-BY 4.0

Taiwan has a big mosquito problem. Not only do the mosquitoes in Taiwan carry dengue – among other dangerous diseases – but they’ve urbanized. Not urbanized in the sense that they’ve acquired a taste for organic coffee and avocado toast (that would be the millennial mosquito, a separate but even more terrifying creature), but more that they’ve adapted to reproduce literally anywhere and everywhere. Taiwanese mosquitoes like to breed in roadside sewer ditches, and this is where our genocidal robot comes in.

To combat the new, dangerous form of street-savvy mosquito, researchers built a robot armed with both insecticide and high-temperature, high-pressure water jets and sent it into the sewers of Kaohsiung City. The robot’s goal was simple: Whenever it came across signs of heavy mosquito breeding – eggs, larvae, pupae, and so on – the robot went to work. Utilizing both its primary weapons, the robot scrubbed numerous breeding sites across the city clean.

The researchers could just sit back and wait to see how effective their robot was. In the immediate aftermath, at various monitoring sites placed alongside the ditches, adult mosquito density fell by two-thirds in areas targeted by the robot. That’s nothing to sniff at, and it does make sense. After all, mosquitoes are quite difficult to kill in their adult stage, why not target them when they’re young and basically immobile?

The researchers saw promise with their mosquito-killing robot, but we’ve noticed a rather large issue. Killing two-thirds of mosquitoes is fine, but the third that’s left will be very angry. Very angry indeed. After all, we’re targeting the mosquito equivalent of children. Let’s hope our mosquito Terminator managed to kill mosquito Sarah Connor, or we’re going to have a big problem on our hands a bit later down the line.
 

This is knot what you were expecting

Physicians who aren’t surgeons probably don’t realize it, but the big thing that’s been getting between the knot-tying specialists and perfect suturing technique all these years is a lack of physics. Don’t believe us? Well, maybe you’ll believe plastic surgeon Samia Guerid, MD, of Lausanne, Switzerland: “The lack of physics-based analysis has been a limitation.” Nuff said.

Alain Herzog / EPFL

That’s not enough for you, is it? Fine, we were warned.

Any surgical knot, Dr. Guerid and associates explained in a written statement, involves the “complex interplay” between six key factors: topology, geometry, elasticity, contact, friction, and polymer plasticity of the suturing filament. The strength of a suture “depends on the tension applied during the tying of the knot, [which] permanently deforms, or stretches the filament, creating a holding force.” Not enough tension and the knot comes undone, while too much snaps the filament.

For the experiment, Dr. Guerid tied a few dozen surgical knots, which were then scanned using x-ray micro–computed tomography to facilitate finite element modeling with a “3D continuum-level constitutive model for elastic-viscoplastic mechanical behavior” – no, we have no idea what that means, either – developed by the research team.

That model, and a great deal of math – so much math – allowed the researchers to define a threshold between loose and tight knots and uncover “relationships between knot strength and pretension, friction, and number of throws,” they said.

But what about the big question? The one about the ideal amount of tension? You may want to sit down. The answer to the ultimate question of the relationship between knot pretension and strength is … Did we mention that the team had its own mathematician? Their predictive model for safe knot-tying is … You’re not going to like this. The best way to teach safe knot-tying to both trainees and robots is … not ready yet.

The secret to targeting the knot tension sweet spot, for now, anyway, is still intuition gained from years of experience. Nobody ever said science was perfect … or easy … or quick.

A bill in the Maine legislature would have the medical malpractice statute of limitations clock start running when a patient discovers the negligence, which could be years after treatment took place. And other states could follow suit with similar bills. What danger does this pose for doctors?

As it stands, the time limit for patients to be able to bring a medical malpractice lawsuit varies by state. The bill that was introduced in Maine would enable patients to bring suits many years after treatment took place. For physicians, this extends their period of liability and could potentially increase the number of lawsuits against them.

“The theory behind a statute of limitations is that states want to provide a reasonable, but not indefinite, amount of time for someone to bring a case to court,” says Patrick T. O’Rourke, Esq., adjunct professor at University of Colorado School of Law, Boulder.

Without a statute of limitations, people could bring claims many years after the fact, which makes it harder to obtain and preserve evidence, Mr. O’Rourke says.

In most cases, it isn’t necessary for a patient to know the full extent of their injury or that their physician acted wrongfully or negligently for the statute of limitations to begin running.
 

Time of injury versus time of discovery

Most states’ laws dictate that the statute of limitations begins at a set time “after the cause of action accrues.” That means that the clock starts ticking from the date of the procedure, surgery, or treatment. In most states, that time is 2 or 3 years.

This can bar some patients from taking any action at all because the statute of limitations ran out. Because of these hurdles, the proposed bill in Maine would extend the statute of limitations.

Proponents of the bill say that patients would still have 3 years to file suit; it just changes when the clock starts. But opponents feel it could open the door to a limitless system in which people have an indefinite time to sue.

Many states already have discovery rules that extend the statute of limitations when the harm was not immediately obvious to the patient. The legal expectation is that patients who have significant pain or unexpected health conditions will seek medical treatment to investigate what’s wrong. Patients who don’t address the situation promptly are not protected by the discovery rule.

“It is the injured person’s obligation, once learning of the injury, to take action to protect their rights,” says Mr. O’Rourke.

Some states have also enacted other claims requirements in medical malpractice cases that are prerequisites for bringing lawsuits that have periods attached to them. For instance, in Florida, parties have 10 days to provide relevant medical records during the investigation period for a malpractice suit, and in Maine, before filing any malpractice action, a plaintiff must file a complaint with a prelitigation screening panel.
 

Medical malpractice statutes of limitations by state

Although each state has a basic statute of limitations, many states also include clauses for discovery rules. For example, in Vermont, in addition to the 3-year statute of limitations, a patient can pursue legal recourse “2 years from the date the injury is or reasonably should have been discovered, whichever occurs later, but not later than 7 years from the date of the incident.”

In some states, such as Virginia, special extensions apply in cases in which fraud, concealment, or intentional misrepresentation prevented discovery of the injury within the statute of limitations. And in most states, the statute of limitations is much longer for cases in which medical malpractice involves a child, usually at least until the child turns 18.
 

Statutes of limitations by state

1 Year: California, Kentucky, Louisiana, Ohio, Tennessee

2 Years: Alabama, Alaska, Arizona, Arkansas, Colorado, Connecticut, Delaware, Florida, Georgia, Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Michigan, Mississippi, Missouri, Nebraska, New Hampshire, New Jersey, North Dakota, Oklahoma, Oregon, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wyoming

2.5 Years: New York

3 Years: Washington D.C., Maine, Maryland, Massachusetts, Montana, Nevada, New Mexico, North Carolina, Rhode Island, South Carolina, Vermont, Washington, Wisconsin

4 Years: Minnesota
 

To protect yourself

Mr. O’Rourke says that if your state enacts a law that extends the statute of limitations for medical malpractice, there aren’t any proactive changes you need to make in terms of your day-to-day practice of medicine.

“Physicians should continue to provide care that is consistent with the standards of care for their specialty and ensure that the documentation accurately reflects the care they rendered,” he says.

Always be candid and up-front about a patient’s condition, Mr. O’Rourke says, especially if malpractice is on the table.

“If a physician misleads a patient about the nature or extent of an injury, that could prevent the statute of limitations from beginning to run,” he says. “Being open and honest about an injury doesn’t mean that a physician must admit any fault. The patient is owed timely, accurate, and candid information about their condition.”
 

Keep good records

If the statute of limitations increases, you’ll need to have access to the medical records for as long as the statute is in place, but this shouldn’t have an effect on your records keeping if you’re up to date with HIPAA compliance, says Mr. O’Rourke.

“I don’t think an extension of the statute should cause physicians to change their practices, particularly with the retention of medical records, which should be maintained consistently with HIPAA requirements irrespective of the limitations period in a particular state,” he adds.
 

Keep an eye on malpractice insurance rates

It’s possible that your malpractice insurance could go up as a result of laws that increase the statute of limitations. But Mr. O’Rourke thinks it likely won’t be a significant amount.

He says it’s “theoretically possible” that an increase in a limitations period could result in an increase in your malpractice insurance, since some claims that would otherwise have been barred because of time could then proceed, but the increase would be nominal.

“I would expect any increase to be fairly marginal because the majority of claims will already be accounted for on an actuarial basis,” he says. “I also don’t think that the extension of a limitations period would increase the award of damages in a particular case. The injuries should be the same under either limitations period, so the compensable loss should not increase.”

Anything that makes it easier for patients to recover should increase the cost of professional liability insurance, and vice versa, says Charles Silver, McDonald Endowed Chair in Civil Procedure at University of Texas at Austin School of Law and coauthor of “Medical Malpractice Litigation: How It Works – Why Tort Reform Hasn’t Helped.” But the long-term trend across the country is toward declining rates of liability and declining payouts on claims.

“The likelihood of being sued successfully by a former patient is low, as is the risk of having to pay out of pocket to settle a claim,” he says. In 2022, the number of adverse reports nationally was 38,938, and out of those, 10,807 resulted in a payout.

In his research on medical malpractice in Texas, Mr. Silver says physicians who carried $1 million in coverage essentially never faced any personal liability on medical malpractice claims. “[This means] that they never had to write a check to a victim,” he says. “Insurers provided all the money. I suspect that the same is true nationwide.”
 

Key takeaways

Ultimately, to protect yourself and your practice, you can do the following:

• Know the statute of limitations and discovery rules for your state.
• Review your coverage with your insurer to better understand your liability.
• Keep accurate records for as long as your statute requires.
• Notify your insurer or risk management department as soon as possible in the event of an adverse outcome with a patient, Mr. O’Rourke advises.

“The most important thing a physician can do to avoid being sued, even when negligent, is to treat patients with kindness and respect,” says Mr. Silver. “Patients don’t expect doctors to be perfect, and they rarely sue doctors they like.”

A version of this article first appeared on Medscape.com.

A bill in the Maine legislature would have the medical malpractice statute of limitations clock start running when a patient discovers the negligence, which could be years after treatment took place. And other states could follow suit with similar bills. What danger does this pose for doctors?

As it stands, the time limit for patients to be able to bring a medical malpractice lawsuit varies by state. The bill that was introduced in Maine would enable patients to bring suits many years after treatment took place. For physicians, this extends their period of liability and could potentially increase the number of lawsuits against them.

“The theory behind a statute of limitations is that states want to provide a reasonable, but not indefinite, amount of time for someone to bring a case to court,” says Patrick T. O’Rourke, Esq., adjunct professor at University of Colorado School of Law, Boulder.

Without a statute of limitations, people could bring claims many years after the fact, which makes it harder to obtain and preserve evidence, Mr. O’Rourke says.

In most cases, it isn’t necessary for a patient to know the full extent of their injury or that their physician acted wrongfully or negligently for the statute of limitations to begin running.
 

Time of injury versus time of discovery

Most states’ laws dictate that the statute of limitations begins at a set time “after the cause of action accrues.” That means that the clock starts ticking from the date of the procedure, surgery, or treatment. In most states, that time is 2 or 3 years.

This can bar some patients from taking any action at all because the statute of limitations ran out. Because of these hurdles, the proposed bill in Maine would extend the statute of limitations.

Proponents of the bill say that patients would still have 3 years to file suit; it just changes when the clock starts. But opponents feel it could open the door to a limitless system in which people have an indefinite time to sue.

Many states already have discovery rules that extend the statute of limitations when the harm was not immediately obvious to the patient. The legal expectation is that patients who have significant pain or unexpected health conditions will seek medical treatment to investigate what’s wrong. Patients who don’t address the situation promptly are not protected by the discovery rule.

“It is the injured person’s obligation, once learning of the injury, to take action to protect their rights,” says Mr. O’Rourke.

Some states have also enacted other claims requirements in medical malpractice cases that are prerequisites for bringing lawsuits that have periods attached to them. For instance, in Florida, parties have 10 days to provide relevant medical records during the investigation period for a malpractice suit, and in Maine, before filing any malpractice action, a plaintiff must file a complaint with a prelitigation screening panel.
 

Medical malpractice statutes of limitations by state

Although each state has a basic statute of limitations, many states also include clauses for discovery rules. For example, in Vermont, in addition to the 3-year statute of limitations, a patient can pursue legal recourse “2 years from the date the injury is or reasonably should have been discovered, whichever occurs later, but not later than 7 years from the date of the incident.”

In some states, such as Virginia, special extensions apply in cases in which fraud, concealment, or intentional misrepresentation prevented discovery of the injury within the statute of limitations. And in most states, the statute of limitations is much longer for cases in which medical malpractice involves a child, usually at least until the child turns 18.
 

Statutes of limitations by state

1 Year: California, Kentucky, Louisiana, Ohio, Tennessee

2 Years: Alabama, Alaska, Arizona, Arkansas, Colorado, Connecticut, Delaware, Florida, Georgia, Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Michigan, Mississippi, Missouri, Nebraska, New Hampshire, New Jersey, North Dakota, Oklahoma, Oregon, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wyoming

2.5 Years: New York

3 Years: Washington D.C., Maine, Maryland, Massachusetts, Montana, Nevada, New Mexico, North Carolina, Rhode Island, South Carolina, Vermont, Washington, Wisconsin

4 Years: Minnesota
 

To protect yourself

Mr. O’Rourke says that if your state enacts a law that extends the statute of limitations for medical malpractice, there aren’t any proactive changes you need to make in terms of your day-to-day practice of medicine.

“Physicians should continue to provide care that is consistent with the standards of care for their specialty and ensure that the documentation accurately reflects the care they rendered,” he says.

Always be candid and up-front about a patient’s condition, Mr. O’Rourke says, especially if malpractice is on the table.

“If a physician misleads a patient about the nature or extent of an injury, that could prevent the statute of limitations from beginning to run,” he says. “Being open and honest about an injury doesn’t mean that a physician must admit any fault. The patient is owed timely, accurate, and candid information about their condition.”
 

Keep good records

If the statute of limitations increases, you’ll need to have access to the medical records for as long as the statute is in place, but this shouldn’t have an effect on your records keeping if you’re up to date with HIPAA compliance, says Mr. O’Rourke.

“I don’t think an extension of the statute should cause physicians to change their practices, particularly with the retention of medical records, which should be maintained consistently with HIPAA requirements irrespective of the limitations period in a particular state,” he adds.
 

Keep an eye on malpractice insurance rates

It’s possible that your malpractice insurance could go up as a result of laws that increase the statute of limitations. But Mr. O’Rourke thinks it likely won’t be a significant amount.

He says it’s “theoretically possible” that an increase in a limitations period could result in an increase in your malpractice insurance, since some claims that would otherwise have been barred because of time could then proceed, but the increase would be nominal.

“I would expect any increase to be fairly marginal because the majority of claims will already be accounted for on an actuarial basis,” he says. “I also don’t think that the extension of a limitations period would increase the award of damages in a particular case. The injuries should be the same under either limitations period, so the compensable loss should not increase.”

Anything that makes it easier for patients to recover should increase the cost of professional liability insurance, and vice versa, says Charles Silver, McDonald Endowed Chair in Civil Procedure at University of Texas at Austin School of Law and coauthor of “Medical Malpractice Litigation: How It Works – Why Tort Reform Hasn’t Helped.” But the long-term trend across the country is toward declining rates of liability and declining payouts on claims.

“The likelihood of being sued successfully by a former patient is low, as is the risk of having to pay out of pocket to settle a claim,” he says. In 2022, the number of adverse reports nationally was 38,938, and out of those, 10,807 resulted in a payout.

In his research on medical malpractice in Texas, Mr. Silver says physicians who carried $1 million in coverage essentially never faced any personal liability on medical malpractice claims. “[This means] that they never had to write a check to a victim,” he says. “Insurers provided all the money. I suspect that the same is true nationwide.”
 

Key takeaways

Ultimately, to protect yourself and your practice, you can do the following:

• Know the statute of limitations and discovery rules for your state.
• Review your coverage with your insurer to better understand your liability.
• Keep accurate records for as long as your statute requires.
• Notify your insurer or risk management department as soon as possible in the event of an adverse outcome with a patient, Mr. O’Rourke advises.

“The most important thing a physician can do to avoid being sued, even when negligent, is to treat patients with kindness and respect,” says Mr. Silver. “Patients don’t expect doctors to be perfect, and they rarely sue doctors they like.”

A version of this article first appeared on Medscape.com.

A bill in the Maine legislature would have the medical malpractice statute of limitations clock start running when a patient discovers the negligence, which could be years after treatment took place. And other states could follow suit with similar bills. What danger does this pose for doctors?

As it stands, the time limit for patients to be able to bring a medical malpractice lawsuit varies by state. The bill that was introduced in Maine would enable patients to bring suits many years after treatment took place. For physicians, this extends their period of liability and could potentially increase the number of lawsuits against them.

“The theory behind a statute of limitations is that states want to provide a reasonable, but not indefinite, amount of time for someone to bring a case to court,” says Patrick T. O’Rourke, Esq., adjunct professor at University of Colorado School of Law, Boulder.

Without a statute of limitations, people could bring claims many years after the fact, which makes it harder to obtain and preserve evidence, Mr. O’Rourke says.

In most cases, it isn’t necessary for a patient to know the full extent of their injury or that their physician acted wrongfully or negligently for the statute of limitations to begin running.
 

Time of injury versus time of discovery

Most states’ laws dictate that the statute of limitations begins at a set time “after the cause of action accrues.” That means that the clock starts ticking from the date of the procedure, surgery, or treatment. In most states, that time is 2 or 3 years.

This can bar some patients from taking any action at all because the statute of limitations ran out. Because of these hurdles, the proposed bill in Maine would extend the statute of limitations.

Proponents of the bill say that patients would still have 3 years to file suit; it just changes when the clock starts. But opponents feel it could open the door to a limitless system in which people have an indefinite time to sue.

Many states already have discovery rules that extend the statute of limitations when the harm was not immediately obvious to the patient. The legal expectation is that patients who have significant pain or unexpected health conditions will seek medical treatment to investigate what’s wrong. Patients who don’t address the situation promptly are not protected by the discovery rule.

“It is the injured person’s obligation, once learning of the injury, to take action to protect their rights,” says Mr. O’Rourke.

Some states have also enacted other claims requirements in medical malpractice cases that are prerequisites for bringing lawsuits that have periods attached to them. For instance, in Florida, parties have 10 days to provide relevant medical records during the investigation period for a malpractice suit, and in Maine, before filing any malpractice action, a plaintiff must file a complaint with a prelitigation screening panel.
 

Medical malpractice statutes of limitations by state

Although each state has a basic statute of limitations, many states also include clauses for discovery rules. For example, in Vermont, in addition to the 3-year statute of limitations, a patient can pursue legal recourse “2 years from the date the injury is or reasonably should have been discovered, whichever occurs later, but not later than 7 years from the date of the incident.”

In some states, such as Virginia, special extensions apply in cases in which fraud, concealment, or intentional misrepresentation prevented discovery of the injury within the statute of limitations. And in most states, the statute of limitations is much longer for cases in which medical malpractice involves a child, usually at least until the child turns 18.
 

Statutes of limitations by state

1 Year: California, Kentucky, Louisiana, Ohio, Tennessee

2 Years: Alabama, Alaska, Arizona, Arkansas, Colorado, Connecticut, Delaware, Florida, Georgia, Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Michigan, Mississippi, Missouri, Nebraska, New Hampshire, New Jersey, North Dakota, Oklahoma, Oregon, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wyoming

2.5 Years: New York

3 Years: Washington D.C., Maine, Maryland, Massachusetts, Montana, Nevada, New Mexico, North Carolina, Rhode Island, South Carolina, Vermont, Washington, Wisconsin

4 Years: Minnesota
 

To protect yourself

Mr. O’Rourke says that if your state enacts a law that extends the statute of limitations for medical malpractice, there aren’t any proactive changes you need to make in terms of your day-to-day practice of medicine.

“Physicians should continue to provide care that is consistent with the standards of care for their specialty and ensure that the documentation accurately reflects the care they rendered,” he says.

Always be candid and up-front about a patient’s condition, Mr. O’Rourke says, especially if malpractice is on the table.

“If a physician misleads a patient about the nature or extent of an injury, that could prevent the statute of limitations from beginning to run,” he says. “Being open and honest about an injury doesn’t mean that a physician must admit any fault. The patient is owed timely, accurate, and candid information about their condition.”
 

Keep good records

If the statute of limitations increases, you’ll need to have access to the medical records for as long as the statute is in place, but this shouldn’t have an effect on your records keeping if you’re up to date with HIPAA compliance, says Mr. O’Rourke.

“I don’t think an extension of the statute should cause physicians to change their practices, particularly with the retention of medical records, which should be maintained consistently with HIPAA requirements irrespective of the limitations period in a particular state,” he adds.
 

Keep an eye on malpractice insurance rates

It’s possible that your malpractice insurance could go up as a result of laws that increase the statute of limitations. But Mr. O’Rourke thinks it likely won’t be a significant amount.

He says it’s “theoretically possible” that an increase in a limitations period could result in an increase in your malpractice insurance, since some claims that would otherwise have been barred because of time could then proceed, but the increase would be nominal.

“I would expect any increase to be fairly marginal because the majority of claims will already be accounted for on an actuarial basis,” he says. “I also don’t think that the extension of a limitations period would increase the award of damages in a particular case. The injuries should be the same under either limitations period, so the compensable loss should not increase.”

Anything that makes it easier for patients to recover should increase the cost of professional liability insurance, and vice versa, says Charles Silver, McDonald Endowed Chair in Civil Procedure at University of Texas at Austin School of Law and coauthor of “Medical Malpractice Litigation: How It Works – Why Tort Reform Hasn’t Helped.” But the long-term trend across the country is toward declining rates of liability and declining payouts on claims.

“The likelihood of being sued successfully by a former patient is low, as is the risk of having to pay out of pocket to settle a claim,” he says. In 2022, the number of adverse reports nationally was 38,938, and out of those, 10,807 resulted in a payout.

In his research on medical malpractice in Texas, Mr. Silver says physicians who carried $1 million in coverage essentially never faced any personal liability on medical malpractice claims. “[This means] that they never had to write a check to a victim,” he says. “Insurers provided all the money. I suspect that the same is true nationwide.”
 

Key takeaways

Ultimately, to protect yourself and your practice, you can do the following:

• Know the statute of limitations and discovery rules for your state.
• Review your coverage with your insurer to better understand your liability.
• Keep accurate records for as long as your statute requires.
• Notify your insurer or risk management department as soon as possible in the event of an adverse outcome with a patient, Mr. O’Rourke advises.

“The most important thing a physician can do to avoid being sued, even when negligent, is to treat patients with kindness and respect,” says Mr. Silver. “Patients don’t expect doctors to be perfect, and they rarely sue doctors they like.”

A version of this article first appeared on Medscape.com.

Insomnia may increase vulnerability to influenza-like illness, a novel finding that was revealed by the passive collection of biometric data from a smart bed.

The study of smart-bed sleepers found that there was a statistically significant correlation between a higher number of episodes of influenza-like illnesses (ILI) per year with longer duration compared to people without insomnia.

However, more research is needed to determine causality and whether insomnia may predispose to ILI or whether ILI affects long-term sleep behavior, the researchers noted. 

“Several lines of evidence make me think that it’s more likely that insomnia makes one more vulnerable to influenza through pathways that involve decreased immune function,” study investigator Gary Garcia-Molina, PhD, with Sleep Number Labs, San Jose, Calif., said in an interview.

Sleep disorders, including insomnia, can dampen immune function and an individual’s ability to fight off illness, he noted.

The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
 

Smart, connected devices

Pathophysiological responses to respiratory viral infection affect sleep duration and quality in addition to breathing function. “Smart” and “connected” devices that monitor biosignals over time have shown promise for monitoring infectious disease.

In an earlier study presented at SLEEP 2021, Dr. Garcia-Molina and colleagues found that real-world biometric data obtained from a smart bed can help predict and track symptoms of COVID-19 and other respiratory infections. They showed that worsening of COVID-19 symptoms correlated with an increase in sleep duration, breathing rate, and heart rate and a decrease in sleep quality.

In the new study, the researchers evaluated vulnerability to ILI in people with insomnia.

They quantified insomnia over time using the insomnia severity index (ISI). They quantified ILI vulnerability using an established artificial intelligence model they developed that estimates the daily probability of ILI symptoms from a Sleep Number smart bed using ballistocardiograph sensors.

Smart bed data – including daily and restful sleep duration, sleep latency, sleep quality, heart rate, breathing rate and motion level – were queried from 2019 (pre-COVID) and 2021.

A total of 1,680 smart sleepers had nearly constant ISI scores over the study period, with 249 having insomnia and 1,431 not having insomnia.

Data from both 2019 and 2021 show that smart sleepers with insomnia had significantly more and longer ILI episodes per year, compared with peers without insomnia.

For 2019, individuals without insomnia had 1.2 ILI episodes on average, which was significantly less (P < .01) than individuals with insomnia, at 1.5 episodes. The average ILI episode duration for those without insomnia was 4.3 days, which was significantly lower (P < .01) in those with insomnia group, at 6.1 days.

The data for 2021 show similar results, with the no-insomnia group having significantly fewer (P < .01) ILI episodes (about 1.2), compared with the insomnia group (about 1.5).

The average ILI episode duration for the no-insomnia group was 5 days, which was significantly less (P < .01) than the insomnia group, at 6.1 days.

The researchers said their study adds to other data on the relationship between sleep and overall health and well-being. It also highlights the potential health risk of insomnia and the importance of identifying and treating sleep disorders.

“Sleep has such a profound influence on health and wellness and the ability to capture these data unobtrusively in such an easy way and with such a large number of participants paves the way to investigate different aspects of health and disease,” Dr. Garcia-Molina said.
 

Rich data source

In a comment, Adam C. Powell, PhD, president of Payer+Provider Syndicate, a management advisory and operational consulting firm, said “smart beds provide a new data source for passively monitoring the health of individuals.”

“Unlike active monitoring methods requiring self-report, passive monitoring enables data to be captured without an individual taking any action. This data can be potentially integrated with data from other sources, such as pedometers, smart scales, and smart blood pressure cuffs, to gain a more holistic understanding of how an individual’s activities and behaviors impact their well-being,” said Dr. Powell, who wasn’t involved in the study.

There are some methodological limitations to the study, he noted.

“While the dependent variables examined were the duration and presence of episodes of influenza-like illness, they did not directly measure these episodes. Instead, they calculated the daily probability of influenza-like illness symptoms using a model that received input from the ballistocardiograph sensors in the smart beds,” Dr. Powell noted.

“The model used to calculate daily probability of influenza-like illness was created by examining associations between individuals’ smart-bed sensor data and population-level trends in influenza-like illness reported by the Centers for Disease Control and Prevention,” he explained.

Nonetheless, the findings are “consistent with the literature. It has been established by other researchers that impaired sleep is associated with greater risk of influenza, as well as other illnesses,” Dr. Powell said.

Funding for the study was provided by Sleep Number. Dr. Garcia-Molina and five coauthors are employed by Sleep Number. Dr. Powell reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Insomnia may increase vulnerability to influenza-like illness, a novel finding that was revealed by the passive collection of biometric data from a smart bed.

The study of smart-bed sleepers found that there was a statistically significant correlation between a higher number of episodes of influenza-like illnesses (ILI) per year with longer duration compared to people without insomnia.

However, more research is needed to determine causality and whether insomnia may predispose to ILI or whether ILI affects long-term sleep behavior, the researchers noted. 

“Several lines of evidence make me think that it’s more likely that insomnia makes one more vulnerable to influenza through pathways that involve decreased immune function,” study investigator Gary Garcia-Molina, PhD, with Sleep Number Labs, San Jose, Calif., said in an interview.

Sleep disorders, including insomnia, can dampen immune function and an individual’s ability to fight off illness, he noted.

The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
 

Smart, connected devices

Pathophysiological responses to respiratory viral infection affect sleep duration and quality in addition to breathing function. “Smart” and “connected” devices that monitor biosignals over time have shown promise for monitoring infectious disease.

In an earlier study presented at SLEEP 2021, Dr. Garcia-Molina and colleagues found that real-world biometric data obtained from a smart bed can help predict and track symptoms of COVID-19 and other respiratory infections. They showed that worsening of COVID-19 symptoms correlated with an increase in sleep duration, breathing rate, and heart rate and a decrease in sleep quality.

In the new study, the researchers evaluated vulnerability to ILI in people with insomnia.

They quantified insomnia over time using the insomnia severity index (ISI). They quantified ILI vulnerability using an established artificial intelligence model they developed that estimates the daily probability of ILI symptoms from a Sleep Number smart bed using ballistocardiograph sensors.

Smart bed data – including daily and restful sleep duration, sleep latency, sleep quality, heart rate, breathing rate and motion level – were queried from 2019 (pre-COVID) and 2021.

A total of 1,680 smart sleepers had nearly constant ISI scores over the study period, with 249 having insomnia and 1,431 not having insomnia.

Data from both 2019 and 2021 show that smart sleepers with insomnia had significantly more and longer ILI episodes per year, compared with peers without insomnia.

For 2019, individuals without insomnia had 1.2 ILI episodes on average, which was significantly less (P < .01) than individuals with insomnia, at 1.5 episodes. The average ILI episode duration for those without insomnia was 4.3 days, which was significantly lower (P < .01) in those with insomnia group, at 6.1 days.

The data for 2021 show similar results, with the no-insomnia group having significantly fewer (P < .01) ILI episodes (about 1.2), compared with the insomnia group (about 1.5).

The average ILI episode duration for the no-insomnia group was 5 days, which was significantly less (P < .01) than the insomnia group, at 6.1 days.

The researchers said their study adds to other data on the relationship between sleep and overall health and well-being. It also highlights the potential health risk of insomnia and the importance of identifying and treating sleep disorders.

“Sleep has such a profound influence on health and wellness and the ability to capture these data unobtrusively in such an easy way and with such a large number of participants paves the way to investigate different aspects of health and disease,” Dr. Garcia-Molina said.
 

Rich data source

In a comment, Adam C. Powell, PhD, president of Payer+Provider Syndicate, a management advisory and operational consulting firm, said “smart beds provide a new data source for passively monitoring the health of individuals.”

“Unlike active monitoring methods requiring self-report, passive monitoring enables data to be captured without an individual taking any action. This data can be potentially integrated with data from other sources, such as pedometers, smart scales, and smart blood pressure cuffs, to gain a more holistic understanding of how an individual’s activities and behaviors impact their well-being,” said Dr. Powell, who wasn’t involved in the study.

There are some methodological limitations to the study, he noted.

“While the dependent variables examined were the duration and presence of episodes of influenza-like illness, they did not directly measure these episodes. Instead, they calculated the daily probability of influenza-like illness symptoms using a model that received input from the ballistocardiograph sensors in the smart beds,” Dr. Powell noted.

“The model used to calculate daily probability of influenza-like illness was created by examining associations between individuals’ smart-bed sensor data and population-level trends in influenza-like illness reported by the Centers for Disease Control and Prevention,” he explained.

Nonetheless, the findings are “consistent with the literature. It has been established by other researchers that impaired sleep is associated with greater risk of influenza, as well as other illnesses,” Dr. Powell said.

Funding for the study was provided by Sleep Number. Dr. Garcia-Molina and five coauthors are employed by Sleep Number. Dr. Powell reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Insomnia may increase vulnerability to influenza-like illness, a novel finding that was revealed by the passive collection of biometric data from a smart bed.

The study of smart-bed sleepers found that there was a statistically significant correlation between a higher number of episodes of influenza-like illnesses (ILI) per year with longer duration compared to people without insomnia.

However, more research is needed to determine causality and whether insomnia may predispose to ILI or whether ILI affects long-term sleep behavior, the researchers noted. 

“Several lines of evidence make me think that it’s more likely that insomnia makes one more vulnerable to influenza through pathways that involve decreased immune function,” study investigator Gary Garcia-Molina, PhD, with Sleep Number Labs, San Jose, Calif., said in an interview.

Sleep disorders, including insomnia, can dampen immune function and an individual’s ability to fight off illness, he noted.

The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
 

Smart, connected devices

Pathophysiological responses to respiratory viral infection affect sleep duration and quality in addition to breathing function. “Smart” and “connected” devices that monitor biosignals over time have shown promise for monitoring infectious disease.

In an earlier study presented at SLEEP 2021, Dr. Garcia-Molina and colleagues found that real-world biometric data obtained from a smart bed can help predict and track symptoms of COVID-19 and other respiratory infections. They showed that worsening of COVID-19 symptoms correlated with an increase in sleep duration, breathing rate, and heart rate and a decrease in sleep quality.

In the new study, the researchers evaluated vulnerability to ILI in people with insomnia.

They quantified insomnia over time using the insomnia severity index (ISI). They quantified ILI vulnerability using an established artificial intelligence model they developed that estimates the daily probability of ILI symptoms from a Sleep Number smart bed using ballistocardiograph sensors.

Smart bed data – including daily and restful sleep duration, sleep latency, sleep quality, heart rate, breathing rate and motion level – were queried from 2019 (pre-COVID) and 2021.

A total of 1,680 smart sleepers had nearly constant ISI scores over the study period, with 249 having insomnia and 1,431 not having insomnia.

Data from both 2019 and 2021 show that smart sleepers with insomnia had significantly more and longer ILI episodes per year, compared with peers without insomnia.

For 2019, individuals without insomnia had 1.2 ILI episodes on average, which was significantly less (P < .01) than individuals with insomnia, at 1.5 episodes. The average ILI episode duration for those without insomnia was 4.3 days, which was significantly lower (P < .01) in those with insomnia group, at 6.1 days.

The data for 2021 show similar results, with the no-insomnia group having significantly fewer (P < .01) ILI episodes (about 1.2), compared with the insomnia group (about 1.5).

The average ILI episode duration for the no-insomnia group was 5 days, which was significantly less (P < .01) than the insomnia group, at 6.1 days.

The researchers said their study adds to other data on the relationship between sleep and overall health and well-being. It also highlights the potential health risk of insomnia and the importance of identifying and treating sleep disorders.

“Sleep has such a profound influence on health and wellness and the ability to capture these data unobtrusively in such an easy way and with such a large number of participants paves the way to investigate different aspects of health and disease,” Dr. Garcia-Molina said.
 

Rich data source

In a comment, Adam C. Powell, PhD, president of Payer+Provider Syndicate, a management advisory and operational consulting firm, said “smart beds provide a new data source for passively monitoring the health of individuals.”

“Unlike active monitoring methods requiring self-report, passive monitoring enables data to be captured without an individual taking any action. This data can be potentially integrated with data from other sources, such as pedometers, smart scales, and smart blood pressure cuffs, to gain a more holistic understanding of how an individual’s activities and behaviors impact their well-being,” said Dr. Powell, who wasn’t involved in the study.

There are some methodological limitations to the study, he noted.

“While the dependent variables examined were the duration and presence of episodes of influenza-like illness, they did not directly measure these episodes. Instead, they calculated the daily probability of influenza-like illness symptoms using a model that received input from the ballistocardiograph sensors in the smart beds,” Dr. Powell noted.

“The model used to calculate daily probability of influenza-like illness was created by examining associations between individuals’ smart-bed sensor data and population-level trends in influenza-like illness reported by the Centers for Disease Control and Prevention,” he explained.

Nonetheless, the findings are “consistent with the literature. It has been established by other researchers that impaired sleep is associated with greater risk of influenza, as well as other illnesses,” Dr. Powell said.

Funding for the study was provided by Sleep Number. Dr. Garcia-Molina and five coauthors are employed by Sleep Number. Dr. Powell reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Not everyone will suffer an episode of posttraumatic stress disorder, even though everyday American life is characterized by a lot of uncertainty these days, particularly considering the proliferation of gun violence.

Robert T. London

Also, everyone who does experience a traumatic event will not suffer an episode of PTSD – just as not everyone develops a heart attack or cancer, nor will everyone get every illness.

The data suggest that of those exposed to trauma, up to 25% of people will develop PTSD, according to Massachusetts General/McLean Hospital, Belmont, psychiatrist Kerry J. Ressler, MD, PhD, chief of the division of depression and anxiety disorders.

As I wrote in December 2022, our “kids” are not all right and psychiatry can help. I would say that many adolescents, and adults as well, may not be all right as we are terrorized not only by mass school shootings, but shootings happening almost anywhere and everywhere in our country: in supermarkets, hospitals, and shopping malls, at graduation parties, and on the streets.

According to a report published in Clinical Psychiatry News, a poll conducted by the American Psychiatric Association showed that most American adults [70%] reported that they were anxious or extremely anxious about keeping themselves or their families safe. APA President Rebecca W. Brendel, MD, JD, pointed out that there is “a lot of worry out there about economic uncertainty, about violence and how we are going to come out of this time period.”

Meanwhile, PTSD is still defined in the DSM-5 as exposure to actual or threatened death, serious injury, or sexual violence experienced directly, witnessing the traumatic event as it occurs to others, learning that a traumatic event occurred to a close family member or friend, or experiencing of traumatic events plus extreme exposure to aversive details of the event.

Examples of traumatic events can be numerous. They include natural disasters, man-made disasters, various types of assaults, war trauma, and severe illness with ICU experiences. I would add encounters with racism and bigotry – including homophobia when one fears for their very life or physical injury. This list includes only a few triggers that may invoke this disorder.

Interestingly, the DSM-5 excludes aversive exposure through electronic media, television, movies, or pictures. Including these aspects of trauma exposure would indeed increase PTSD diagnoses, and I believe this type of exposure needs to be included, especially considering how different people process information. Some viewers of media remain “outside” the events depicted on television, movies, or electronic media while others fit directly “into” the film or TV show. Even, for example, a news program, as evidenced by those people suffering from PTSD after viewing the Sept. 11, 2001, disaster on TV.

I have interviewed numerous people who witnessed Sept. 11 tragedies on TV, some during and some after the event, and they genuinely had experienced key factors of PTSD, including nightmares and intrusive recollections of the event. It’s important to include the ways in which people process information and events in order to make a correct diagnosis, in that “one [diagnostic] size does not fit all.”
 

PTSD at school

In my December column, I noted the fear of death that my generation and beyond experienced with the endless threat of nuclear war, which by its very nature meant death, and if not, the saying went “the living would envy the dead” – that is, in post–nuclear war.

As I pointed out in the column, that war never came and hopefully never will, yet the intensity of those many decades of threatened terror with regular school exercises of “hide under the desk” and “don’t look at the flash” left some with intrusive fearful thoughts, nightmares, and even visualization of atomic destruction, as well as the many scenes of destruction portrayed in news casts and films of nuclear explosions.

Clearly, most U.S. school children who participate in school lockdown drills will not suffer from PTSD episodes, but some will. If that “some” approaches 20% or even 10% or less, that will amount to a lot of kids.

I decided to interview two of my grandchildren, each living in different communities and attending different school systems, but both experiencing “lockdown drills.”

Jack, who is 13 and going into eighth grade, was quite clear regarding the drills and reported that in his age group, both he and the kids in his class felt scared while in lockdown. He told me some kids looked nervous. He mentioned that they were taught in school that if the “real thing” happened, the message was “hide, run, and fight.” I was curious and asked why not run first. He was quick to answer and said if you run, you might run into danger, so it’s better to hide and wait for help to arrive. I said to myself, if not PTSD, then being scared or nervous may also lead to anxiety or even to an anxiety disorder.

Next, I interviewed almost 11-year-old Charley, who is going into sixth grade. She was very clear about not at all being fearful or nervous during these drills and was confident that her classmates felt the same way. Then she explained that the school did a great job with a security officer and had locked doors all around that only opened from the inside. She was proud of the school and not fearful or worried at all.

The diverse views of these two young people surprised me but confirm that PTSD is not at all a given based on what is occurring in society. However, it should always be considered by clinicians if a child or adolescent begins to show signs consistent with PTSD.

These two interviews were quite short, but after I finished talking with Charley, she reported spontaneously that while she and her classmates were neither worried nor scared, some of their teachers did look nervous and seemed scared.

I was quite impressed with her sharpness and nuanced observation, and as noted, adults as well may be adversely affected by the entire concept of school lockdowns, as the awareness of their purpose rests in the forefront of their minds.
 

The way forward

So how do we prepare kids and adolescents for potential emotional problems like PTSD arising from lockdowns, even though most children or adults will not suffer any of these PTSD issues?

First, I believe that as we develop and teach health education in schools, mental health issues should be included according to grade level without generating fear or worry. Second, it is important that school children be aware that if they feel bad in any way emotionally, they should speak to their parents, guardians, teachers, or school nurses.

Clearly, communicating simple problems without embarrassment or shame can lead to solutions, often quickly. Larger, more complicated issues may need professional intervention. Equally important, many mental health interventions need not be long in duration but client-centered, focused, and short term.

But what needs to be emphasized is that speaking and addressing what’s going on, if your thoughts and emotions are troubling, are in themselves therapeutic. Talk therapy works – especially if you get a new perspective on the old set of problems.

Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

Not everyone will suffer an episode of posttraumatic stress disorder, even though everyday American life is characterized by a lot of uncertainty these days, particularly considering the proliferation of gun violence.

Robert T. London

Also, everyone who does experience a traumatic event will not suffer an episode of PTSD – just as not everyone develops a heart attack or cancer, nor will everyone get every illness.

The data suggest that of those exposed to trauma, up to 25% of people will develop PTSD, according to Massachusetts General/McLean Hospital, Belmont, psychiatrist Kerry J. Ressler, MD, PhD, chief of the division of depression and anxiety disorders.

As I wrote in December 2022, our “kids” are not all right and psychiatry can help. I would say that many adolescents, and adults as well, may not be all right as we are terrorized not only by mass school shootings, but shootings happening almost anywhere and everywhere in our country: in supermarkets, hospitals, and shopping malls, at graduation parties, and on the streets.

According to a report published in Clinical Psychiatry News, a poll conducted by the American Psychiatric Association showed that most American adults [70%] reported that they were anxious or extremely anxious about keeping themselves or their families safe. APA President Rebecca W. Brendel, MD, JD, pointed out that there is “a lot of worry out there about economic uncertainty, about violence and how we are going to come out of this time period.”

Meanwhile, PTSD is still defined in the DSM-5 as exposure to actual or threatened death, serious injury, or sexual violence experienced directly, witnessing the traumatic event as it occurs to others, learning that a traumatic event occurred to a close family member or friend, or experiencing of traumatic events plus extreme exposure to aversive details of the event.

Examples of traumatic events can be numerous. They include natural disasters, man-made disasters, various types of assaults, war trauma, and severe illness with ICU experiences. I would add encounters with racism and bigotry – including homophobia when one fears for their very life or physical injury. This list includes only a few triggers that may invoke this disorder.

Interestingly, the DSM-5 excludes aversive exposure through electronic media, television, movies, or pictures. Including these aspects of trauma exposure would indeed increase PTSD diagnoses, and I believe this type of exposure needs to be included, especially considering how different people process information. Some viewers of media remain “outside” the events depicted on television, movies, or electronic media while others fit directly “into” the film or TV show. Even, for example, a news program, as evidenced by those people suffering from PTSD after viewing the Sept. 11, 2001, disaster on TV.

I have interviewed numerous people who witnessed Sept. 11 tragedies on TV, some during and some after the event, and they genuinely had experienced key factors of PTSD, including nightmares and intrusive recollections of the event. It’s important to include the ways in which people process information and events in order to make a correct diagnosis, in that “one [diagnostic] size does not fit all.”
 

PTSD at school

In my December column, I noted the fear of death that my generation and beyond experienced with the endless threat of nuclear war, which by its very nature meant death, and if not, the saying went “the living would envy the dead” – that is, in post–nuclear war.

As I pointed out in the column, that war never came and hopefully never will, yet the intensity of those many decades of threatened terror with regular school exercises of “hide under the desk” and “don’t look at the flash” left some with intrusive fearful thoughts, nightmares, and even visualization of atomic destruction, as well as the many scenes of destruction portrayed in news casts and films of nuclear explosions.

Clearly, most U.S. school children who participate in school lockdown drills will not suffer from PTSD episodes, but some will. If that “some” approaches 20% or even 10% or less, that will amount to a lot of kids.

I decided to interview two of my grandchildren, each living in different communities and attending different school systems, but both experiencing “lockdown drills.”

Jack, who is 13 and going into eighth grade, was quite clear regarding the drills and reported that in his age group, both he and the kids in his class felt scared while in lockdown. He told me some kids looked nervous. He mentioned that they were taught in school that if the “real thing” happened, the message was “hide, run, and fight.” I was curious and asked why not run first. He was quick to answer and said if you run, you might run into danger, so it’s better to hide and wait for help to arrive. I said to myself, if not PTSD, then being scared or nervous may also lead to anxiety or even to an anxiety disorder.

Next, I interviewed almost 11-year-old Charley, who is going into sixth grade. She was very clear about not at all being fearful or nervous during these drills and was confident that her classmates felt the same way. Then she explained that the school did a great job with a security officer and had locked doors all around that only opened from the inside. She was proud of the school and not fearful or worried at all.

The diverse views of these two young people surprised me but confirm that PTSD is not at all a given based on what is occurring in society. However, it should always be considered by clinicians if a child or adolescent begins to show signs consistent with PTSD.

These two interviews were quite short, but after I finished talking with Charley, she reported spontaneously that while she and her classmates were neither worried nor scared, some of their teachers did look nervous and seemed scared.

I was quite impressed with her sharpness and nuanced observation, and as noted, adults as well may be adversely affected by the entire concept of school lockdowns, as the awareness of their purpose rests in the forefront of their minds.
 

The way forward

So how do we prepare kids and adolescents for potential emotional problems like PTSD arising from lockdowns, even though most children or adults will not suffer any of these PTSD issues?

First, I believe that as we develop and teach health education in schools, mental health issues should be included according to grade level without generating fear or worry. Second, it is important that school children be aware that if they feel bad in any way emotionally, they should speak to their parents, guardians, teachers, or school nurses.

Clearly, communicating simple problems without embarrassment or shame can lead to solutions, often quickly. Larger, more complicated issues may need professional intervention. Equally important, many mental health interventions need not be long in duration but client-centered, focused, and short term.

But what needs to be emphasized is that speaking and addressing what’s going on, if your thoughts and emotions are troubling, are in themselves therapeutic. Talk therapy works – especially if you get a new perspective on the old set of problems.

Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

Not everyone will suffer an episode of posttraumatic stress disorder, even though everyday American life is characterized by a lot of uncertainty these days, particularly considering the proliferation of gun violence.

Robert T. London

Also, everyone who does experience a traumatic event will not suffer an episode of PTSD – just as not everyone develops a heart attack or cancer, nor will everyone get every illness.

The data suggest that of those exposed to trauma, up to 25% of people will develop PTSD, according to Massachusetts General/McLean Hospital, Belmont, psychiatrist Kerry J. Ressler, MD, PhD, chief of the division of depression and anxiety disorders.

As I wrote in December 2022, our “kids” are not all right and psychiatry can help. I would say that many adolescents, and adults as well, may not be all right as we are terrorized not only by mass school shootings, but shootings happening almost anywhere and everywhere in our country: in supermarkets, hospitals, and shopping malls, at graduation parties, and on the streets.

According to a report published in Clinical Psychiatry News, a poll conducted by the American Psychiatric Association showed that most American adults [70%] reported that they were anxious or extremely anxious about keeping themselves or their families safe. APA President Rebecca W. Brendel, MD, JD, pointed out that there is “a lot of worry out there about economic uncertainty, about violence and how we are going to come out of this time period.”

Meanwhile, PTSD is still defined in the DSM-5 as exposure to actual or threatened death, serious injury, or sexual violence experienced directly, witnessing the traumatic event as it occurs to others, learning that a traumatic event occurred to a close family member or friend, or experiencing of traumatic events plus extreme exposure to aversive details of the event.

Examples of traumatic events can be numerous. They include natural disasters, man-made disasters, various types of assaults, war trauma, and severe illness with ICU experiences. I would add encounters with racism and bigotry – including homophobia when one fears for their very life or physical injury. This list includes only a few triggers that may invoke this disorder.

Interestingly, the DSM-5 excludes aversive exposure through electronic media, television, movies, or pictures. Including these aspects of trauma exposure would indeed increase PTSD diagnoses, and I believe this type of exposure needs to be included, especially considering how different people process information. Some viewers of media remain “outside” the events depicted on television, movies, or electronic media while others fit directly “into” the film or TV show. Even, for example, a news program, as evidenced by those people suffering from PTSD after viewing the Sept. 11, 2001, disaster on TV.

I have interviewed numerous people who witnessed Sept. 11 tragedies on TV, some during and some after the event, and they genuinely had experienced key factors of PTSD, including nightmares and intrusive recollections of the event. It’s important to include the ways in which people process information and events in order to make a correct diagnosis, in that “one [diagnostic] size does not fit all.”
 

PTSD at school

In my December column, I noted the fear of death that my generation and beyond experienced with the endless threat of nuclear war, which by its very nature meant death, and if not, the saying went “the living would envy the dead” – that is, in post–nuclear war.

As I pointed out in the column, that war never came and hopefully never will, yet the intensity of those many decades of threatened terror with regular school exercises of “hide under the desk” and “don’t look at the flash” left some with intrusive fearful thoughts, nightmares, and even visualization of atomic destruction, as well as the many scenes of destruction portrayed in news casts and films of nuclear explosions.

Clearly, most U.S. school children who participate in school lockdown drills will not suffer from PTSD episodes, but some will. If that “some” approaches 20% or even 10% or less, that will amount to a lot of kids.

I decided to interview two of my grandchildren, each living in different communities and attending different school systems, but both experiencing “lockdown drills.”

Jack, who is 13 and going into eighth grade, was quite clear regarding the drills and reported that in his age group, both he and the kids in his class felt scared while in lockdown. He told me some kids looked nervous. He mentioned that they were taught in school that if the “real thing” happened, the message was “hide, run, and fight.” I was curious and asked why not run first. He was quick to answer and said if you run, you might run into danger, so it’s better to hide and wait for help to arrive. I said to myself, if not PTSD, then being scared or nervous may also lead to anxiety or even to an anxiety disorder.

Next, I interviewed almost 11-year-old Charley, who is going into sixth grade. She was very clear about not at all being fearful or nervous during these drills and was confident that her classmates felt the same way. Then she explained that the school did a great job with a security officer and had locked doors all around that only opened from the inside. She was proud of the school and not fearful or worried at all.

The diverse views of these two young people surprised me but confirm that PTSD is not at all a given based on what is occurring in society. However, it should always be considered by clinicians if a child or adolescent begins to show signs consistent with PTSD.

These two interviews were quite short, but after I finished talking with Charley, she reported spontaneously that while she and her classmates were neither worried nor scared, some of their teachers did look nervous and seemed scared.

I was quite impressed with her sharpness and nuanced observation, and as noted, adults as well may be adversely affected by the entire concept of school lockdowns, as the awareness of their purpose rests in the forefront of their minds.
 

The way forward

So how do we prepare kids and adolescents for potential emotional problems like PTSD arising from lockdowns, even though most children or adults will not suffer any of these PTSD issues?

First, I believe that as we develop and teach health education in schools, mental health issues should be included according to grade level without generating fear or worry. Second, it is important that school children be aware that if they feel bad in any way emotionally, they should speak to their parents, guardians, teachers, or school nurses.

Clearly, communicating simple problems without embarrassment or shame can lead to solutions, often quickly. Larger, more complicated issues may need professional intervention. Equally important, many mental health interventions need not be long in duration but client-centered, focused, and short term.

But what needs to be emphasized is that speaking and addressing what’s going on, if your thoughts and emotions are troubling, are in themselves therapeutic. Talk therapy works – especially if you get a new perspective on the old set of problems.

Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

Patients with “treatment-resistant depression” may be taking other medications with side effects that interfere with antidepressant efficacy.

Investigators studied over 800 patients who were taking antidepressants for major depressive disorder (MDD) and found that close to two-thirds were taking at least one nonpsychiatric medication with potential depressive symptom side effects (PDSS), more than 30% were taking two or more such medications, and 20% at least three such medications.

These medications, which included antihypertensive medications and corticosteroids, among others, were associated with higher odds of moderate-to-severe depressive symptoms, compared with medications without PDSS.

“When evaluating the reasons for inadequate response to treatment for depression, clinicians should consider whether their patient is also receiving a nonpsychiatric medication with a potential for depressive symptom side effects,” study investigator Mark Olfson, MD, MPH, Elizabeth K. Dollard professor of psychiatry, medicine, and law and professor of epidemiology, Columbia University Irving Medical Center, New York, said in an interview.

Columbia University

Previous research limited

“In earlier research, we found that people who were taking medications with a potential to cause depressive symptom side effects were at increased risk of depression, especially those adults who were taking more than one of these medications,” said Dr. Olfson.

This finding led Dr. Olfson and his team to “wonder whether the risks of depressive symptoms associated with these medications extended to people who were being actively treated with antidepressants for depression.”

To investigate, they turned to the National Health and Nutrition Examination Survey (NHANES) – a nationally representative cross-sectional survey of the United States general population.

The study was based on the 2013-2014, 2015-2016, and 2017-2018 waves and included 885 adults who reported using antidepressant medications for greater than or equal to 6 weeks for depression and whose depression could be ascertained.

Prescription medications with PDSS were identified through Micromedex, whose accuracy is “established” and primarily based on the U.S. Food and Drug Administration’s labeled side effects.

Nonantidepressant psychiatric medications and medications for Alzheimer’s disease or substance use disorders were not included in the analysis.

Antidepressant-treated MDD was defined as taking an antidepressant for MDD for greater than or equal to 6 weeks. Depressive symptoms were ascertained using the Patient Health Questionnaire-9 (PHQ-9) with a score of less than 5 representing no/minimal depressive symptoms and a score of greater than or equal to 10 indicating moderate/severe symptoms.

Other variables included self-reported sex, age, race/ethnicity, income, education, health insurance, and common chronic medical conditions such as hypertension, arthritis, lung disease, diabetes mellitus, thyroid disease, cancer, heart disease, liver disease, stroke, and congestive heart failure.
 

Recovery interrupted

Of the patients in the study treated with antidepressants, most were female, greater than or equal to 50 years, non-Hispanic White, and with a college education (70.55, 62.0%, 81.7%, and 69.4%, respectively).

Selective serotonin reuptake inhibitors were used by 67.9% of participants with MDD. Most had been on the same antidepressant medication for a “long time,” the authors report, with 79.2% and 67.8% taking them for greater than 1 year and greater than 2 years, respectively.

Despite the large number of patients on antidepressants, only 43.0% scored in the no/minimal symptoms range, based on the PHQ-9, while 28.4% scored in the moderate/severe range.

Most patients (85%) took at least one medication for medical conditions, with the majority medications with PDSS: 66.7% took at least one medication with PDSS, 37.3% took at least two, 21.6% took at least three, 10.7% took at least four, and 4.9% took at least five.

Almost 75% were using greater than or equal to 1 medication without PDSS, and about 50% were using greater than 1.

The number of medications with PDSS was significantly associated with lower odds of no/minimal depressive symptoms (AOR, 0.75 [95% CI, 0.64-0.87]; P < .001) and higher odds of moderate/severe symptoms (AOR, 1.14 [1.004-1.29]; P = .044).

“The predicted probability of no/minimal symptoms in those taking 5 medications with PDSS was less than half the predicted probability in those taking no medications with PDSS (0.23 vs. 0.52),” the authors report.

Conversely, the predicted probability of moderate/severe symptoms was ~50% higher in individuals taking 5 versus 0 medications with PDSS (0.36 vs. 0.24).

No corresponding associations were found for medications without PDSS.

The results were even stronger when the researchers repeated their adjusted regression analyses to focus on the 10 individual medications most associated with the severity of depressive symptoms. These were omeprazole, gabapentin, meloxicam, tramadol, ranitidine, baclofen, oxycodone, tizanidine, propranolol, and morphine, with an AOR of 0.42 [0.30-0.60] for no/minimal symptoms and 1.68 [1.24-2.27] for moderate/severe symptoms.

“Many widely prescribed medications, from antihypertensives, such as atenolol and metoprolol to corticosteroids, such as dexamethasone and triamcinolone, are associated with depression side effects,” said Dr. Olfson.

“These medications could interfere with recovery from depression. When available, consideration should be given to selecting a substitute with lower risk for depressive symptoms,” he said.
 

Role in treatment-resistant depression

In a comment, Dima Qato, PharmD, MPH, PhD, Hygeia Centennial chair and associate professor, University of Southern California School of Pharmacy, Los Angeles, said the study “is an important reminder that the use of medications with depressive symptoms side effects is increasingly common and may contribute to delays in responsiveness or worsen depressive symptoms among individuals being treated for depression.”

University of Southern California

Dr. Qato, who is also the director of the Program on Medicines and Public Health, USC School of Pharmacy, and was not involved with the study, recommended that clinicians “consider the role of medications with depression side effects when evaluating patients with treatment-resistant depression.”

The study was not supported by any funding agency. Dr. Olfson and coauthors have disclosed no relevant financial relationships. Dr. Qato is a consultant for the Public Citizen Health Research Group.

A version of this article first appeared on Medscape.com.

Patients with “treatment-resistant depression” may be taking other medications with side effects that interfere with antidepressant efficacy.

Investigators studied over 800 patients who were taking antidepressants for major depressive disorder (MDD) and found that close to two-thirds were taking at least one nonpsychiatric medication with potential depressive symptom side effects (PDSS), more than 30% were taking two or more such medications, and 20% at least three such medications.

These medications, which included antihypertensive medications and corticosteroids, among others, were associated with higher odds of moderate-to-severe depressive symptoms, compared with medications without PDSS.

“When evaluating the reasons for inadequate response to treatment for depression, clinicians should consider whether their patient is also receiving a nonpsychiatric medication with a potential for depressive symptom side effects,” study investigator Mark Olfson, MD, MPH, Elizabeth K. Dollard professor of psychiatry, medicine, and law and professor of epidemiology, Columbia University Irving Medical Center, New York, said in an interview.

Columbia University

Previous research limited

“In earlier research, we found that people who were taking medications with a potential to cause depressive symptom side effects were at increased risk of depression, especially those adults who were taking more than one of these medications,” said Dr. Olfson.

This finding led Dr. Olfson and his team to “wonder whether the risks of depressive symptoms associated with these medications extended to people who were being actively treated with antidepressants for depression.”

To investigate, they turned to the National Health and Nutrition Examination Survey (NHANES) – a nationally representative cross-sectional survey of the United States general population.

The study was based on the 2013-2014, 2015-2016, and 2017-2018 waves and included 885 adults who reported using antidepressant medications for greater than or equal to 6 weeks for depression and whose depression could be ascertained.

Prescription medications with PDSS were identified through Micromedex, whose accuracy is “established” and primarily based on the U.S. Food and Drug Administration’s labeled side effects.

Nonantidepressant psychiatric medications and medications for Alzheimer’s disease or substance use disorders were not included in the analysis.

Antidepressant-treated MDD was defined as taking an antidepressant for MDD for greater than or equal to 6 weeks. Depressive symptoms were ascertained using the Patient Health Questionnaire-9 (PHQ-9) with a score of less than 5 representing no/minimal depressive symptoms and a score of greater than or equal to 10 indicating moderate/severe symptoms.

Other variables included self-reported sex, age, race/ethnicity, income, education, health insurance, and common chronic medical conditions such as hypertension, arthritis, lung disease, diabetes mellitus, thyroid disease, cancer, heart disease, liver disease, stroke, and congestive heart failure.
 

Recovery interrupted

Of the patients in the study treated with antidepressants, most were female, greater than or equal to 50 years, non-Hispanic White, and with a college education (70.55, 62.0%, 81.7%, and 69.4%, respectively).

Selective serotonin reuptake inhibitors were used by 67.9% of participants with MDD. Most had been on the same antidepressant medication for a “long time,” the authors report, with 79.2% and 67.8% taking them for greater than 1 year and greater than 2 years, respectively.

Despite the large number of patients on antidepressants, only 43.0% scored in the no/minimal symptoms range, based on the PHQ-9, while 28.4% scored in the moderate/severe range.

Most patients (85%) took at least one medication for medical conditions, with the majority medications with PDSS: 66.7% took at least one medication with PDSS, 37.3% took at least two, 21.6% took at least three, 10.7% took at least four, and 4.9% took at least five.

Almost 75% were using greater than or equal to 1 medication without PDSS, and about 50% were using greater than 1.

The number of medications with PDSS was significantly associated with lower odds of no/minimal depressive symptoms (AOR, 0.75 [95% CI, 0.64-0.87]; P < .001) and higher odds of moderate/severe symptoms (AOR, 1.14 [1.004-1.29]; P = .044).

“The predicted probability of no/minimal symptoms in those taking 5 medications with PDSS was less than half the predicted probability in those taking no medications with PDSS (0.23 vs. 0.52),” the authors report.

Conversely, the predicted probability of moderate/severe symptoms was ~50% higher in individuals taking 5 versus 0 medications with PDSS (0.36 vs. 0.24).

No corresponding associations were found for medications without PDSS.

The results were even stronger when the researchers repeated their adjusted regression analyses to focus on the 10 individual medications most associated with the severity of depressive symptoms. These were omeprazole, gabapentin, meloxicam, tramadol, ranitidine, baclofen, oxycodone, tizanidine, propranolol, and morphine, with an AOR of 0.42 [0.30-0.60] for no/minimal symptoms and 1.68 [1.24-2.27] for moderate/severe symptoms.

“Many widely prescribed medications, from antihypertensives, such as atenolol and metoprolol to corticosteroids, such as dexamethasone and triamcinolone, are associated with depression side effects,” said Dr. Olfson.

“These medications could interfere with recovery from depression. When available, consideration should be given to selecting a substitute with lower risk for depressive symptoms,” he said.
 

Role in treatment-resistant depression

In a comment, Dima Qato, PharmD, MPH, PhD, Hygeia Centennial chair and associate professor, University of Southern California School of Pharmacy, Los Angeles, said the study “is an important reminder that the use of medications with depressive symptoms side effects is increasingly common and may contribute to delays in responsiveness or worsen depressive symptoms among individuals being treated for depression.”

University of Southern California

Dr. Qato, who is also the director of the Program on Medicines and Public Health, USC School of Pharmacy, and was not involved with the study, recommended that clinicians “consider the role of medications with depression side effects when evaluating patients with treatment-resistant depression.”

The study was not supported by any funding agency. Dr. Olfson and coauthors have disclosed no relevant financial relationships. Dr. Qato is a consultant for the Public Citizen Health Research Group.

A version of this article first appeared on Medscape.com.

Patients with “treatment-resistant depression” may be taking other medications with side effects that interfere with antidepressant efficacy.

Investigators studied over 800 patients who were taking antidepressants for major depressive disorder (MDD) and found that close to two-thirds were taking at least one nonpsychiatric medication with potential depressive symptom side effects (PDSS), more than 30% were taking two or more such medications, and 20% at least three such medications.

These medications, which included antihypertensive medications and corticosteroids, among others, were associated with higher odds of moderate-to-severe depressive symptoms, compared with medications without PDSS.

“When evaluating the reasons for inadequate response to treatment for depression, clinicians should consider whether their patient is also receiving a nonpsychiatric medication with a potential for depressive symptom side effects,” study investigator Mark Olfson, MD, MPH, Elizabeth K. Dollard professor of psychiatry, medicine, and law and professor of epidemiology, Columbia University Irving Medical Center, New York, said in an interview.

Columbia University

Previous research limited

“In earlier research, we found that people who were taking medications with a potential to cause depressive symptom side effects were at increased risk of depression, especially those adults who were taking more than one of these medications,” said Dr. Olfson.

This finding led Dr. Olfson and his team to “wonder whether the risks of depressive symptoms associated with these medications extended to people who were being actively treated with antidepressants for depression.”

To investigate, they turned to the National Health and Nutrition Examination Survey (NHANES) – a nationally representative cross-sectional survey of the United States general population.

The study was based on the 2013-2014, 2015-2016, and 2017-2018 waves and included 885 adults who reported using antidepressant medications for greater than or equal to 6 weeks for depression and whose depression could be ascertained.

Prescription medications with PDSS were identified through Micromedex, whose accuracy is “established” and primarily based on the U.S. Food and Drug Administration’s labeled side effects.

Nonantidepressant psychiatric medications and medications for Alzheimer’s disease or substance use disorders were not included in the analysis.

Antidepressant-treated MDD was defined as taking an antidepressant for MDD for greater than or equal to 6 weeks. Depressive symptoms were ascertained using the Patient Health Questionnaire-9 (PHQ-9) with a score of less than 5 representing no/minimal depressive symptoms and a score of greater than or equal to 10 indicating moderate/severe symptoms.

Other variables included self-reported sex, age, race/ethnicity, income, education, health insurance, and common chronic medical conditions such as hypertension, arthritis, lung disease, diabetes mellitus, thyroid disease, cancer, heart disease, liver disease, stroke, and congestive heart failure.
 

Recovery interrupted

Of the patients in the study treated with antidepressants, most were female, greater than or equal to 50 years, non-Hispanic White, and with a college education (70.55, 62.0%, 81.7%, and 69.4%, respectively).

Selective serotonin reuptake inhibitors were used by 67.9% of participants with MDD. Most had been on the same antidepressant medication for a “long time,” the authors report, with 79.2% and 67.8% taking them for greater than 1 year and greater than 2 years, respectively.

Despite the large number of patients on antidepressants, only 43.0% scored in the no/minimal symptoms range, based on the PHQ-9, while 28.4% scored in the moderate/severe range.

Most patients (85%) took at least one medication for medical conditions, with the majority medications with PDSS: 66.7% took at least one medication with PDSS, 37.3% took at least two, 21.6% took at least three, 10.7% took at least four, and 4.9% took at least five.

Almost 75% were using greater than or equal to 1 medication without PDSS, and about 50% were using greater than 1.

The number of medications with PDSS was significantly associated with lower odds of no/minimal depressive symptoms (AOR, 0.75 [95% CI, 0.64-0.87]; P < .001) and higher odds of moderate/severe symptoms (AOR, 1.14 [1.004-1.29]; P = .044).

“The predicted probability of no/minimal symptoms in those taking 5 medications with PDSS was less than half the predicted probability in those taking no medications with PDSS (0.23 vs. 0.52),” the authors report.

Conversely, the predicted probability of moderate/severe symptoms was ~50% higher in individuals taking 5 versus 0 medications with PDSS (0.36 vs. 0.24).

No corresponding associations were found for medications without PDSS.

The results were even stronger when the researchers repeated their adjusted regression analyses to focus on the 10 individual medications most associated with the severity of depressive symptoms. These were omeprazole, gabapentin, meloxicam, tramadol, ranitidine, baclofen, oxycodone, tizanidine, propranolol, and morphine, with an AOR of 0.42 [0.30-0.60] for no/minimal symptoms and 1.68 [1.24-2.27] for moderate/severe symptoms.

“Many widely prescribed medications, from antihypertensives, such as atenolol and metoprolol to corticosteroids, such as dexamethasone and triamcinolone, are associated with depression side effects,” said Dr. Olfson.

“These medications could interfere with recovery from depression. When available, consideration should be given to selecting a substitute with lower risk for depressive symptoms,” he said.
 

Role in treatment-resistant depression

In a comment, Dima Qato, PharmD, MPH, PhD, Hygeia Centennial chair and associate professor, University of Southern California School of Pharmacy, Los Angeles, said the study “is an important reminder that the use of medications with depressive symptoms side effects is increasingly common and may contribute to delays in responsiveness or worsen depressive symptoms among individuals being treated for depression.”

University of Southern California

Dr. Qato, who is also the director of the Program on Medicines and Public Health, USC School of Pharmacy, and was not involved with the study, recommended that clinicians “consider the role of medications with depression side effects when evaluating patients with treatment-resistant depression.”

The study was not supported by any funding agency. Dr. Olfson and coauthors have disclosed no relevant financial relationships. Dr. Qato is a consultant for the Public Citizen Health Research Group.

A version of this article first appeared on Medscape.com.

TOPLINE

Patients who received zuranolone 50 mg/d demonstrated significantly greater improvement in depressive symptoms than those who received placebo, with a rapid onset of effect.

METHODOLOGY

The Food and Drug Administration has accepted filing of a new drug application for zuranolone, a neuroactive steroid that targets g-aminobutyric acid type A receptors (GABAAR), for the treatment of major depressive disorder (MDD) and postpartum depression.

The study included 543 mostly White female patients with MDD. The mean age of the patients was 40 years. Participants were randomly assigned to receive oral zuranolone 50 mg or placebo once daily for 14 days.

About 30% of patients were taking an antidepressant.

The primary endpoint was change in Hamilton Depression Rating Scale (HAM-D) score at day 15.
 

TAKEAWAY

The zuranolone group showed significantly greater improvement in depressive symptoms at 15 days compared with the placebo group (least square mean [LSM] change on HAM-D, –14.1, vs. –12.3; P = .01; Cohen’s d = 0.23).

Improvements were observed on day 3, the earliest assessment, and were sustained at all subsequent visits during the treatment and follow-up period (through day 42).

Results favored zuranolone regardless of the use of antidepressant therapies.

Patients with anxiety who received the active drug experienced improvement in anxiety symptoms compared to the patients who received placebo.

The drug was well tolerated, and there were no new safety findings. The most common treatment-emergent adverse events were somnolence and headache. There was no weight gain, sexual dysfunction, withdrawal symptoms, or increased suicidal ideation or behavior.
 

IN PRACTICE

The study adds to evidence suggesting zuranolone is a promising novel therapy for treating MDD, the authors noted.

STUDY DETAILS

The study was conducted by Anita H. Clayton, MD, department of psychiatry and neurobehavioral sciences, University of Virginia, Charlottesville, and colleagues. It was published online May 3 in The American Journal of Psychiatry.

LIMITATIONS

The study was short term, and the patient population was severely depressed at study entry, which may limit application to those with mild or moderate symptoms. There was a robust placebo response, possibly partly due to the COVID-19 pandemic, when there was an increase in depressive symptoms in the U.S. population, and so frequent in-person visits may have led to an improvement in symptoms even if the patient was receiving placebo.

DISCLOSURES

The study was funded by Sage Therapeutics and Biogen.

A version of this article first appeared on Medscape.com.

TOPLINE

Patients who received zuranolone 50 mg/d demonstrated significantly greater improvement in depressive symptoms than those who received placebo, with a rapid onset of effect.

METHODOLOGY

The Food and Drug Administration has accepted filing of a new drug application for zuranolone, a neuroactive steroid that targets g-aminobutyric acid type A receptors (GABAAR), for the treatment of major depressive disorder (MDD) and postpartum depression.

The study included 543 mostly White female patients with MDD. The mean age of the patients was 40 years. Participants were randomly assigned to receive oral zuranolone 50 mg or placebo once daily for 14 days.

About 30% of patients were taking an antidepressant.

The primary endpoint was change in Hamilton Depression Rating Scale (HAM-D) score at day 15.
 

TAKEAWAY

The zuranolone group showed significantly greater improvement in depressive symptoms at 15 days compared with the placebo group (least square mean [LSM] change on HAM-D, –14.1, vs. –12.3; P = .01; Cohen’s d = 0.23).

Improvements were observed on day 3, the earliest assessment, and were sustained at all subsequent visits during the treatment and follow-up period (through day 42).

Results favored zuranolone regardless of the use of antidepressant therapies.

Patients with anxiety who received the active drug experienced improvement in anxiety symptoms compared to the patients who received placebo.

The drug was well tolerated, and there were no new safety findings. The most common treatment-emergent adverse events were somnolence and headache. There was no weight gain, sexual dysfunction, withdrawal symptoms, or increased suicidal ideation or behavior.
 

IN PRACTICE

The study adds to evidence suggesting zuranolone is a promising novel therapy for treating MDD, the authors noted.

STUDY DETAILS

The study was conducted by Anita H. Clayton, MD, department of psychiatry and neurobehavioral sciences, University of Virginia, Charlottesville, and colleagues. It was published online May 3 in The American Journal of Psychiatry.

LIMITATIONS

The study was short term, and the patient population was severely depressed at study entry, which may limit application to those with mild or moderate symptoms. There was a robust placebo response, possibly partly due to the COVID-19 pandemic, when there was an increase in depressive symptoms in the U.S. population, and so frequent in-person visits may have led to an improvement in symptoms even if the patient was receiving placebo.

DISCLOSURES

The study was funded by Sage Therapeutics and Biogen.

A version of this article first appeared on Medscape.com.

TOPLINE

Patients who received zuranolone 50 mg/d demonstrated significantly greater improvement in depressive symptoms than those who received placebo, with a rapid onset of effect.

METHODOLOGY

The Food and Drug Administration has accepted filing of a new drug application for zuranolone, a neuroactive steroid that targets g-aminobutyric acid type A receptors (GABAAR), for the treatment of major depressive disorder (MDD) and postpartum depression.

The study included 543 mostly White female patients with MDD. The mean age of the patients was 40 years. Participants were randomly assigned to receive oral zuranolone 50 mg or placebo once daily for 14 days.

About 30% of patients were taking an antidepressant.

The primary endpoint was change in Hamilton Depression Rating Scale (HAM-D) score at day 15.
 

TAKEAWAY

The zuranolone group showed significantly greater improvement in depressive symptoms at 15 days compared with the placebo group (least square mean [LSM] change on HAM-D, –14.1, vs. –12.3; P = .01; Cohen’s d = 0.23).

Improvements were observed on day 3, the earliest assessment, and were sustained at all subsequent visits during the treatment and follow-up period (through day 42).

Results favored zuranolone regardless of the use of antidepressant therapies.

Patients with anxiety who received the active drug experienced improvement in anxiety symptoms compared to the patients who received placebo.

The drug was well tolerated, and there were no new safety findings. The most common treatment-emergent adverse events were somnolence and headache. There was no weight gain, sexual dysfunction, withdrawal symptoms, or increased suicidal ideation or behavior.
 

IN PRACTICE

The study adds to evidence suggesting zuranolone is a promising novel therapy for treating MDD, the authors noted.

STUDY DETAILS

The study was conducted by Anita H. Clayton, MD, department of psychiatry and neurobehavioral sciences, University of Virginia, Charlottesville, and colleagues. It was published online May 3 in The American Journal of Psychiatry.

LIMITATIONS

The study was short term, and the patient population was severely depressed at study entry, which may limit application to those with mild or moderate symptoms. There was a robust placebo response, possibly partly due to the COVID-19 pandemic, when there was an increase in depressive symptoms in the U.S. population, and so frequent in-person visits may have led to an improvement in symptoms even if the patient was receiving placebo.

DISCLOSURES

The study was funded by Sage Therapeutics and Biogen.

A version of this article first appeared on Medscape.com.