User login
VAM on Demand Coming Soon
If you missed the Vascular Annual Meeting, would like to review some sessions or view the ones you missed, purchase VAM on Demand. The online library will hold audio and slide presentations of most sessions from the meeting. It will become available in four-six weeks, at which time a notification will be distributed. Attendees will pay $199 and non-attendees will pay $499. Contact the SVS Education Department for more information at [email protected].
If you missed the Vascular Annual Meeting, would like to review some sessions or view the ones you missed, purchase VAM on Demand. The online library will hold audio and slide presentations of most sessions from the meeting. It will become available in four-six weeks, at which time a notification will be distributed. Attendees will pay $199 and non-attendees will pay $499. Contact the SVS Education Department for more information at [email protected].
If you missed the Vascular Annual Meeting, would like to review some sessions or view the ones you missed, purchase VAM on Demand. The online library will hold audio and slide presentations of most sessions from the meeting. It will become available in four-six weeks, at which time a notification will be distributed. Attendees will pay $199 and non-attendees will pay $499. Contact the SVS Education Department for more information at [email protected].
New single-dose influenza therapy effective among outpatients
Clinical question: Is baloxavir marboxil, a selective inhibitor of influenza cap-dependent endonuclease, a safe and effective treatment for acute uncomplicated influenza?
Background: The emergence of oseltamivir-resistant influenza A(H1NI) infection in 2007 highlights the risk of future neuraminidase-resistant global pandemics. Baloxavir represents a new class of antiviral agent that may help treat such outbreaks.
Study design: Phase 3 randomized, double-blind, placebo-controlled trial.
Setting: Outpatients in the United States and Japan.
Synopsis: The trial recruited 1,436 otherwise healthy patients aged 12-64 years of age (median age, 33 years) with a clinical diagnosis of acute uncomplicated influenza pneumonia. The patients were randomly assigned to receive either a single dose of oral baloxavir, oseltamivir 75 mg twice daily for 5 days, or matching placebo within 48 hours of symptom onset. The primary outcome was patient self-assessment of symptomatology.
Among the 1,064 adult patients (age 20-64) with influenza diagnosis confirmed by reverse transcription polymerase chain reaction (RT-PCR), the median time to alleviation of symptoms was lower in the baloxavir group than it was in the placebo group (53.7 hours vs. 80.2 hours; P less than .001). There was no significant difference in time to alleviation of symptoms in the baloxavir group when compared with the oseltamivir group. Adverse events were reported in 21% of baloxavir patients, 25% of placebo patients, and 25% of oseltamivir patients.
The enrolled patients were predominantly young, healthy, and treated as an outpatient. Patients hospitalized with influenza pneumonia are often older, have significant comorbidities, and are at higher risk of poor outcomes. This trial does not directly support the safety or efficacy of baloxavir in this population.
Bottom line: A single dose of baloxavir provides similar clinical benefit as 5 days of oseltamivir therapy in the early treatment of healthy patients with acute influenza.
Citation: Hayden FG et al. Baloxavir marboxil for uncomplicated influenza in adults and adolescents. N Eng J Med. 2018:379(10):914-23.
Dr. Holzer is an assistant professor of medicine in the division of hospital medicine at Mount Sinai Hospital, New York.
Clinical question: Is baloxavir marboxil, a selective inhibitor of influenza cap-dependent endonuclease, a safe and effective treatment for acute uncomplicated influenza?
Background: The emergence of oseltamivir-resistant influenza A(H1NI) infection in 2007 highlights the risk of future neuraminidase-resistant global pandemics. Baloxavir represents a new class of antiviral agent that may help treat such outbreaks.
Study design: Phase 3 randomized, double-blind, placebo-controlled trial.
Setting: Outpatients in the United States and Japan.
Synopsis: The trial recruited 1,436 otherwise healthy patients aged 12-64 years of age (median age, 33 years) with a clinical diagnosis of acute uncomplicated influenza pneumonia. The patients were randomly assigned to receive either a single dose of oral baloxavir, oseltamivir 75 mg twice daily for 5 days, or matching placebo within 48 hours of symptom onset. The primary outcome was patient self-assessment of symptomatology.
Among the 1,064 adult patients (age 20-64) with influenza diagnosis confirmed by reverse transcription polymerase chain reaction (RT-PCR), the median time to alleviation of symptoms was lower in the baloxavir group than it was in the placebo group (53.7 hours vs. 80.2 hours; P less than .001). There was no significant difference in time to alleviation of symptoms in the baloxavir group when compared with the oseltamivir group. Adverse events were reported in 21% of baloxavir patients, 25% of placebo patients, and 25% of oseltamivir patients.
The enrolled patients were predominantly young, healthy, and treated as an outpatient. Patients hospitalized with influenza pneumonia are often older, have significant comorbidities, and are at higher risk of poor outcomes. This trial does not directly support the safety or efficacy of baloxavir in this population.
Bottom line: A single dose of baloxavir provides similar clinical benefit as 5 days of oseltamivir therapy in the early treatment of healthy patients with acute influenza.
Citation: Hayden FG et al. Baloxavir marboxil for uncomplicated influenza in adults and adolescents. N Eng J Med. 2018:379(10):914-23.
Dr. Holzer is an assistant professor of medicine in the division of hospital medicine at Mount Sinai Hospital, New York.
Clinical question: Is baloxavir marboxil, a selective inhibitor of influenza cap-dependent endonuclease, a safe and effective treatment for acute uncomplicated influenza?
Background: The emergence of oseltamivir-resistant influenza A(H1NI) infection in 2007 highlights the risk of future neuraminidase-resistant global pandemics. Baloxavir represents a new class of antiviral agent that may help treat such outbreaks.
Study design: Phase 3 randomized, double-blind, placebo-controlled trial.
Setting: Outpatients in the United States and Japan.
Synopsis: The trial recruited 1,436 otherwise healthy patients aged 12-64 years of age (median age, 33 years) with a clinical diagnosis of acute uncomplicated influenza pneumonia. The patients were randomly assigned to receive either a single dose of oral baloxavir, oseltamivir 75 mg twice daily for 5 days, or matching placebo within 48 hours of symptom onset. The primary outcome was patient self-assessment of symptomatology.
Among the 1,064 adult patients (age 20-64) with influenza diagnosis confirmed by reverse transcription polymerase chain reaction (RT-PCR), the median time to alleviation of symptoms was lower in the baloxavir group than it was in the placebo group (53.7 hours vs. 80.2 hours; P less than .001). There was no significant difference in time to alleviation of symptoms in the baloxavir group when compared with the oseltamivir group. Adverse events were reported in 21% of baloxavir patients, 25% of placebo patients, and 25% of oseltamivir patients.
The enrolled patients were predominantly young, healthy, and treated as an outpatient. Patients hospitalized with influenza pneumonia are often older, have significant comorbidities, and are at higher risk of poor outcomes. This trial does not directly support the safety or efficacy of baloxavir in this population.
Bottom line: A single dose of baloxavir provides similar clinical benefit as 5 days of oseltamivir therapy in the early treatment of healthy patients with acute influenza.
Citation: Hayden FG et al. Baloxavir marboxil for uncomplicated influenza in adults and adolescents. N Eng J Med. 2018:379(10):914-23.
Dr. Holzer is an assistant professor of medicine in the division of hospital medicine at Mount Sinai Hospital, New York.
Elevated monocyte count predicts poor outcomes in idiopathic pulmonary fibrosis
, including hypertrophic cardiomyopathy, systemic sclerosis, and myelofibrosis, according to research published in The Lancet Respiratory Medicine.
The data indicate that “a single threshold value of absolute monocyte counts of 0.95 K/mcL could be used to identify high-risk patients with a fibrotic disease,” said Madeleine K. D. Scott, a researcher at Stanford (Calif.) University, and coauthors. The results “suggest that monocyte count should be incorporated into the clinical assessment” and may “enable more conscientious allocation of scarce resources, including lung transplantations,” they said.
While other published biomarkers – including gene panels and multicytokine signatures – may be expensive and not readily available, “absolute monocyte count is routinely measured as part of a complete blood count, an inexpensive test used in clinical practice worldwide,” the authors said.
Further study of monocytes’ mechanistic role in fibrosis ultimately could point to new treatment approaches.
A retrospective multicenter cohort study
To assess whether immune cells may identify patients with idiopathic pulmonary fibrosis at greater risk of poor outcomes, Ms. Scott and her collaborators conducted a retrospective multicenter cohort study.
They first analyzed transcriptome data from 120 peripheral blood mononuclear cell samples of patients with idiopathic pulmonary fibrosis, which they obtained from the Gene Expression Omnibus at the National Center for Biotechnology Information. They used statistical deconvolution to estimate percentages of 13 immune cell types and examined their associations with transplant-free survival. Their discovery analysis found that estimated CD14+ classical monocyte percentages above the mean correlated with shorter transplant-free survival times (hazard ratio, 1.82), but percentages of T cells and B cells did not.
The researchers then validated these results using samples from patients with idiopathic pulmonary fibrosis in two independent cohorts. In the COMET validation cohort, which included 45 patients with idiopathic pulmonary fibrosis whose monocyte counts were measured using flow cytometry, higher monocyte counts were significantly associated with greater risk of disease progression. In the Yale cohort, which included 15 patients with idiopathic pulmonary fibrosis, the 6 patients who were classified as high risk on the basis of a 52-gene signature had more CD14+ monocytes than the 9 low-risk patients did.
In addition, Ms. Scott and her collaborators looked at complete blood count values in the electronic health records of 45,068 patients with idiopathic pulmonary fibrosis, systemic sclerosis, hypertrophic cardiomyopathy, or myelofibrosis in Stanford, Northwestern, Vanderbilt, and Optum Clinformatics Data Mart cohorts.
Among patients in the COMET, Stanford, and Northwestern datasets, monocyte counts of 0.95 K/mcL or greater were associated with mortality after adjustment for forced vital capacity (HR, 2.47) and the gender, age, and physiology index (HR, 2.06). Data from 7,459 patients with idiopathic pulmonary fibrosis “showed that patients with monocyte counts of 0.95 K/mcL or greater were at increased risk of mortality with lung transplantation as a censoring event, after adjusting for age at diagnosis and sex” in the Stanford (HR, 2.30), Vanderbilt (HR, 1.52), and Optum (HR, 1.74) cohorts. “Likewise, higher absolute monocyte count was associated with shortened survival in patients with hypertrophic cardiomyopathy across all three cohorts, and in patients with systemic sclerosis or myelofibrosis in two of the three cohorts,” the researchers said.
The study was funded by grants from the Bill & Melinda Gates Foundation, U.S. National Institute of Allergy and Infectious Diseases, and U.S. National Library of Medicine. Ms. Scott had no competing interests. Coauthors disclosed grants, compensation, and support from foundations, agencies, and companies.
SOURCE: Scott MKD et al. Lancet Respir Med. 2019 Jun. doi: 10.1016/S2213-2600(18)30508-3.
The study by Scott et al. provides evidence that monocyte count may be a “novel, simple, and inexpensive prognostic biomarker in idiopathic pulmonary fibrosis,” according to an accompanying editorial.
Progress has been made in the treatment of idiopathic pulmonary fibrosis, but patient prognosis remains “challenging to predict,” wrote Michael Kreuter, MD, of University of Heidelberg, Germany, and Toby M. Maher, MB, MSc, PhD, of Royal Brompton Hospital in London and Imperial College London. “One lesson that can be learned from other respiratory disorders is that routinely measured cellular biomarkers, such as blood eosinophil counts in chronic obstructive pulmonary disease (COPD), can predict treatment responses” (Lancet Respir Med. 2019 Jun. doi: 10.1016/S2213-2600[19]30050-5).
Increased blood monocyte counts in idiopathic pulmonary fibrosis may reflect disease activity, which “could explain the outcome differences,” said Dr. Kreuter and Dr. Maher. “As highlighted by the investigators themselves, before introducing assessment of monocyte counts as part of routine clinical care for individuals with idiopathic pulmonary fibrosis, the limitations of this research should be taken into account. These include uncertainty around diagnosis and disease severity in a substantial subset of the patients, and the unknown effect of medical therapies (including corticosteroids and immunosuppressant and antifibrotic drugs) on monocyte counts and prognosis.” Researchers should validate the clinical value of blood monocyte counts in existing and future cohorts and evaluate the biomarker in clinical trials.
The editorialists have received compensation and funding from various pharmaceutical companies.
The study by Scott et al. provides evidence that monocyte count may be a “novel, simple, and inexpensive prognostic biomarker in idiopathic pulmonary fibrosis,” according to an accompanying editorial.
Progress has been made in the treatment of idiopathic pulmonary fibrosis, but patient prognosis remains “challenging to predict,” wrote Michael Kreuter, MD, of University of Heidelberg, Germany, and Toby M. Maher, MB, MSc, PhD, of Royal Brompton Hospital in London and Imperial College London. “One lesson that can be learned from other respiratory disorders is that routinely measured cellular biomarkers, such as blood eosinophil counts in chronic obstructive pulmonary disease (COPD), can predict treatment responses” (Lancet Respir Med. 2019 Jun. doi: 10.1016/S2213-2600[19]30050-5).
Increased blood monocyte counts in idiopathic pulmonary fibrosis may reflect disease activity, which “could explain the outcome differences,” said Dr. Kreuter and Dr. Maher. “As highlighted by the investigators themselves, before introducing assessment of monocyte counts as part of routine clinical care for individuals with idiopathic pulmonary fibrosis, the limitations of this research should be taken into account. These include uncertainty around diagnosis and disease severity in a substantial subset of the patients, and the unknown effect of medical therapies (including corticosteroids and immunosuppressant and antifibrotic drugs) on monocyte counts and prognosis.” Researchers should validate the clinical value of blood monocyte counts in existing and future cohorts and evaluate the biomarker in clinical trials.
The editorialists have received compensation and funding from various pharmaceutical companies.
The study by Scott et al. provides evidence that monocyte count may be a “novel, simple, and inexpensive prognostic biomarker in idiopathic pulmonary fibrosis,” according to an accompanying editorial.
Progress has been made in the treatment of idiopathic pulmonary fibrosis, but patient prognosis remains “challenging to predict,” wrote Michael Kreuter, MD, of University of Heidelberg, Germany, and Toby M. Maher, MB, MSc, PhD, of Royal Brompton Hospital in London and Imperial College London. “One lesson that can be learned from other respiratory disorders is that routinely measured cellular biomarkers, such as blood eosinophil counts in chronic obstructive pulmonary disease (COPD), can predict treatment responses” (Lancet Respir Med. 2019 Jun. doi: 10.1016/S2213-2600[19]30050-5).
Increased blood monocyte counts in idiopathic pulmonary fibrosis may reflect disease activity, which “could explain the outcome differences,” said Dr. Kreuter and Dr. Maher. “As highlighted by the investigators themselves, before introducing assessment of monocyte counts as part of routine clinical care for individuals with idiopathic pulmonary fibrosis, the limitations of this research should be taken into account. These include uncertainty around diagnosis and disease severity in a substantial subset of the patients, and the unknown effect of medical therapies (including corticosteroids and immunosuppressant and antifibrotic drugs) on monocyte counts and prognosis.” Researchers should validate the clinical value of blood monocyte counts in existing and future cohorts and evaluate the biomarker in clinical trials.
The editorialists have received compensation and funding from various pharmaceutical companies.
, including hypertrophic cardiomyopathy, systemic sclerosis, and myelofibrosis, according to research published in The Lancet Respiratory Medicine.
The data indicate that “a single threshold value of absolute monocyte counts of 0.95 K/mcL could be used to identify high-risk patients with a fibrotic disease,” said Madeleine K. D. Scott, a researcher at Stanford (Calif.) University, and coauthors. The results “suggest that monocyte count should be incorporated into the clinical assessment” and may “enable more conscientious allocation of scarce resources, including lung transplantations,” they said.
While other published biomarkers – including gene panels and multicytokine signatures – may be expensive and not readily available, “absolute monocyte count is routinely measured as part of a complete blood count, an inexpensive test used in clinical practice worldwide,” the authors said.
Further study of monocytes’ mechanistic role in fibrosis ultimately could point to new treatment approaches.
A retrospective multicenter cohort study
To assess whether immune cells may identify patients with idiopathic pulmonary fibrosis at greater risk of poor outcomes, Ms. Scott and her collaborators conducted a retrospective multicenter cohort study.
They first analyzed transcriptome data from 120 peripheral blood mononuclear cell samples of patients with idiopathic pulmonary fibrosis, which they obtained from the Gene Expression Omnibus at the National Center for Biotechnology Information. They used statistical deconvolution to estimate percentages of 13 immune cell types and examined their associations with transplant-free survival. Their discovery analysis found that estimated CD14+ classical monocyte percentages above the mean correlated with shorter transplant-free survival times (hazard ratio, 1.82), but percentages of T cells and B cells did not.
The researchers then validated these results using samples from patients with idiopathic pulmonary fibrosis in two independent cohorts. In the COMET validation cohort, which included 45 patients with idiopathic pulmonary fibrosis whose monocyte counts were measured using flow cytometry, higher monocyte counts were significantly associated with greater risk of disease progression. In the Yale cohort, which included 15 patients with idiopathic pulmonary fibrosis, the 6 patients who were classified as high risk on the basis of a 52-gene signature had more CD14+ monocytes than the 9 low-risk patients did.
In addition, Ms. Scott and her collaborators looked at complete blood count values in the electronic health records of 45,068 patients with idiopathic pulmonary fibrosis, systemic sclerosis, hypertrophic cardiomyopathy, or myelofibrosis in Stanford, Northwestern, Vanderbilt, and Optum Clinformatics Data Mart cohorts.
Among patients in the COMET, Stanford, and Northwestern datasets, monocyte counts of 0.95 K/mcL or greater were associated with mortality after adjustment for forced vital capacity (HR, 2.47) and the gender, age, and physiology index (HR, 2.06). Data from 7,459 patients with idiopathic pulmonary fibrosis “showed that patients with monocyte counts of 0.95 K/mcL or greater were at increased risk of mortality with lung transplantation as a censoring event, after adjusting for age at diagnosis and sex” in the Stanford (HR, 2.30), Vanderbilt (HR, 1.52), and Optum (HR, 1.74) cohorts. “Likewise, higher absolute monocyte count was associated with shortened survival in patients with hypertrophic cardiomyopathy across all three cohorts, and in patients with systemic sclerosis or myelofibrosis in two of the three cohorts,” the researchers said.
The study was funded by grants from the Bill & Melinda Gates Foundation, U.S. National Institute of Allergy and Infectious Diseases, and U.S. National Library of Medicine. Ms. Scott had no competing interests. Coauthors disclosed grants, compensation, and support from foundations, agencies, and companies.
SOURCE: Scott MKD et al. Lancet Respir Med. 2019 Jun. doi: 10.1016/S2213-2600(18)30508-3.
, including hypertrophic cardiomyopathy, systemic sclerosis, and myelofibrosis, according to research published in The Lancet Respiratory Medicine.
The data indicate that “a single threshold value of absolute monocyte counts of 0.95 K/mcL could be used to identify high-risk patients with a fibrotic disease,” said Madeleine K. D. Scott, a researcher at Stanford (Calif.) University, and coauthors. The results “suggest that monocyte count should be incorporated into the clinical assessment” and may “enable more conscientious allocation of scarce resources, including lung transplantations,” they said.
While other published biomarkers – including gene panels and multicytokine signatures – may be expensive and not readily available, “absolute monocyte count is routinely measured as part of a complete blood count, an inexpensive test used in clinical practice worldwide,” the authors said.
Further study of monocytes’ mechanistic role in fibrosis ultimately could point to new treatment approaches.
A retrospective multicenter cohort study
To assess whether immune cells may identify patients with idiopathic pulmonary fibrosis at greater risk of poor outcomes, Ms. Scott and her collaborators conducted a retrospective multicenter cohort study.
They first analyzed transcriptome data from 120 peripheral blood mononuclear cell samples of patients with idiopathic pulmonary fibrosis, which they obtained from the Gene Expression Omnibus at the National Center for Biotechnology Information. They used statistical deconvolution to estimate percentages of 13 immune cell types and examined their associations with transplant-free survival. Their discovery analysis found that estimated CD14+ classical monocyte percentages above the mean correlated with shorter transplant-free survival times (hazard ratio, 1.82), but percentages of T cells and B cells did not.
The researchers then validated these results using samples from patients with idiopathic pulmonary fibrosis in two independent cohorts. In the COMET validation cohort, which included 45 patients with idiopathic pulmonary fibrosis whose monocyte counts were measured using flow cytometry, higher monocyte counts were significantly associated with greater risk of disease progression. In the Yale cohort, which included 15 patients with idiopathic pulmonary fibrosis, the 6 patients who were classified as high risk on the basis of a 52-gene signature had more CD14+ monocytes than the 9 low-risk patients did.
In addition, Ms. Scott and her collaborators looked at complete blood count values in the electronic health records of 45,068 patients with idiopathic pulmonary fibrosis, systemic sclerosis, hypertrophic cardiomyopathy, or myelofibrosis in Stanford, Northwestern, Vanderbilt, and Optum Clinformatics Data Mart cohorts.
Among patients in the COMET, Stanford, and Northwestern datasets, monocyte counts of 0.95 K/mcL or greater were associated with mortality after adjustment for forced vital capacity (HR, 2.47) and the gender, age, and physiology index (HR, 2.06). Data from 7,459 patients with idiopathic pulmonary fibrosis “showed that patients with monocyte counts of 0.95 K/mcL or greater were at increased risk of mortality with lung transplantation as a censoring event, after adjusting for age at diagnosis and sex” in the Stanford (HR, 2.30), Vanderbilt (HR, 1.52), and Optum (HR, 1.74) cohorts. “Likewise, higher absolute monocyte count was associated with shortened survival in patients with hypertrophic cardiomyopathy across all three cohorts, and in patients with systemic sclerosis or myelofibrosis in two of the three cohorts,” the researchers said.
The study was funded by grants from the Bill & Melinda Gates Foundation, U.S. National Institute of Allergy and Infectious Diseases, and U.S. National Library of Medicine. Ms. Scott had no competing interests. Coauthors disclosed grants, compensation, and support from foundations, agencies, and companies.
SOURCE: Scott MKD et al. Lancet Respir Med. 2019 Jun. doi: 10.1016/S2213-2600(18)30508-3.
FROM THE LANCET RESPIRATORY MEDICINE
Key clinical point: An increased monocyte count predicts poor outcomes among patients with idiopathic pulmonary fibrosis and other fibrotic diseases.
Major finding: Among patients in three cohorts, monocyte counts of 0.95 K/mcL or greater were associated with mortality after adjustment for forced vital capacity (hazard ratio, 2.47) and the gender, age, and physiology index (HR, 2.06).
Study details: A retrospective analysis of data from 7,000 patients with idiopathic pulmonary fibrosis from five independent cohorts.
Disclosures: The study was funded by grants from the Bill & Melinda Gates Foundation, U.S. National Institute of Allergy and Infectious Diseases, and U.S. National Library of Medicine. Ms. Scott had no competing interests. Coauthors disclosed grants, compensation, and support from foundations, agencies, and companies.
Source: Scott MKD et al. Lancet Respir Med. 2019 Jun. doi: 10.1016/S2213-2600(18)30508-3.
Briefest flash of light can alter the human circadian system
SAN ANTONIO –
“This becomes a complementary way to help people with various kinds of circadian phase disorders,” the study’s first author, Jamie M. Zeitzer, PhD, said during an interview at the annual meeting of the Associated Professional Sleep Societies. “Right now under ideal laboratory circumstances, you can change someone’s circadian timing by about 3 hours. That’s not happening in the real world; that’s what you do in a lab. That’s with very bright light for 6 hours and very dim light the rest of the time.”
In an effort to build on previous literature related to circadian phase shifting and continuous light exposure in rodents and in humans, Dr. Zeitzer, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University, and colleagues enrolled 56 healthy young men and women in their 20s and 30s to take part in two parallel 16-day studies. For the first 14 days, study participants maintained a regular sleep/wake cycle at home as confirmed through actigraphy and sleep logs. They spent the final 2 days in a specialized time-isolation laboratory, during which the phase of the circadian pacemaker (salivary melatonin onset) was determined in constant routine conditions on evening one and two; light exposure occurred between these two phase determinations on night one.
Light exposure consisted of 1 hour of a sequence of light flashes delivered through a pair of modified welding goggles during enforced wake starting 2 hours after habitual bedtime. Flashes were presented every 15 seconds and varied either by duration (from 10 microseconds to 10 seconds at a fixed intensity of 2,200 lux) or intensity (a range between 3 and 9,500 lux, with a duration fixed at 2 milliseconds).
Dr. Zeitzer and colleagues observed no significant difference in the phase shift created between flashes that were given at 10 microseconds and flashes that were given at 10 seconds. “That’s a six-log unit variation,” he said during a presentation of the results at the meeting. “There are a million times more photons given in 10-second flashes over the hour than there are in the 10-microsecond flashes. Despite the fact that there are a million more photons, you get the exact same phase shift in both of these conditions. You need very little light in order to generate these phase shifts. You’re talking about less than 1 second of light stretched out over 1 hour.”
The researchers also observed that flash intensity showed a sigmoidal relationship with phase shifting, with a half-maximal shift observed at 8 lux and 90% of the maximal shift occurring after exposure to flashes as dim as 50 lux. None of the flash sequences caused acute suppression of melatonin.
“We did not anticipate the invariance, that anything from 10 microseconds to 10 seconds gives us no difference [in phase shifting],” Dr. Zeitzer said. “That was surprising. I thought that more light would be slightly less effective in terms of photons but still give a bigger [phase] shift, but that didn’t happen. In the intensity response, we see things are more sensitive to light flashes than they are to continuous light, which is also surprising. It implies that a different part of the eye is responding to light flashes than it is to continuous light. It provides more information about how to minimize the amount of light we’re using and maximize the amount of shift.”
Which photoreceptors underlie the responses remains unclear, he continued, “but given the characteristics of photoreceptors, our hypothesis is that flashes are being mediated through a cone cell response, while the response to continuous light is being primarily mediated through a melanopsin response. A future question we plan to investigate is, can selective sequential simultaneous activation of different photoreceptors create enhanced phase shifts?”
The study was supported by the Department of Defense. Dr. Zeitzer reported having no financial disclosures.
SAN ANTONIO –
“This becomes a complementary way to help people with various kinds of circadian phase disorders,” the study’s first author, Jamie M. Zeitzer, PhD, said during an interview at the annual meeting of the Associated Professional Sleep Societies. “Right now under ideal laboratory circumstances, you can change someone’s circadian timing by about 3 hours. That’s not happening in the real world; that’s what you do in a lab. That’s with very bright light for 6 hours and very dim light the rest of the time.”
In an effort to build on previous literature related to circadian phase shifting and continuous light exposure in rodents and in humans, Dr. Zeitzer, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University, and colleagues enrolled 56 healthy young men and women in their 20s and 30s to take part in two parallel 16-day studies. For the first 14 days, study participants maintained a regular sleep/wake cycle at home as confirmed through actigraphy and sleep logs. They spent the final 2 days in a specialized time-isolation laboratory, during which the phase of the circadian pacemaker (salivary melatonin onset) was determined in constant routine conditions on evening one and two; light exposure occurred between these two phase determinations on night one.
Light exposure consisted of 1 hour of a sequence of light flashes delivered through a pair of modified welding goggles during enforced wake starting 2 hours after habitual bedtime. Flashes were presented every 15 seconds and varied either by duration (from 10 microseconds to 10 seconds at a fixed intensity of 2,200 lux) or intensity (a range between 3 and 9,500 lux, with a duration fixed at 2 milliseconds).
Dr. Zeitzer and colleagues observed no significant difference in the phase shift created between flashes that were given at 10 microseconds and flashes that were given at 10 seconds. “That’s a six-log unit variation,” he said during a presentation of the results at the meeting. “There are a million times more photons given in 10-second flashes over the hour than there are in the 10-microsecond flashes. Despite the fact that there are a million more photons, you get the exact same phase shift in both of these conditions. You need very little light in order to generate these phase shifts. You’re talking about less than 1 second of light stretched out over 1 hour.”
The researchers also observed that flash intensity showed a sigmoidal relationship with phase shifting, with a half-maximal shift observed at 8 lux and 90% of the maximal shift occurring after exposure to flashes as dim as 50 lux. None of the flash sequences caused acute suppression of melatonin.
“We did not anticipate the invariance, that anything from 10 microseconds to 10 seconds gives us no difference [in phase shifting],” Dr. Zeitzer said. “That was surprising. I thought that more light would be slightly less effective in terms of photons but still give a bigger [phase] shift, but that didn’t happen. In the intensity response, we see things are more sensitive to light flashes than they are to continuous light, which is also surprising. It implies that a different part of the eye is responding to light flashes than it is to continuous light. It provides more information about how to minimize the amount of light we’re using and maximize the amount of shift.”
Which photoreceptors underlie the responses remains unclear, he continued, “but given the characteristics of photoreceptors, our hypothesis is that flashes are being mediated through a cone cell response, while the response to continuous light is being primarily mediated through a melanopsin response. A future question we plan to investigate is, can selective sequential simultaneous activation of different photoreceptors create enhanced phase shifts?”
The study was supported by the Department of Defense. Dr. Zeitzer reported having no financial disclosures.
SAN ANTONIO –
“This becomes a complementary way to help people with various kinds of circadian phase disorders,” the study’s first author, Jamie M. Zeitzer, PhD, said during an interview at the annual meeting of the Associated Professional Sleep Societies. “Right now under ideal laboratory circumstances, you can change someone’s circadian timing by about 3 hours. That’s not happening in the real world; that’s what you do in a lab. That’s with very bright light for 6 hours and very dim light the rest of the time.”
In an effort to build on previous literature related to circadian phase shifting and continuous light exposure in rodents and in humans, Dr. Zeitzer, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University, and colleagues enrolled 56 healthy young men and women in their 20s and 30s to take part in two parallel 16-day studies. For the first 14 days, study participants maintained a regular sleep/wake cycle at home as confirmed through actigraphy and sleep logs. They spent the final 2 days in a specialized time-isolation laboratory, during which the phase of the circadian pacemaker (salivary melatonin onset) was determined in constant routine conditions on evening one and two; light exposure occurred between these two phase determinations on night one.
Light exposure consisted of 1 hour of a sequence of light flashes delivered through a pair of modified welding goggles during enforced wake starting 2 hours after habitual bedtime. Flashes were presented every 15 seconds and varied either by duration (from 10 microseconds to 10 seconds at a fixed intensity of 2,200 lux) or intensity (a range between 3 and 9,500 lux, with a duration fixed at 2 milliseconds).
Dr. Zeitzer and colleagues observed no significant difference in the phase shift created between flashes that were given at 10 microseconds and flashes that were given at 10 seconds. “That’s a six-log unit variation,” he said during a presentation of the results at the meeting. “There are a million times more photons given in 10-second flashes over the hour than there are in the 10-microsecond flashes. Despite the fact that there are a million more photons, you get the exact same phase shift in both of these conditions. You need very little light in order to generate these phase shifts. You’re talking about less than 1 second of light stretched out over 1 hour.”
The researchers also observed that flash intensity showed a sigmoidal relationship with phase shifting, with a half-maximal shift observed at 8 lux and 90% of the maximal shift occurring after exposure to flashes as dim as 50 lux. None of the flash sequences caused acute suppression of melatonin.
“We did not anticipate the invariance, that anything from 10 microseconds to 10 seconds gives us no difference [in phase shifting],” Dr. Zeitzer said. “That was surprising. I thought that more light would be slightly less effective in terms of photons but still give a bigger [phase] shift, but that didn’t happen. In the intensity response, we see things are more sensitive to light flashes than they are to continuous light, which is also surprising. It implies that a different part of the eye is responding to light flashes than it is to continuous light. It provides more information about how to minimize the amount of light we’re using and maximize the amount of shift.”
Which photoreceptors underlie the responses remains unclear, he continued, “but given the characteristics of photoreceptors, our hypothesis is that flashes are being mediated through a cone cell response, while the response to continuous light is being primarily mediated through a melanopsin response. A future question we plan to investigate is, can selective sequential simultaneous activation of different photoreceptors create enhanced phase shifts?”
The study was supported by the Department of Defense. Dr. Zeitzer reported having no financial disclosures.
REPORTING FROM SLEEP 2019
Key clinical point: When distributed as flashes, the human circadian system can be phase shifted by extraordinarily brief and dim light.
Major finding: The researchers observed no significant difference in the phase shift created between flashes that were given at 10 microseconds and flashes that were given at 10 seconds.
Study details: Two parallel 16-day studies involving 56 healthy men and women in their 20s and 30s.
Disclosures: The study was supported by the Department of Defense. Dr. Zeitzer reported having no financial disclosures.
CF drug picks up indication for children as young as 6
to include children as young as 6 years old who have cystic fibrosis.
The drug was approved in 2018 for patients aged 12 years and older who have the most common cause of the disease, two alleles for the F508del mutation in the gene that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein, or at least one other CFTR mutation responsive to the combination, as listed in labeling.
The original approval was based on three phase 3, double blind, placebo-controlled trials, which demonstrated improvements in lung function and other key measures of the disease. One trial that found a 6.8% mean improvement in lung function testing over placebo at 8 weeks, and another that found a 4% improvement at 24 weeks, with fewer respiratory exacerbations and improved respiratory-related quality of life. A third trial in patients without the indicated genetic mutations was ended early for futility.
The efficacy in children under 12 years was extrapolated from those trials, plus an open-label study that found similar effects.
Labeling warns of elevated liver enzymes and cataracts in children, and notes that the drug should be taken with food that contains fat. Labeling also recommends against use with strong cytochrome P450 3A4 (CYP3A) inducers – rifampin, phenobarbital, St. John’s wort, among others – because they might reduce efficacy, and against use with CYP3A inhibitors – ketoconazole, clarithromycin, Seville oranges, grapefruit juice, etc. – because of the risk of increased exposure.
The most common side effects are headache, nausea, sinus congestion, and dizziness. The FDA has cleared a CF gene test to check for the required mutations. Symdeko is marketed by Vertex Pharmaceuticals.
to include children as young as 6 years old who have cystic fibrosis.
The drug was approved in 2018 for patients aged 12 years and older who have the most common cause of the disease, two alleles for the F508del mutation in the gene that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein, or at least one other CFTR mutation responsive to the combination, as listed in labeling.
The original approval was based on three phase 3, double blind, placebo-controlled trials, which demonstrated improvements in lung function and other key measures of the disease. One trial that found a 6.8% mean improvement in lung function testing over placebo at 8 weeks, and another that found a 4% improvement at 24 weeks, with fewer respiratory exacerbations and improved respiratory-related quality of life. A third trial in patients without the indicated genetic mutations was ended early for futility.
The efficacy in children under 12 years was extrapolated from those trials, plus an open-label study that found similar effects.
Labeling warns of elevated liver enzymes and cataracts in children, and notes that the drug should be taken with food that contains fat. Labeling also recommends against use with strong cytochrome P450 3A4 (CYP3A) inducers – rifampin, phenobarbital, St. John’s wort, among others – because they might reduce efficacy, and against use with CYP3A inhibitors – ketoconazole, clarithromycin, Seville oranges, grapefruit juice, etc. – because of the risk of increased exposure.
The most common side effects are headache, nausea, sinus congestion, and dizziness. The FDA has cleared a CF gene test to check for the required mutations. Symdeko is marketed by Vertex Pharmaceuticals.
to include children as young as 6 years old who have cystic fibrosis.
The drug was approved in 2018 for patients aged 12 years and older who have the most common cause of the disease, two alleles for the F508del mutation in the gene that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein, or at least one other CFTR mutation responsive to the combination, as listed in labeling.
The original approval was based on three phase 3, double blind, placebo-controlled trials, which demonstrated improvements in lung function and other key measures of the disease. One trial that found a 6.8% mean improvement in lung function testing over placebo at 8 weeks, and another that found a 4% improvement at 24 weeks, with fewer respiratory exacerbations and improved respiratory-related quality of life. A third trial in patients without the indicated genetic mutations was ended early for futility.
The efficacy in children under 12 years was extrapolated from those trials, plus an open-label study that found similar effects.
Labeling warns of elevated liver enzymes and cataracts in children, and notes that the drug should be taken with food that contains fat. Labeling also recommends against use with strong cytochrome P450 3A4 (CYP3A) inducers – rifampin, phenobarbital, St. John’s wort, among others – because they might reduce efficacy, and against use with CYP3A inhibitors – ketoconazole, clarithromycin, Seville oranges, grapefruit juice, etc. – because of the risk of increased exposure.
The most common side effects are headache, nausea, sinus congestion, and dizziness. The FDA has cleared a CF gene test to check for the required mutations. Symdeko is marketed by Vertex Pharmaceuticals.
Cannabis vaping among teens tied to tobacco use
and that practice is associated with cigars, waterpipe and e-cigarette use, findings from a survey of nearly 3,000 adolescents have shown.
“Although the prevalence of e-cigarette use among youth has increased dramatically in the past decade, little epidemiologic data exist on the prevalence of using e-cigarette devices or other specialised devices to vaporise (‘vape’) cannabis in the form of hash oil, tetrahydrocannabinol (THC) wax or oil, or dried cannabis buds or leaves,” wrote Sarah D. Kowitt, PhD, of the University of North Carolina, Chapel Hill, and colleagues. “This is surprising given that (1) cannabis (also referred to as marijuana) and e-cigarettes are the most commonly used substances by adolescents in the USA, (2) evidence exists that adolescents dual use both tobacco e-cigarettes and cannabis, and (3) longitudinal research suggests that use of e-cigarettes is associated with progression to use of cannabis.”
In a study published in BMJ Open, the researchers used data from the 2017 North Carolina Youth Tobacco Survey, a school-based survey of students in grades 6-12. The study population included 2,835 adolescents in grades 9-12.
Overall, 9.6% of students reported ever vaping cannabis. In multivariate analysis, cannabis vaping was significantly more likely among adolescents who reported using e-cigarettes (adjusted odds ratio 3.18), cigars (aOR 3.76), or water pipes (aOR 2.32) in the past 30 days, compared with peers who didn’t use tobacco.
The researchers found no significant association between smokeless tobacco use or traditional cigarette use in the past 30 days and vaping cannabis.
In a bivariate analysis, vaping cannabis was significantly more common among males vs. females (11% vs. 8.2%) and among non-Hispanic white students (11.3%), Hispanic students (10.5%), and other non-Hispanic students (11.8%) compared with non-Hispanic black students (5.0%).
In addition, prevalence of cannabis vaping increased with grade level, from 4.7% of 9th graders to 15.5% of 12th graders.
The health impacts of vaping cannabis are not well researched, but the researchers note that among the potential safety issues are earlier initiation of tobacco or cannabis use, concomitant tobacco and cannabis use, increased frequency of use or misuse of tobacco or cannabis, or increased potency of cannabis.
The results of the study were limited by several factors including the use of data only from the state of North Carolina, the lack of data on frequency or current vaping cannabis behavior, lack of data on specific products, and lack of data on whether teens used specialized devices or e-cigarettes for cannabis vaping. However, the findings are consistent with studies on prevalence of cannabis vaping in other states such as Connecticut and California. “No studies to our knowledge have examined how adolescents who vape cannabis use other specific tobacco products (i.e., cigarettes, cigars, waterpipe, smokeless tobacco),” the researchers wrote.
The findings confirm that a large number of adolescents who use tobacco products have vaped cannabis as well, and this growing public health issue “is likely to affect and be affected by tobacco control and cannabis policies in states and at the federal level in the USA,” the researchers concluded.
“Increased research investigating how youth use e-cigarette devices for other purposes beyond vaping nicotine, like the current study, is needed,” they added.
The study was supported in part by the National Cancer Institute and the Food and Drug Administration’s Center for Tobacco Products. The researchers had no financial conflicts to disclose.
SOURCE: Kowitt SD et al. BMJ Open. 2019 Jun 13. doi: 10.1136/bmjopen-2018-028535.
and that practice is associated with cigars, waterpipe and e-cigarette use, findings from a survey of nearly 3,000 adolescents have shown.
“Although the prevalence of e-cigarette use among youth has increased dramatically in the past decade, little epidemiologic data exist on the prevalence of using e-cigarette devices or other specialised devices to vaporise (‘vape’) cannabis in the form of hash oil, tetrahydrocannabinol (THC) wax or oil, or dried cannabis buds or leaves,” wrote Sarah D. Kowitt, PhD, of the University of North Carolina, Chapel Hill, and colleagues. “This is surprising given that (1) cannabis (also referred to as marijuana) and e-cigarettes are the most commonly used substances by adolescents in the USA, (2) evidence exists that adolescents dual use both tobacco e-cigarettes and cannabis, and (3) longitudinal research suggests that use of e-cigarettes is associated with progression to use of cannabis.”
In a study published in BMJ Open, the researchers used data from the 2017 North Carolina Youth Tobacco Survey, a school-based survey of students in grades 6-12. The study population included 2,835 adolescents in grades 9-12.
Overall, 9.6% of students reported ever vaping cannabis. In multivariate analysis, cannabis vaping was significantly more likely among adolescents who reported using e-cigarettes (adjusted odds ratio 3.18), cigars (aOR 3.76), or water pipes (aOR 2.32) in the past 30 days, compared with peers who didn’t use tobacco.
The researchers found no significant association between smokeless tobacco use or traditional cigarette use in the past 30 days and vaping cannabis.
In a bivariate analysis, vaping cannabis was significantly more common among males vs. females (11% vs. 8.2%) and among non-Hispanic white students (11.3%), Hispanic students (10.5%), and other non-Hispanic students (11.8%) compared with non-Hispanic black students (5.0%).
In addition, prevalence of cannabis vaping increased with grade level, from 4.7% of 9th graders to 15.5% of 12th graders.
The health impacts of vaping cannabis are not well researched, but the researchers note that among the potential safety issues are earlier initiation of tobacco or cannabis use, concomitant tobacco and cannabis use, increased frequency of use or misuse of tobacco or cannabis, or increased potency of cannabis.
The results of the study were limited by several factors including the use of data only from the state of North Carolina, the lack of data on frequency or current vaping cannabis behavior, lack of data on specific products, and lack of data on whether teens used specialized devices or e-cigarettes for cannabis vaping. However, the findings are consistent with studies on prevalence of cannabis vaping in other states such as Connecticut and California. “No studies to our knowledge have examined how adolescents who vape cannabis use other specific tobacco products (i.e., cigarettes, cigars, waterpipe, smokeless tobacco),” the researchers wrote.
The findings confirm that a large number of adolescents who use tobacco products have vaped cannabis as well, and this growing public health issue “is likely to affect and be affected by tobacco control and cannabis policies in states and at the federal level in the USA,” the researchers concluded.
“Increased research investigating how youth use e-cigarette devices for other purposes beyond vaping nicotine, like the current study, is needed,” they added.
The study was supported in part by the National Cancer Institute and the Food and Drug Administration’s Center for Tobacco Products. The researchers had no financial conflicts to disclose.
SOURCE: Kowitt SD et al. BMJ Open. 2019 Jun 13. doi: 10.1136/bmjopen-2018-028535.
and that practice is associated with cigars, waterpipe and e-cigarette use, findings from a survey of nearly 3,000 adolescents have shown.
“Although the prevalence of e-cigarette use among youth has increased dramatically in the past decade, little epidemiologic data exist on the prevalence of using e-cigarette devices or other specialised devices to vaporise (‘vape’) cannabis in the form of hash oil, tetrahydrocannabinol (THC) wax or oil, or dried cannabis buds or leaves,” wrote Sarah D. Kowitt, PhD, of the University of North Carolina, Chapel Hill, and colleagues. “This is surprising given that (1) cannabis (also referred to as marijuana) and e-cigarettes are the most commonly used substances by adolescents in the USA, (2) evidence exists that adolescents dual use both tobacco e-cigarettes and cannabis, and (3) longitudinal research suggests that use of e-cigarettes is associated with progression to use of cannabis.”
In a study published in BMJ Open, the researchers used data from the 2017 North Carolina Youth Tobacco Survey, a school-based survey of students in grades 6-12. The study population included 2,835 adolescents in grades 9-12.
Overall, 9.6% of students reported ever vaping cannabis. In multivariate analysis, cannabis vaping was significantly more likely among adolescents who reported using e-cigarettes (adjusted odds ratio 3.18), cigars (aOR 3.76), or water pipes (aOR 2.32) in the past 30 days, compared with peers who didn’t use tobacco.
The researchers found no significant association between smokeless tobacco use or traditional cigarette use in the past 30 days and vaping cannabis.
In a bivariate analysis, vaping cannabis was significantly more common among males vs. females (11% vs. 8.2%) and among non-Hispanic white students (11.3%), Hispanic students (10.5%), and other non-Hispanic students (11.8%) compared with non-Hispanic black students (5.0%).
In addition, prevalence of cannabis vaping increased with grade level, from 4.7% of 9th graders to 15.5% of 12th graders.
The health impacts of vaping cannabis are not well researched, but the researchers note that among the potential safety issues are earlier initiation of tobacco or cannabis use, concomitant tobacco and cannabis use, increased frequency of use or misuse of tobacco or cannabis, or increased potency of cannabis.
The results of the study were limited by several factors including the use of data only from the state of North Carolina, the lack of data on frequency or current vaping cannabis behavior, lack of data on specific products, and lack of data on whether teens used specialized devices or e-cigarettes for cannabis vaping. However, the findings are consistent with studies on prevalence of cannabis vaping in other states such as Connecticut and California. “No studies to our knowledge have examined how adolescents who vape cannabis use other specific tobacco products (i.e., cigarettes, cigars, waterpipe, smokeless tobacco),” the researchers wrote.
The findings confirm that a large number of adolescents who use tobacco products have vaped cannabis as well, and this growing public health issue “is likely to affect and be affected by tobacco control and cannabis policies in states and at the federal level in the USA,” the researchers concluded.
“Increased research investigating how youth use e-cigarette devices for other purposes beyond vaping nicotine, like the current study, is needed,” they added.
The study was supported in part by the National Cancer Institute and the Food and Drug Administration’s Center for Tobacco Products. The researchers had no financial conflicts to disclose.
SOURCE: Kowitt SD et al. BMJ Open. 2019 Jun 13. doi: 10.1136/bmjopen-2018-028535.
FROM BMJ OPEN
Key clinical point: Use of tobacco products was significantly associated with cannabis vaping in teens.
Major finding: Approximately 10% of adolescents reported vaping cannabis.
Study details: The data come from a survey of 2,835 adolescents in North Carolina.
Disclosures: The study was supported in part by the National Cancer Institute and the FDA Center for Tobacco Products. The researchers had no financial conflicts to disclose.
Source: Kowitt SD et al. BMJ Open. 2019 Jun 13. doi: 10.1136/bmjopen-2018-028535.
Inhaler technique not to blame for uncontrolled asthma in inner-city study
, a study has found.
“Incorrect inhaler technique cannot explain the poor disease control in our patient population,” wrote Patrick K. Gleeson, MD, of the University of Pennsylvania, Philadelphia, and coinvestigators. Their report is in the Journal of Allergy and Clinical Immunology: In Practice. “In individuals with poorly controlled asthma, other factors contributing to disease mortality must be considered.”
The 586 patients in the study were observed using their inhalers, and their technique was scored by way of a checklist developed for the study. Inhaler technique – widely regarded as a risk factor for poor disease control – was “better than expected,” the investigators reported, with 56% of patients using metered dose inhalers and 64% of those using dry powder inhalers not making any errors.
“The seeming disassociation between subjects’ asthma control and inhaler technique is counterintuitive, and may be explained by important baseline characteristics in our patients,” they wrote. For instance, participants had suboptimal living conditions in lower income Philadelphia neighborhoods. Almost a quarter – 23% – were current smokers, and almost half were Medicaid recipients. In addition, their mean body mass index was 35.1 kg/m2.
The investigators hypothesized that patients with lower health literacy would have poorer technique but found instead that technique did not vary by reading comprehension or numeracy levels.
More than half of the adults in the study had uncontrolled asthma as defined by prednisone use, an emergency department visit, or a hospitalization for asthma in the past 12 months. A subset had moderate to severe disease per a physician’s diagnosis, forced expiratory volume in 1 second less than 80% predicted, and improvement with a bronchodilator. All patients, however, were considered to have uncontrolled asthma.
There is “uncertainty” in the field about how to measure inhaler technique, and the technique checklist used in the study “may have omitted potentially important errors,” the investigators noted. Still, “good technique predominated among our [population of vulnerable patients].”
The project was supported through awards from the National Institutes of Health/National Heart, Lung, and Blood Institute and the Patient-Centered Outcomes Research Institute.
Coinvestigator Andrea J. Apter, MD, reported that she consults for UpToDate and is an associate editor for the journal. Coinvestigator Knashawn H. Morales, ScD, reported owning stock in Altria Group, British American Tobacco, and Philip Morris International. The other authors reported having no conflicts of interest.
SOURCE: Gleeson PK. J Allergy Clin Immunol Pract. 2019 Jun 5. doi: 10.1016/j.jaip.2019.05.048.
, a study has found.
“Incorrect inhaler technique cannot explain the poor disease control in our patient population,” wrote Patrick K. Gleeson, MD, of the University of Pennsylvania, Philadelphia, and coinvestigators. Their report is in the Journal of Allergy and Clinical Immunology: In Practice. “In individuals with poorly controlled asthma, other factors contributing to disease mortality must be considered.”
The 586 patients in the study were observed using their inhalers, and their technique was scored by way of a checklist developed for the study. Inhaler technique – widely regarded as a risk factor for poor disease control – was “better than expected,” the investigators reported, with 56% of patients using metered dose inhalers and 64% of those using dry powder inhalers not making any errors.
“The seeming disassociation between subjects’ asthma control and inhaler technique is counterintuitive, and may be explained by important baseline characteristics in our patients,” they wrote. For instance, participants had suboptimal living conditions in lower income Philadelphia neighborhoods. Almost a quarter – 23% – were current smokers, and almost half were Medicaid recipients. In addition, their mean body mass index was 35.1 kg/m2.
The investigators hypothesized that patients with lower health literacy would have poorer technique but found instead that technique did not vary by reading comprehension or numeracy levels.
More than half of the adults in the study had uncontrolled asthma as defined by prednisone use, an emergency department visit, or a hospitalization for asthma in the past 12 months. A subset had moderate to severe disease per a physician’s diagnosis, forced expiratory volume in 1 second less than 80% predicted, and improvement with a bronchodilator. All patients, however, were considered to have uncontrolled asthma.
There is “uncertainty” in the field about how to measure inhaler technique, and the technique checklist used in the study “may have omitted potentially important errors,” the investigators noted. Still, “good technique predominated among our [population of vulnerable patients].”
The project was supported through awards from the National Institutes of Health/National Heart, Lung, and Blood Institute and the Patient-Centered Outcomes Research Institute.
Coinvestigator Andrea J. Apter, MD, reported that she consults for UpToDate and is an associate editor for the journal. Coinvestigator Knashawn H. Morales, ScD, reported owning stock in Altria Group, British American Tobacco, and Philip Morris International. The other authors reported having no conflicts of interest.
SOURCE: Gleeson PK. J Allergy Clin Immunol Pract. 2019 Jun 5. doi: 10.1016/j.jaip.2019.05.048.
, a study has found.
“Incorrect inhaler technique cannot explain the poor disease control in our patient population,” wrote Patrick K. Gleeson, MD, of the University of Pennsylvania, Philadelphia, and coinvestigators. Their report is in the Journal of Allergy and Clinical Immunology: In Practice. “In individuals with poorly controlled asthma, other factors contributing to disease mortality must be considered.”
The 586 patients in the study were observed using their inhalers, and their technique was scored by way of a checklist developed for the study. Inhaler technique – widely regarded as a risk factor for poor disease control – was “better than expected,” the investigators reported, with 56% of patients using metered dose inhalers and 64% of those using dry powder inhalers not making any errors.
“The seeming disassociation between subjects’ asthma control and inhaler technique is counterintuitive, and may be explained by important baseline characteristics in our patients,” they wrote. For instance, participants had suboptimal living conditions in lower income Philadelphia neighborhoods. Almost a quarter – 23% – were current smokers, and almost half were Medicaid recipients. In addition, their mean body mass index was 35.1 kg/m2.
The investigators hypothesized that patients with lower health literacy would have poorer technique but found instead that technique did not vary by reading comprehension or numeracy levels.
More than half of the adults in the study had uncontrolled asthma as defined by prednisone use, an emergency department visit, or a hospitalization for asthma in the past 12 months. A subset had moderate to severe disease per a physician’s diagnosis, forced expiratory volume in 1 second less than 80% predicted, and improvement with a bronchodilator. All patients, however, were considered to have uncontrolled asthma.
There is “uncertainty” in the field about how to measure inhaler technique, and the technique checklist used in the study “may have omitted potentially important errors,” the investigators noted. Still, “good technique predominated among our [population of vulnerable patients].”
The project was supported through awards from the National Institutes of Health/National Heart, Lung, and Blood Institute and the Patient-Centered Outcomes Research Institute.
Coinvestigator Andrea J. Apter, MD, reported that she consults for UpToDate and is an associate editor for the journal. Coinvestigator Knashawn H. Morales, ScD, reported owning stock in Altria Group, British American Tobacco, and Philip Morris International. The other authors reported having no conflicts of interest.
SOURCE: Gleeson PK. J Allergy Clin Immunol Pract. 2019 Jun 5. doi: 10.1016/j.jaip.2019.05.048.
FROM THE JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY: IN PRACTICE
Key clinical point: Factors other than inhaler technique should be considered to explain uncontrolled asthma in a low-income, inner-city population.
Major finding: In the study, 56% of patients using metered dose inhalers and 64% of those using dry powder inhalers were using their devices correctly.
Study details: In all, 586 patients were observed using their inhalers, and their technique was scored by way of a checklist developed for the study.
Disclosures: The National Institutes of Health/National Heart, Lung, and Blood Institute and the Patient-Centered Outcomes Research Institute supported the study. Coinvestigator Andrea J. Apter, MD, consults for UpToDate and is an associate editor for the journal. Coinvestigator Knashawn H. Morales, ScD, reported owning stock in Altria Group, British American Tobacco, and Philip Morris International. The other authors reported having no conflicts of interest.
Source: Gleeson PK. J Allergy Clin Immunol Pract. 2019 Jun 5. doi: 10.1016/j.jaip.2019.05.048.
Sleep quality linked to gut microbiome biodiversity
SAN ANTONIO – , according to results from a population sample of adults.
“These findings are preliminary and very early in the growth of this field,” lead study author Erika W. Hagen, PhD, said during an interview at the annual meeting of the Associated Professional Sleep Societies
According to Dr. Hagen, an epidemiologist at the University of Wisconsin–Madison, experimental studies in mice have shown that disturbed sleep is associated with gut microbiota composition, and a few small experimental studies in humans have found associations between curtailed sleep and measures of gut microbiota richness and diversity.
In an effort to examine associations of subjectively and objectively assessed sleep metrics with indices of gut microbiome richness and diversity, Dr. Hagen and colleagues assessed 482 individuals who participated in the Survey of the Health of Wisconsin and completed in-home study visits in 2016. They provided fecal samples, participated in a week-long wrist actigraphy protocol to measure sleep, and completed questionnaires about sleep, diet, and other health and sociodemographic factors, and an assessment of physical activity by waist-worn actigraphy.
Metrics of species richness included the Chao1 and the ACE, which estimate the number of species. Metrics of the diversity of the gut microbiome included the Inverse Simpson index and the Shannon index. All metrics were regressed on self-reported sleep duration, extreme daytime sleepiness, the Epworth Sleepiness Scale (ESS), and actigraphy-measured sleep duration and wake after sleep onset (WASO). Next, the researchers estimated associations between each of the sleep and diversity measures separately, adjusting for age and sex and then additionally adjusting for body mass index, moderate-vigorous physical activity, and dietary fat and fiber.
The mean age of the 482 subjects was 56 years, 57% were female, and the mean body mass index was 30 kg/m2. After the researchers adjusted for gender and age, they found that greater WASO was statistically significantly associated with lower richness and alpha diversity (P less than .05). These associations remained significant on the Chao1 measure and borderline significant on the ACE and Shannon measures after further adjustment for BMI, physical activity, and dietary fiber and fat. For example, 60 minutes greater WASO was associated with an approximate 26% population standard deviation reduction in microbial richness as measured by Chao1. In fully-adjusted models, greater daytime sleepiness was associated with lower richness and diversity on all indices (P = .01-.06). The ESS and sleep duration were not associated with microbiota richness or diversity.
“Our results suggest that sleep quality is associated with gut microbiome richness and diversity,” Dr. Hagen said. “Our results are in line with other research on this topic. What’s interesting is how your sleep over a period of time is affecting these measures of your microbiome. That’s something people can do something about with [eating] habits over time. What would be great is to collect longitudinal data so that you could characterize sleep over a longer period of time, but also so you could measure the microbiome at different time points to see what’s changing with changes in sleep. That would be interesting to untangle.”
She acknowledged certain limitations of the study, including the small sample size and the cross-sectional design. The study was supported by the University of Wisconsin School of Medicine and Public Health through the Wisconsin Partnership Program.
SOURCE: Hagen EW et al. SLEEP 2019, Abstract 0106.
SAN ANTONIO – , according to results from a population sample of adults.
“These findings are preliminary and very early in the growth of this field,” lead study author Erika W. Hagen, PhD, said during an interview at the annual meeting of the Associated Professional Sleep Societies
According to Dr. Hagen, an epidemiologist at the University of Wisconsin–Madison, experimental studies in mice have shown that disturbed sleep is associated with gut microbiota composition, and a few small experimental studies in humans have found associations between curtailed sleep and measures of gut microbiota richness and diversity.
In an effort to examine associations of subjectively and objectively assessed sleep metrics with indices of gut microbiome richness and diversity, Dr. Hagen and colleagues assessed 482 individuals who participated in the Survey of the Health of Wisconsin and completed in-home study visits in 2016. They provided fecal samples, participated in a week-long wrist actigraphy protocol to measure sleep, and completed questionnaires about sleep, diet, and other health and sociodemographic factors, and an assessment of physical activity by waist-worn actigraphy.
Metrics of species richness included the Chao1 and the ACE, which estimate the number of species. Metrics of the diversity of the gut microbiome included the Inverse Simpson index and the Shannon index. All metrics were regressed on self-reported sleep duration, extreme daytime sleepiness, the Epworth Sleepiness Scale (ESS), and actigraphy-measured sleep duration and wake after sleep onset (WASO). Next, the researchers estimated associations between each of the sleep and diversity measures separately, adjusting for age and sex and then additionally adjusting for body mass index, moderate-vigorous physical activity, and dietary fat and fiber.
The mean age of the 482 subjects was 56 years, 57% were female, and the mean body mass index was 30 kg/m2. After the researchers adjusted for gender and age, they found that greater WASO was statistically significantly associated with lower richness and alpha diversity (P less than .05). These associations remained significant on the Chao1 measure and borderline significant on the ACE and Shannon measures after further adjustment for BMI, physical activity, and dietary fiber and fat. For example, 60 minutes greater WASO was associated with an approximate 26% population standard deviation reduction in microbial richness as measured by Chao1. In fully-adjusted models, greater daytime sleepiness was associated with lower richness and diversity on all indices (P = .01-.06). The ESS and sleep duration were not associated with microbiota richness or diversity.
“Our results suggest that sleep quality is associated with gut microbiome richness and diversity,” Dr. Hagen said. “Our results are in line with other research on this topic. What’s interesting is how your sleep over a period of time is affecting these measures of your microbiome. That’s something people can do something about with [eating] habits over time. What would be great is to collect longitudinal data so that you could characterize sleep over a longer period of time, but also so you could measure the microbiome at different time points to see what’s changing with changes in sleep. That would be interesting to untangle.”
She acknowledged certain limitations of the study, including the small sample size and the cross-sectional design. The study was supported by the University of Wisconsin School of Medicine and Public Health through the Wisconsin Partnership Program.
SOURCE: Hagen EW et al. SLEEP 2019, Abstract 0106.
SAN ANTONIO – , according to results from a population sample of adults.
“These findings are preliminary and very early in the growth of this field,” lead study author Erika W. Hagen, PhD, said during an interview at the annual meeting of the Associated Professional Sleep Societies
According to Dr. Hagen, an epidemiologist at the University of Wisconsin–Madison, experimental studies in mice have shown that disturbed sleep is associated with gut microbiota composition, and a few small experimental studies in humans have found associations between curtailed sleep and measures of gut microbiota richness and diversity.
In an effort to examine associations of subjectively and objectively assessed sleep metrics with indices of gut microbiome richness and diversity, Dr. Hagen and colleagues assessed 482 individuals who participated in the Survey of the Health of Wisconsin and completed in-home study visits in 2016. They provided fecal samples, participated in a week-long wrist actigraphy protocol to measure sleep, and completed questionnaires about sleep, diet, and other health and sociodemographic factors, and an assessment of physical activity by waist-worn actigraphy.
Metrics of species richness included the Chao1 and the ACE, which estimate the number of species. Metrics of the diversity of the gut microbiome included the Inverse Simpson index and the Shannon index. All metrics were regressed on self-reported sleep duration, extreme daytime sleepiness, the Epworth Sleepiness Scale (ESS), and actigraphy-measured sleep duration and wake after sleep onset (WASO). Next, the researchers estimated associations between each of the sleep and diversity measures separately, adjusting for age and sex and then additionally adjusting for body mass index, moderate-vigorous physical activity, and dietary fat and fiber.
The mean age of the 482 subjects was 56 years, 57% were female, and the mean body mass index was 30 kg/m2. After the researchers adjusted for gender and age, they found that greater WASO was statistically significantly associated with lower richness and alpha diversity (P less than .05). These associations remained significant on the Chao1 measure and borderline significant on the ACE and Shannon measures after further adjustment for BMI, physical activity, and dietary fiber and fat. For example, 60 minutes greater WASO was associated with an approximate 26% population standard deviation reduction in microbial richness as measured by Chao1. In fully-adjusted models, greater daytime sleepiness was associated with lower richness and diversity on all indices (P = .01-.06). The ESS and sleep duration were not associated with microbiota richness or diversity.
“Our results suggest that sleep quality is associated with gut microbiome richness and diversity,” Dr. Hagen said. “Our results are in line with other research on this topic. What’s interesting is how your sleep over a period of time is affecting these measures of your microbiome. That’s something people can do something about with [eating] habits over time. What would be great is to collect longitudinal data so that you could characterize sleep over a longer period of time, but also so you could measure the microbiome at different time points to see what’s changing with changes in sleep. That would be interesting to untangle.”
She acknowledged certain limitations of the study, including the small sample size and the cross-sectional design. The study was supported by the University of Wisconsin School of Medicine and Public Health through the Wisconsin Partnership Program.
SOURCE: Hagen EW et al. SLEEP 2019, Abstract 0106.
REPORTING FROM SLEEP 2019
Key clinical point: Better quality of sleep, but not duration of sleep, was associated with greater species richness and diversity of the gut microbiome.
Major finding: In fully adjusted models, greater daytime sleepiness was associated with lower richness and diversity of the gut microbiome on all indices (P = .01-.06).
Study details: An assessment of 482 individuals who participated in the Survey of the Health of Wisconsin.
Disclosures: The study was supported by the University of Wisconsin School of Medicine and Public Health through the Wisconsin Partnership Program.
Source: Hagen EW et al. SLEEP 2019, Abstract 0106.
Mortality risk from mild to moderate OSA modified by age
SAN ANTONIO – , results from a large longitudinal analysis showed.
“The association between severe OSA and significant morbidity and mortality – particularly cardiovascular in nature – is well established,” the study’s first author, Alexandros N. Vgontzas, MD, said at the annual meeting of the Associated Professional Sleep Societies. “In contrast, mild to moderate OSA is highly prevalent in the general population but its association with morbidity and mortality is not well established.”
In an effort to examine the association between mild to moderate OSA and all-cause mortality, Dr. Vgontzas and colleagues drew from the Penn State Adult Cohort, a random general population sample of 1,741 men and women who were studied in the sleep lab with an 8-hour polysomnography at baseline and followed for a mean of 19.2 years for all-cause mortality.
The researchers retrieved mortality data from the Centers for Disease Control and Prevention’s National Death Index and defined mild OSA as an apnea/hypopnea index (AHI) of 5-14.9 events per hour, while moderate OSA was defined as an AHI of 15-29.9 events per hour. They used Cox proportional hazards regression to estimate all-cause mortality and adjusted for race, sex, body mass index, smoking, hypertension, diabetes, heart problems, and stroke.
Dr. Vgontzas, of the Sleep Research and Treatment Center at Penn State University, Hershey, Pa., reported that 596 individuals have died since the study began. On adjusted analysis, patients with an AHI between 5 and 29 were 1.28 times as likely to die overall (P = .019). The researchers found that the association with mortality was stronger among patients younger than age 60, compared with those aged 60 and older. The hazard ratio was 1.44 for study participants younger than age 60 (P = .027), and 1.14 for those aged 60 and older (P = .34).
“Mild to moderate sleep apnea is associated with significant all-cause mortality risk, but the strength of the association decreases markedly with age,” Dr. Vgontzas concluded. “These findings are in line with previous findings that the association of mild to moderate OSA with cardiometabolic risk is modified by age and suggests that OSA in older adults is a distinctly different phenotype than in the young and middle-aged.”
The explanation for the association remains unclear. “Is it because the people of older age have some kind of genetic protection, or is because their sleep apnea is milder?” he asked. “We don’t have the data to tell.”
Dr. Vgontzas reported having no financial disclosures.
SOURCE: Vgontzas A et al. SLEEP 2019, abstract 0504.
SAN ANTONIO – , results from a large longitudinal analysis showed.
“The association between severe OSA and significant morbidity and mortality – particularly cardiovascular in nature – is well established,” the study’s first author, Alexandros N. Vgontzas, MD, said at the annual meeting of the Associated Professional Sleep Societies. “In contrast, mild to moderate OSA is highly prevalent in the general population but its association with morbidity and mortality is not well established.”
In an effort to examine the association between mild to moderate OSA and all-cause mortality, Dr. Vgontzas and colleagues drew from the Penn State Adult Cohort, a random general population sample of 1,741 men and women who were studied in the sleep lab with an 8-hour polysomnography at baseline and followed for a mean of 19.2 years for all-cause mortality.
The researchers retrieved mortality data from the Centers for Disease Control and Prevention’s National Death Index and defined mild OSA as an apnea/hypopnea index (AHI) of 5-14.9 events per hour, while moderate OSA was defined as an AHI of 15-29.9 events per hour. They used Cox proportional hazards regression to estimate all-cause mortality and adjusted for race, sex, body mass index, smoking, hypertension, diabetes, heart problems, and stroke.
Dr. Vgontzas, of the Sleep Research and Treatment Center at Penn State University, Hershey, Pa., reported that 596 individuals have died since the study began. On adjusted analysis, patients with an AHI between 5 and 29 were 1.28 times as likely to die overall (P = .019). The researchers found that the association with mortality was stronger among patients younger than age 60, compared with those aged 60 and older. The hazard ratio was 1.44 for study participants younger than age 60 (P = .027), and 1.14 for those aged 60 and older (P = .34).
“Mild to moderate sleep apnea is associated with significant all-cause mortality risk, but the strength of the association decreases markedly with age,” Dr. Vgontzas concluded. “These findings are in line with previous findings that the association of mild to moderate OSA with cardiometabolic risk is modified by age and suggests that OSA in older adults is a distinctly different phenotype than in the young and middle-aged.”
The explanation for the association remains unclear. “Is it because the people of older age have some kind of genetic protection, or is because their sleep apnea is milder?” he asked. “We don’t have the data to tell.”
Dr. Vgontzas reported having no financial disclosures.
SOURCE: Vgontzas A et al. SLEEP 2019, abstract 0504.
SAN ANTONIO – , results from a large longitudinal analysis showed.
“The association between severe OSA and significant morbidity and mortality – particularly cardiovascular in nature – is well established,” the study’s first author, Alexandros N. Vgontzas, MD, said at the annual meeting of the Associated Professional Sleep Societies. “In contrast, mild to moderate OSA is highly prevalent in the general population but its association with morbidity and mortality is not well established.”
In an effort to examine the association between mild to moderate OSA and all-cause mortality, Dr. Vgontzas and colleagues drew from the Penn State Adult Cohort, a random general population sample of 1,741 men and women who were studied in the sleep lab with an 8-hour polysomnography at baseline and followed for a mean of 19.2 years for all-cause mortality.
The researchers retrieved mortality data from the Centers for Disease Control and Prevention’s National Death Index and defined mild OSA as an apnea/hypopnea index (AHI) of 5-14.9 events per hour, while moderate OSA was defined as an AHI of 15-29.9 events per hour. They used Cox proportional hazards regression to estimate all-cause mortality and adjusted for race, sex, body mass index, smoking, hypertension, diabetes, heart problems, and stroke.
Dr. Vgontzas, of the Sleep Research and Treatment Center at Penn State University, Hershey, Pa., reported that 596 individuals have died since the study began. On adjusted analysis, patients with an AHI between 5 and 29 were 1.28 times as likely to die overall (P = .019). The researchers found that the association with mortality was stronger among patients younger than age 60, compared with those aged 60 and older. The hazard ratio was 1.44 for study participants younger than age 60 (P = .027), and 1.14 for those aged 60 and older (P = .34).
“Mild to moderate sleep apnea is associated with significant all-cause mortality risk, but the strength of the association decreases markedly with age,” Dr. Vgontzas concluded. “These findings are in line with previous findings that the association of mild to moderate OSA with cardiometabolic risk is modified by age and suggests that OSA in older adults is a distinctly different phenotype than in the young and middle-aged.”
The explanation for the association remains unclear. “Is it because the people of older age have some kind of genetic protection, or is because their sleep apnea is milder?” he asked. “We don’t have the data to tell.”
Dr. Vgontzas reported having no financial disclosures.
SOURCE: Vgontzas A et al. SLEEP 2019, abstract 0504.
REPORTING FROM SLEEP 2019
Key clinical point: Among adults with mild to moderate obstructive sleep apnea, the risk of mortality is highest among those younger than age 60.
Major finding: The hazard ratio for mortality was 1.44 for study participants younger than age 60 (P = .027), and 1.14 for those aged 60 and older (P = .34).
Study details: An analysis of 1,741 men and women from the Penn State Adult Cohort.
Disclosures: Dr. Vgontzas reported having no financial disclosures.
Source: Vgontzas A et al. SLEEP 2019, Abstract 0504.
Daytime eating schedule found to help with weight management
SAN ANTONIO – In adults of normal weight, a small controlled study has shown that a , independent of caloric intake.
The findings come from an 8-week controlled trial presented at the annual meeting of the Associated Professional Sleep Societies, which set out to examine the impact of a daytime versus delayed eating schedule on body mass, adiposity, and energy homeostasis in adults of normal weight.
“It is best to stop eating as early as possible in the day, and to not eat late at night,” the study’s first author, Namni Goel, PhD, said in an interview at the meeting. “There’s an open question in our field: Should you stop eating at 7:00 p.m.? 8:00 p.m.? My own feeling is, the longer it is between when you stop eating and go to bed, the better off you are metabolically.”
Dr. Goel, associate professor in the division of sleep and chronobiology in the department of psychiatry at the University of Pennsylvania, Philadelphia, and colleagues enrolled 12 healthy adults to participate in a randomized cross-over study in free-living conditions. Three meals and two snacks consisting of comparable energy and macronutrient content were provided during two 8-week counterbalanced phases: 1) daytime eating (food consumed between 8:00 a.m. and 7:00 p.m, and 2) delayed eating (food consumed between 12:00 p.m. and 11:00 p.m. A 2-week washout period occurred between the conditions. “What we wanted to do is just manipulate the timing of eating and we provided all of the meals so we could control the caloric intake,” Dr. Goel said.
The researchers asked participants to maintain a sleep-wake cycle between 11:00 p.m. and 9:00 a.m. (verified by wrist actigraphy) and to limit physical activity. They assessed weight, adiposity, energy metabolism, and hormonal markers during four inpatient visits: 1) baseline; 2) after the first eating condition; 3) after the washout period, before the second eating condition began; and 4) after the second eating condition. They used two-way analysis of variance and Cohen’s d effect sizes to examine changes in anthropometrics and metabolic measures affected by eating schedule (daytime vs. delayed) and time (before vs. after each eating schedule).
The mean age of 12 study participants was 26 years; five were females. Their mean body mass index was 21.9 kg/m2. Dr. Goel reported that participants had excellent adherence to assigned eating schedules, with no differences between the conditions. Weight was decreased on the daytime vs. delayed eating schedule. Specifically, Cohen’s d effect sizes were 0.57 overall: 1.16 for females and 0.33 for males, all in the small to large range. Resting energy expenditure, respiratory quotient, and trunk fat percentage/leg fat percentage were decreased on the daytime vs. delayed eating condition, with Cohen’s d effect sizes of 0.45-1.02, all in the medium to large range. In addition, total cholesterol and insulin were decreased on the daytime eating condition (medium effect sizes of 0.60 and 0.57, respectively), while triglycerides and glucose were increased on the delayed condition (medium effect sizes of 0.46 and 0.52, respectively).
Weight, adiposity, energy metabolism, and hormonal measures did not differ significantly between the pre-daytime and pre-delayed eating conditions, suggesting that they returned to pre-condition levels after the washout period.
“One of the things we’re advocating is that with consistent daytime eating, you can lose weight and/or remain at weight maintenance,” Dr. Goel said. “Consistency is very important. Across 8 weeks, you’re becoming metabolically healthier because you’re not eating that late-night meal or snack. We had shown in previous sleep loss studies that people were eating 500 calories late in the evening on consecutive nights and gaining a substantial amount of weight.”
She and her colleagues are currently enrolling obese individuals into a similarly designed trial, “where we expect much bigger changes metabolically,” she said. The study was funded by a grant from the National Institutes of Health. Dr. Goel reported having no financial disclosures.
SOURCE: Goel N et al. SLEEP 2019, Abstract 0036.
SAN ANTONIO – In adults of normal weight, a small controlled study has shown that a , independent of caloric intake.
The findings come from an 8-week controlled trial presented at the annual meeting of the Associated Professional Sleep Societies, which set out to examine the impact of a daytime versus delayed eating schedule on body mass, adiposity, and energy homeostasis in adults of normal weight.
“It is best to stop eating as early as possible in the day, and to not eat late at night,” the study’s first author, Namni Goel, PhD, said in an interview at the meeting. “There’s an open question in our field: Should you stop eating at 7:00 p.m.? 8:00 p.m.? My own feeling is, the longer it is between when you stop eating and go to bed, the better off you are metabolically.”
Dr. Goel, associate professor in the division of sleep and chronobiology in the department of psychiatry at the University of Pennsylvania, Philadelphia, and colleagues enrolled 12 healthy adults to participate in a randomized cross-over study in free-living conditions. Three meals and two snacks consisting of comparable energy and macronutrient content were provided during two 8-week counterbalanced phases: 1) daytime eating (food consumed between 8:00 a.m. and 7:00 p.m, and 2) delayed eating (food consumed between 12:00 p.m. and 11:00 p.m. A 2-week washout period occurred between the conditions. “What we wanted to do is just manipulate the timing of eating and we provided all of the meals so we could control the caloric intake,” Dr. Goel said.
The researchers asked participants to maintain a sleep-wake cycle between 11:00 p.m. and 9:00 a.m. (verified by wrist actigraphy) and to limit physical activity. They assessed weight, adiposity, energy metabolism, and hormonal markers during four inpatient visits: 1) baseline; 2) after the first eating condition; 3) after the washout period, before the second eating condition began; and 4) after the second eating condition. They used two-way analysis of variance and Cohen’s d effect sizes to examine changes in anthropometrics and metabolic measures affected by eating schedule (daytime vs. delayed) and time (before vs. after each eating schedule).
The mean age of 12 study participants was 26 years; five were females. Their mean body mass index was 21.9 kg/m2. Dr. Goel reported that participants had excellent adherence to assigned eating schedules, with no differences between the conditions. Weight was decreased on the daytime vs. delayed eating schedule. Specifically, Cohen’s d effect sizes were 0.57 overall: 1.16 for females and 0.33 for males, all in the small to large range. Resting energy expenditure, respiratory quotient, and trunk fat percentage/leg fat percentage were decreased on the daytime vs. delayed eating condition, with Cohen’s d effect sizes of 0.45-1.02, all in the medium to large range. In addition, total cholesterol and insulin were decreased on the daytime eating condition (medium effect sizes of 0.60 and 0.57, respectively), while triglycerides and glucose were increased on the delayed condition (medium effect sizes of 0.46 and 0.52, respectively).
Weight, adiposity, energy metabolism, and hormonal measures did not differ significantly between the pre-daytime and pre-delayed eating conditions, suggesting that they returned to pre-condition levels after the washout period.
“One of the things we’re advocating is that with consistent daytime eating, you can lose weight and/or remain at weight maintenance,” Dr. Goel said. “Consistency is very important. Across 8 weeks, you’re becoming metabolically healthier because you’re not eating that late-night meal or snack. We had shown in previous sleep loss studies that people were eating 500 calories late in the evening on consecutive nights and gaining a substantial amount of weight.”
She and her colleagues are currently enrolling obese individuals into a similarly designed trial, “where we expect much bigger changes metabolically,” she said. The study was funded by a grant from the National Institutes of Health. Dr. Goel reported having no financial disclosures.
SOURCE: Goel N et al. SLEEP 2019, Abstract 0036.
SAN ANTONIO – In adults of normal weight, a small controlled study has shown that a , independent of caloric intake.
The findings come from an 8-week controlled trial presented at the annual meeting of the Associated Professional Sleep Societies, which set out to examine the impact of a daytime versus delayed eating schedule on body mass, adiposity, and energy homeostasis in adults of normal weight.
“It is best to stop eating as early as possible in the day, and to not eat late at night,” the study’s first author, Namni Goel, PhD, said in an interview at the meeting. “There’s an open question in our field: Should you stop eating at 7:00 p.m.? 8:00 p.m.? My own feeling is, the longer it is between when you stop eating and go to bed, the better off you are metabolically.”
Dr. Goel, associate professor in the division of sleep and chronobiology in the department of psychiatry at the University of Pennsylvania, Philadelphia, and colleagues enrolled 12 healthy adults to participate in a randomized cross-over study in free-living conditions. Three meals and two snacks consisting of comparable energy and macronutrient content were provided during two 8-week counterbalanced phases: 1) daytime eating (food consumed between 8:00 a.m. and 7:00 p.m, and 2) delayed eating (food consumed between 12:00 p.m. and 11:00 p.m. A 2-week washout period occurred between the conditions. “What we wanted to do is just manipulate the timing of eating and we provided all of the meals so we could control the caloric intake,” Dr. Goel said.
The researchers asked participants to maintain a sleep-wake cycle between 11:00 p.m. and 9:00 a.m. (verified by wrist actigraphy) and to limit physical activity. They assessed weight, adiposity, energy metabolism, and hormonal markers during four inpatient visits: 1) baseline; 2) after the first eating condition; 3) after the washout period, before the second eating condition began; and 4) after the second eating condition. They used two-way analysis of variance and Cohen’s d effect sizes to examine changes in anthropometrics and metabolic measures affected by eating schedule (daytime vs. delayed) and time (before vs. after each eating schedule).
The mean age of 12 study participants was 26 years; five were females. Their mean body mass index was 21.9 kg/m2. Dr. Goel reported that participants had excellent adherence to assigned eating schedules, with no differences between the conditions. Weight was decreased on the daytime vs. delayed eating schedule. Specifically, Cohen’s d effect sizes were 0.57 overall: 1.16 for females and 0.33 for males, all in the small to large range. Resting energy expenditure, respiratory quotient, and trunk fat percentage/leg fat percentage were decreased on the daytime vs. delayed eating condition, with Cohen’s d effect sizes of 0.45-1.02, all in the medium to large range. In addition, total cholesterol and insulin were decreased on the daytime eating condition (medium effect sizes of 0.60 and 0.57, respectively), while triglycerides and glucose were increased on the delayed condition (medium effect sizes of 0.46 and 0.52, respectively).
Weight, adiposity, energy metabolism, and hormonal measures did not differ significantly between the pre-daytime and pre-delayed eating conditions, suggesting that they returned to pre-condition levels after the washout period.
“One of the things we’re advocating is that with consistent daytime eating, you can lose weight and/or remain at weight maintenance,” Dr. Goel said. “Consistency is very important. Across 8 weeks, you’re becoming metabolically healthier because you’re not eating that late-night meal or snack. We had shown in previous sleep loss studies that people were eating 500 calories late in the evening on consecutive nights and gaining a substantial amount of weight.”
She and her colleagues are currently enrolling obese individuals into a similarly designed trial, “where we expect much bigger changes metabolically,” she said. The study was funded by a grant from the National Institutes of Health. Dr. Goel reported having no financial disclosures.
SOURCE: Goel N et al. SLEEP 2019, Abstract 0036.
REPORTING FROM SLEEP 2019
Key clinical point: A daytime eating schedule is likely beneficial for weight management and metabolic health.
Major finding: Weight was decreased on the daytime vs. delayed eating schedule with Cohen’s d effect of 0.57 overall: 1.16 for females and 0.33 for males, all in the small to large range.
Study details: A randomized trial of 12 healthy adults with normal body weight.
Disclosures: The study was funded by a grant from the National Institutes of Health. Dr. Goel reported having no financial disclosures.
Source: Goel N et al. SLEEP 2019, Abstract 0036.