Sleep Medicine

Individuals with preexisting sleep disturbances including obstructive sleep apnea (OSA), insomnia, and abnormal sleep duration showed significantly increased vulnerability to COVID-19, as well as an increased risk for hospitalization, mortality, and long COVID, according to new data from more than 8 million individuals.

Sleep disturbances, though common in the general population, are generally overlooked as a risk factor for COVID-19, wrote Jiawei Zhou, MD, of The First Hospital of China Medical University, Shenyang, China, and colleagues. Most previous research has focused on the impact of COVID-19 on sleep disturbances, not the impact of sleep disturbances on COVID-19, and most studies on the latter topic have focused only on OSA, the researchers wrote.

In a meta-analysis published in eClinicalMedicine, part of The Lancet Discovery Science, the researchers identified 48 observational studies published between October 27, 2023, and May 8, 2024, that involved COVID-19 and sleep disturbances including OSA, insomnia, abnormal sleep duration, and night shift work, among others. The study population included 8,664,026 adults.

The primary outcomes were COVID-19 susceptibility, hospitalization, mortality, and long COVID. Overall, the presence of preexisting sleep disturbances was associated with a significantly increased risk for each of these outcomes, with odds ratios (ORs) of 1.12, 1.25, 1.45, and 1.36, respectively.

In subgroup analyses, the association between preexisting sleep disturbances and greater susceptibility and hospitalization was higher in younger adults (younger than 60 years) than in older adults (aged 60 years and older), but the risk for death was lower in younger adults with sleep disturbances than in older adults with sleep disturbances (OR, 1.22 vs OR, 2.07, respectively). Men with sleep disturbances had a higher risk for COVID-19 mortality than women with sleep disturbances.

Preexisting sleep disturbances overall were significantly associated with long COVID and more so in a subgroup analysis of patients whose definition of long COVID was symptoms lasting 3 or more months vs those lasting 1 month (P = .029).

When the researchers broke down associations with COVID-19 outcomes and specific sleep disturbances, they found significant associations between OSA and all four primary outcomes. Abnormal sleep duration was associated with an increased risk for COVID-19 susceptibility, hospitalization, and long COVID. Night shift work was associated with an increased risk for COVID-19 susceptibility and hospitalization, and insomnia was associated with an increased risk for long COVID.

Although the exact mechanism behind the associations between preexisting sleep disturbances and COVID-19 outcomes is uncertain, persistent sleep deprivation could set the stage in various ways, including the promotion of elevated C-reactive protein and interleukin-6 levels, the researchers wrote.

“Overall, the compromised innate and adaptive immune functions combined with a persistent inflammatory state may explain the higher risk of susceptibility, severity, and longer recovery time observed in patients with sleep disturbances. Fortunately, early intervention for sleep disturbances could attenuate the adverse effects of COVID-19,” they noted in their discussion.

The findings were limited by several factors including the observational nature of the studies and the heterogeneity of outcomes, the researchers wrote. Looking ahead, randomized, controlled trials are needed to examine the effect of interventions for sleep disturbances in the prevention and course of COVID-19, they said.

However, the study is the first known to examine multiple types of sleep disturbances and their possible influences on the full clinical course of COVID-19 and support the need for early evaluation and intervention for individuals with sleep disturbances to reduce short-term and long-term effects of the disease, the researchers concluded.
 

Findings Reflect the Need to Address Sleep Issues Early

Although the results of the current study were not surprising, “it is always worth doing meta-analyses to see if there is a potential signal in the published data to suggest a need for a new study,” Arun Chatterjee, MD, professor of pulmonary, critical care, allergy, and immunologic diseases at Wake Forest University, Winston-Salem, North Carolina, said in an interview.

“Lack of sleep, whether acute active deprivation (zero sleep for one night) or subacute/chronic sleep debt, such as only 5 hours per night, has been demonstrated to affect lymphocyte proliferation, reduce immune globulin levels, increase inflammatory markers, shorten telomeres, and affect the immune system in various ways,” said Dr. Chatterjee, who was not involved in the meta-analysis.

The clinical takeaway from the current meta-analysis is that adequate sleep is important for various reasons, Dr. Chatterjee said. “Sleep disruption affects health across a spectrum of systems; adding an annual sleep wellness and screening event to healthcare visits is probably worth the investment,” he noted.

Much more is needed in the way of additional research, Dr. Chatterjee told this news organization. Notably, studies are needed to examine what sleep disruption does to immune status, as well as all other physiologic and mental health systems, he said.

The study was supported by the National Natural Science Foundation of China and the Key Laboratory of Respiratory Diseases of Liaoning Province. The researchers had no financial conflicts to disclose. Chatterjee had no financial conflicts to disclose.
 

A version of this article appeared on Medscape.com.

Individuals with preexisting sleep disturbances including obstructive sleep apnea (OSA), insomnia, and abnormal sleep duration showed significantly increased vulnerability to COVID-19, as well as an increased risk for hospitalization, mortality, and long COVID, according to new data from more than 8 million individuals.

Sleep disturbances, though common in the general population, are generally overlooked as a risk factor for COVID-19, wrote Jiawei Zhou, MD, of The First Hospital of China Medical University, Shenyang, China, and colleagues. Most previous research has focused on the impact of COVID-19 on sleep disturbances, not the impact of sleep disturbances on COVID-19, and most studies on the latter topic have focused only on OSA, the researchers wrote.

In a meta-analysis published in eClinicalMedicine, part of The Lancet Discovery Science, the researchers identified 48 observational studies published between October 27, 2023, and May 8, 2024, that involved COVID-19 and sleep disturbances including OSA, insomnia, abnormal sleep duration, and night shift work, among others. The study population included 8,664,026 adults.

The primary outcomes were COVID-19 susceptibility, hospitalization, mortality, and long COVID. Overall, the presence of preexisting sleep disturbances was associated with a significantly increased risk for each of these outcomes, with odds ratios (ORs) of 1.12, 1.25, 1.45, and 1.36, respectively.

In subgroup analyses, the association between preexisting sleep disturbances and greater susceptibility and hospitalization was higher in younger adults (younger than 60 years) than in older adults (aged 60 years and older), but the risk for death was lower in younger adults with sleep disturbances than in older adults with sleep disturbances (OR, 1.22 vs OR, 2.07, respectively). Men with sleep disturbances had a higher risk for COVID-19 mortality than women with sleep disturbances.

Preexisting sleep disturbances overall were significantly associated with long COVID and more so in a subgroup analysis of patients whose definition of long COVID was symptoms lasting 3 or more months vs those lasting 1 month (P = .029).

When the researchers broke down associations with COVID-19 outcomes and specific sleep disturbances, they found significant associations between OSA and all four primary outcomes. Abnormal sleep duration was associated with an increased risk for COVID-19 susceptibility, hospitalization, and long COVID. Night shift work was associated with an increased risk for COVID-19 susceptibility and hospitalization, and insomnia was associated with an increased risk for long COVID.

Although the exact mechanism behind the associations between preexisting sleep disturbances and COVID-19 outcomes is uncertain, persistent sleep deprivation could set the stage in various ways, including the promotion of elevated C-reactive protein and interleukin-6 levels, the researchers wrote.

“Overall, the compromised innate and adaptive immune functions combined with a persistent inflammatory state may explain the higher risk of susceptibility, severity, and longer recovery time observed in patients with sleep disturbances. Fortunately, early intervention for sleep disturbances could attenuate the adverse effects of COVID-19,” they noted in their discussion.

The findings were limited by several factors including the observational nature of the studies and the heterogeneity of outcomes, the researchers wrote. Looking ahead, randomized, controlled trials are needed to examine the effect of interventions for sleep disturbances in the prevention and course of COVID-19, they said.

However, the study is the first known to examine multiple types of sleep disturbances and their possible influences on the full clinical course of COVID-19 and support the need for early evaluation and intervention for individuals with sleep disturbances to reduce short-term and long-term effects of the disease, the researchers concluded.
 

Findings Reflect the Need to Address Sleep Issues Early

Although the results of the current study were not surprising, “it is always worth doing meta-analyses to see if there is a potential signal in the published data to suggest a need for a new study,” Arun Chatterjee, MD, professor of pulmonary, critical care, allergy, and immunologic diseases at Wake Forest University, Winston-Salem, North Carolina, said in an interview.

“Lack of sleep, whether acute active deprivation (zero sleep for one night) or subacute/chronic sleep debt, such as only 5 hours per night, has been demonstrated to affect lymphocyte proliferation, reduce immune globulin levels, increase inflammatory markers, shorten telomeres, and affect the immune system in various ways,” said Dr. Chatterjee, who was not involved in the meta-analysis.

The clinical takeaway from the current meta-analysis is that adequate sleep is important for various reasons, Dr. Chatterjee said. “Sleep disruption affects health across a spectrum of systems; adding an annual sleep wellness and screening event to healthcare visits is probably worth the investment,” he noted.

Much more is needed in the way of additional research, Dr. Chatterjee told this news organization. Notably, studies are needed to examine what sleep disruption does to immune status, as well as all other physiologic and mental health systems, he said.

The study was supported by the National Natural Science Foundation of China and the Key Laboratory of Respiratory Diseases of Liaoning Province. The researchers had no financial conflicts to disclose. Chatterjee had no financial conflicts to disclose.
 

A version of this article appeared on Medscape.com.

Individuals with preexisting sleep disturbances including obstructive sleep apnea (OSA), insomnia, and abnormal sleep duration showed significantly increased vulnerability to COVID-19, as well as an increased risk for hospitalization, mortality, and long COVID, according to new data from more than 8 million individuals.

Sleep disturbances, though common in the general population, are generally overlooked as a risk factor for COVID-19, wrote Jiawei Zhou, MD, of The First Hospital of China Medical University, Shenyang, China, and colleagues. Most previous research has focused on the impact of COVID-19 on sleep disturbances, not the impact of sleep disturbances on COVID-19, and most studies on the latter topic have focused only on OSA, the researchers wrote.

In a meta-analysis published in eClinicalMedicine, part of The Lancet Discovery Science, the researchers identified 48 observational studies published between October 27, 2023, and May 8, 2024, that involved COVID-19 and sleep disturbances including OSA, insomnia, abnormal sleep duration, and night shift work, among others. The study population included 8,664,026 adults.

The primary outcomes were COVID-19 susceptibility, hospitalization, mortality, and long COVID. Overall, the presence of preexisting sleep disturbances was associated with a significantly increased risk for each of these outcomes, with odds ratios (ORs) of 1.12, 1.25, 1.45, and 1.36, respectively.

In subgroup analyses, the association between preexisting sleep disturbances and greater susceptibility and hospitalization was higher in younger adults (younger than 60 years) than in older adults (aged 60 years and older), but the risk for death was lower in younger adults with sleep disturbances than in older adults with sleep disturbances (OR, 1.22 vs OR, 2.07, respectively). Men with sleep disturbances had a higher risk for COVID-19 mortality than women with sleep disturbances.

Preexisting sleep disturbances overall were significantly associated with long COVID and more so in a subgroup analysis of patients whose definition of long COVID was symptoms lasting 3 or more months vs those lasting 1 month (P = .029).

When the researchers broke down associations with COVID-19 outcomes and specific sleep disturbances, they found significant associations between OSA and all four primary outcomes. Abnormal sleep duration was associated with an increased risk for COVID-19 susceptibility, hospitalization, and long COVID. Night shift work was associated with an increased risk for COVID-19 susceptibility and hospitalization, and insomnia was associated with an increased risk for long COVID.

Although the exact mechanism behind the associations between preexisting sleep disturbances and COVID-19 outcomes is uncertain, persistent sleep deprivation could set the stage in various ways, including the promotion of elevated C-reactive protein and interleukin-6 levels, the researchers wrote.

“Overall, the compromised innate and adaptive immune functions combined with a persistent inflammatory state may explain the higher risk of susceptibility, severity, and longer recovery time observed in patients with sleep disturbances. Fortunately, early intervention for sleep disturbances could attenuate the adverse effects of COVID-19,” they noted in their discussion.

The findings were limited by several factors including the observational nature of the studies and the heterogeneity of outcomes, the researchers wrote. Looking ahead, randomized, controlled trials are needed to examine the effect of interventions for sleep disturbances in the prevention and course of COVID-19, they said.

However, the study is the first known to examine multiple types of sleep disturbances and their possible influences on the full clinical course of COVID-19 and support the need for early evaluation and intervention for individuals with sleep disturbances to reduce short-term and long-term effects of the disease, the researchers concluded.
 

Findings Reflect the Need to Address Sleep Issues Early

Although the results of the current study were not surprising, “it is always worth doing meta-analyses to see if there is a potential signal in the published data to suggest a need for a new study,” Arun Chatterjee, MD, professor of pulmonary, critical care, allergy, and immunologic diseases at Wake Forest University, Winston-Salem, North Carolina, said in an interview.

“Lack of sleep, whether acute active deprivation (zero sleep for one night) or subacute/chronic sleep debt, such as only 5 hours per night, has been demonstrated to affect lymphocyte proliferation, reduce immune globulin levels, increase inflammatory markers, shorten telomeres, and affect the immune system in various ways,” said Dr. Chatterjee, who was not involved in the meta-analysis.

The clinical takeaway from the current meta-analysis is that adequate sleep is important for various reasons, Dr. Chatterjee said. “Sleep disruption affects health across a spectrum of systems; adding an annual sleep wellness and screening event to healthcare visits is probably worth the investment,” he noted.

Much more is needed in the way of additional research, Dr. Chatterjee told this news organization. Notably, studies are needed to examine what sleep disruption does to immune status, as well as all other physiologic and mental health systems, he said.

The study was supported by the National Natural Science Foundation of China and the Key Laboratory of Respiratory Diseases of Liaoning Province. The researchers had no financial conflicts to disclose. Chatterjee had no financial conflicts to disclose.
 

A version of this article appeared on Medscape.com.

Individuals who are more active in the evening performed better on cognitive tests than did those who are typically more active in the morning hours, new research suggests. 

“Rather than just being personal preferences, these chronotypes could impact our cognitive function,” said study investigator, Raha West, MBChB, with Imperial College London, London, England, in a statement.

But the researchers also urged caution when interpreting the findings.

“It’s important to note that this doesn’t mean all morning people have worse cognitive performance. The findings reflect an overall trend where the majority might lean toward better cognition in the evening types,” Dr. West added. 

In addition, across the board, getting the recommended 7-9 hours of nightly sleep was best for cognitive function, and sleeping for less than 7 or more than 9 hours had detrimental effects on brain function regardless of whether an individual was a night owl or lark. 

The study was published online in BMJ Public Health. 
 

A UK Biobank Cohort Study 

The findings are based on a cross-sectional analysis of 26,820 adults aged 53-86 years from the UK Biobank database, who were categorized into two cohorts. 

Cohort 1 had 10,067 participants (56% women) who completed four cognitive tests measuring fluid intelligence/reasoning, pairs matching, reaction time, and prospective memory. Cohort 2 had 16,753 participants (56% women) who completed two cognitive assessments (pairs matching and reaction time).

Participants self-reported sleep duration, chronotype, and quality. Cognitive test scores were evaluated against sleep parameters and health and lifestyle factors including sex, age, vascular and cardiac conditions, diabetes,alcohol use, smoking habits, and body mass index.

The results revealed a positive association between normal sleep duration (7-9 hours) and cognitive scores in Cohort 1 (beta, 0.0567), while extended sleep duration negatively impacted scores across in Cohort 1 and 2 (beta, –0.188 and beta, –0.2619, respectively). 

An individual’s preference for evening or morning activity correlated strongly with their test scores. In particular, night owls consistently performed better on cognitive tests than early birds. 

“While understanding and working with your natural sleep tendencies is essential, it’s equally important to remember to get just enough sleep, not too long or too short,” Dr. West noted. “This is crucial for keeping your brain healthy and functioning at its best.”

Contrary to some previous findings, the study did not find a significant relationship between sleep, sleepiness/insomnia, and cognitive performance. This may be because specific aspects of insomnia, such as severity and chronicity, as well as comorbid conditions need to be considered, the investigators wrote. 

They added that age and diabetes consistently emerged as negative predictors of cognitive functioning across both cohorts, in line with previous research. 

Limitations of the study include the cross-sectional design, which limits causal inferences; the possibility of residual confounding; and reliance on self-reported sleep data.

Also, the study did not adjust for educational attainment, a factor potentially influential on cognitive performance and sleep patterns, because of incomplete data. The study also did not factor in depression and social isolation, which have been shown to increase the risk for cognitive decline.
 

No Real-World Implications

Several outside experts offered their perspective on the study in a statement from the UK nonprofit Science Media Centre. 

The study provides “interesting insights” into the difference in memory and thinking in people who identify themselves as a “morning” or “evening” person, Jacqui Hanley, PhD, with Alzheimer’s Research UK, said in the statement. 

However, without a detailed picture of what is going on in the brain, it’s not clear whether being a morning or evening person affects memory and thinking or whether a decline in cognition is causing changes to sleeping patterns, Dr. Hanley added. 

Roi Cohen Kadosh, PhD, CPsychol, professor of cognitive neuroscience, University of Surrey, Guildford, England, cautioned that there are “multiple potential reasons” for these associations. 

“Therefore, there are no implications in my view for the real world. I fear that the general public will not be able to understand that and will change their sleep pattern, while this study does not give any evidence that this will lead to any benefit,” Dr. Cohen Kadosh said. 

Jessica Chelekis, PhD, MBA, a sleep expert from Brunel University London, Uxbridge, England, said that the “main takeaway should be that the cultural belief that early risers are more productive than ‘night owls’ does not hold up to scientific scrutiny.” 

“While everyone should aim to get good-quality sleep each night, we should also try to be aware of what time of day we are at our (cognitive) best and work in ways that suit us. Night owls, in particular, should not be shamed into fitting a stereotype that favors an ‘early to bed, early to rise’ practice,” Dr. Chelekis said. 

Funding for the study was provided by the Korea Institute of Oriental Medicine in collaboration with Imperial College London. Dr. Hanley, Dr. Cohen Kadosh, and Dr. Chelekis have no relevant disclosures.

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

Individuals who are more active in the evening performed better on cognitive tests than did those who are typically more active in the morning hours, new research suggests. 

“Rather than just being personal preferences, these chronotypes could impact our cognitive function,” said study investigator, Raha West, MBChB, with Imperial College London, London, England, in a statement.

But the researchers also urged caution when interpreting the findings.

“It’s important to note that this doesn’t mean all morning people have worse cognitive performance. The findings reflect an overall trend where the majority might lean toward better cognition in the evening types,” Dr. West added. 

In addition, across the board, getting the recommended 7-9 hours of nightly sleep was best for cognitive function, and sleeping for less than 7 or more than 9 hours had detrimental effects on brain function regardless of whether an individual was a night owl or lark. 

The study was published online in BMJ Public Health. 
 

A UK Biobank Cohort Study 

The findings are based on a cross-sectional analysis of 26,820 adults aged 53-86 years from the UK Biobank database, who were categorized into two cohorts. 

Cohort 1 had 10,067 participants (56% women) who completed four cognitive tests measuring fluid intelligence/reasoning, pairs matching, reaction time, and prospective memory. Cohort 2 had 16,753 participants (56% women) who completed two cognitive assessments (pairs matching and reaction time).

Participants self-reported sleep duration, chronotype, and quality. Cognitive test scores were evaluated against sleep parameters and health and lifestyle factors including sex, age, vascular and cardiac conditions, diabetes,alcohol use, smoking habits, and body mass index.

The results revealed a positive association between normal sleep duration (7-9 hours) and cognitive scores in Cohort 1 (beta, 0.0567), while extended sleep duration negatively impacted scores across in Cohort 1 and 2 (beta, –0.188 and beta, –0.2619, respectively). 

An individual’s preference for evening or morning activity correlated strongly with their test scores. In particular, night owls consistently performed better on cognitive tests than early birds. 

“While understanding and working with your natural sleep tendencies is essential, it’s equally important to remember to get just enough sleep, not too long or too short,” Dr. West noted. “This is crucial for keeping your brain healthy and functioning at its best.”

Contrary to some previous findings, the study did not find a significant relationship between sleep, sleepiness/insomnia, and cognitive performance. This may be because specific aspects of insomnia, such as severity and chronicity, as well as comorbid conditions need to be considered, the investigators wrote. 

They added that age and diabetes consistently emerged as negative predictors of cognitive functioning across both cohorts, in line with previous research. 

Limitations of the study include the cross-sectional design, which limits causal inferences; the possibility of residual confounding; and reliance on self-reported sleep data.

Also, the study did not adjust for educational attainment, a factor potentially influential on cognitive performance and sleep patterns, because of incomplete data. The study also did not factor in depression and social isolation, which have been shown to increase the risk for cognitive decline.
 

No Real-World Implications

Several outside experts offered their perspective on the study in a statement from the UK nonprofit Science Media Centre. 

The study provides “interesting insights” into the difference in memory and thinking in people who identify themselves as a “morning” or “evening” person, Jacqui Hanley, PhD, with Alzheimer’s Research UK, said in the statement. 

However, without a detailed picture of what is going on in the brain, it’s not clear whether being a morning or evening person affects memory and thinking or whether a decline in cognition is causing changes to sleeping patterns, Dr. Hanley added. 

Roi Cohen Kadosh, PhD, CPsychol, professor of cognitive neuroscience, University of Surrey, Guildford, England, cautioned that there are “multiple potential reasons” for these associations. 

“Therefore, there are no implications in my view for the real world. I fear that the general public will not be able to understand that and will change their sleep pattern, while this study does not give any evidence that this will lead to any benefit,” Dr. Cohen Kadosh said. 

Jessica Chelekis, PhD, MBA, a sleep expert from Brunel University London, Uxbridge, England, said that the “main takeaway should be that the cultural belief that early risers are more productive than ‘night owls’ does not hold up to scientific scrutiny.” 

“While everyone should aim to get good-quality sleep each night, we should also try to be aware of what time of day we are at our (cognitive) best and work in ways that suit us. Night owls, in particular, should not be shamed into fitting a stereotype that favors an ‘early to bed, early to rise’ practice,” Dr. Chelekis said. 

Funding for the study was provided by the Korea Institute of Oriental Medicine in collaboration with Imperial College London. Dr. Hanley, Dr. Cohen Kadosh, and Dr. Chelekis have no relevant disclosures.

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

Individuals who are more active in the evening performed better on cognitive tests than did those who are typically more active in the morning hours, new research suggests. 

“Rather than just being personal preferences, these chronotypes could impact our cognitive function,” said study investigator, Raha West, MBChB, with Imperial College London, London, England, in a statement.

But the researchers also urged caution when interpreting the findings.

“It’s important to note that this doesn’t mean all morning people have worse cognitive performance. The findings reflect an overall trend where the majority might lean toward better cognition in the evening types,” Dr. West added. 

In addition, across the board, getting the recommended 7-9 hours of nightly sleep was best for cognitive function, and sleeping for less than 7 or more than 9 hours had detrimental effects on brain function regardless of whether an individual was a night owl or lark. 

The study was published online in BMJ Public Health. 
 

A UK Biobank Cohort Study 

The findings are based on a cross-sectional analysis of 26,820 adults aged 53-86 years from the UK Biobank database, who were categorized into two cohorts. 

Cohort 1 had 10,067 participants (56% women) who completed four cognitive tests measuring fluid intelligence/reasoning, pairs matching, reaction time, and prospective memory. Cohort 2 had 16,753 participants (56% women) who completed two cognitive assessments (pairs matching and reaction time).

Participants self-reported sleep duration, chronotype, and quality. Cognitive test scores were evaluated against sleep parameters and health and lifestyle factors including sex, age, vascular and cardiac conditions, diabetes,alcohol use, smoking habits, and body mass index.

The results revealed a positive association between normal sleep duration (7-9 hours) and cognitive scores in Cohort 1 (beta, 0.0567), while extended sleep duration negatively impacted scores across in Cohort 1 and 2 (beta, –0.188 and beta, –0.2619, respectively). 

An individual’s preference for evening or morning activity correlated strongly with their test scores. In particular, night owls consistently performed better on cognitive tests than early birds. 

“While understanding and working with your natural sleep tendencies is essential, it’s equally important to remember to get just enough sleep, not too long or too short,” Dr. West noted. “This is crucial for keeping your brain healthy and functioning at its best.”

Contrary to some previous findings, the study did not find a significant relationship between sleep, sleepiness/insomnia, and cognitive performance. This may be because specific aspects of insomnia, such as severity and chronicity, as well as comorbid conditions need to be considered, the investigators wrote. 

They added that age and diabetes consistently emerged as negative predictors of cognitive functioning across both cohorts, in line with previous research. 

Limitations of the study include the cross-sectional design, which limits causal inferences; the possibility of residual confounding; and reliance on self-reported sleep data.

Also, the study did not adjust for educational attainment, a factor potentially influential on cognitive performance and sleep patterns, because of incomplete data. The study also did not factor in depression and social isolation, which have been shown to increase the risk for cognitive decline.
 

No Real-World Implications

Several outside experts offered their perspective on the study in a statement from the UK nonprofit Science Media Centre. 

The study provides “interesting insights” into the difference in memory and thinking in people who identify themselves as a “morning” or “evening” person, Jacqui Hanley, PhD, with Alzheimer’s Research UK, said in the statement. 

However, without a detailed picture of what is going on in the brain, it’s not clear whether being a morning or evening person affects memory and thinking or whether a decline in cognition is causing changes to sleeping patterns, Dr. Hanley added. 

Roi Cohen Kadosh, PhD, CPsychol, professor of cognitive neuroscience, University of Surrey, Guildford, England, cautioned that there are “multiple potential reasons” for these associations. 

“Therefore, there are no implications in my view for the real world. I fear that the general public will not be able to understand that and will change their sleep pattern, while this study does not give any evidence that this will lead to any benefit,” Dr. Cohen Kadosh said. 

Jessica Chelekis, PhD, MBA, a sleep expert from Brunel University London, Uxbridge, England, said that the “main takeaway should be that the cultural belief that early risers are more productive than ‘night owls’ does not hold up to scientific scrutiny.” 

“While everyone should aim to get good-quality sleep each night, we should also try to be aware of what time of day we are at our (cognitive) best and work in ways that suit us. Night owls, in particular, should not be shamed into fitting a stereotype that favors an ‘early to bed, early to rise’ practice,” Dr. Chelekis said. 

Funding for the study was provided by the Korea Institute of Oriental Medicine in collaboration with Imperial College London. Dr. Hanley, Dr. Cohen Kadosh, and Dr. Chelekis have no relevant disclosures.

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

Concerned about your patient’s type 2 diabetes risk? Along with the usual preventive strategies — like diet and exercise and, when appropriate, glucagon-like peptide 1 (GLP-1) agonists — there’s another simple, no-risk strategy that just might help: Turning off the light at night.

A study in The Lancet found that people who were exposed to the most light between 12:30 a.m. and 6 a.m. were 1.5 times more likely to develop diabetes than those who remained in darkness during that time frame.

The study builds on growing evidence linking nighttime light exposure to type 2 diabetes risk. But unlike previous large studies that relied on satellite data of outdoor light levels (an indirect measure of light exposure), the recent study looked at personal light exposure — that is, light measured directly on individuals — as recorded by a wrist-worn sensor.

“Those previous studies likely underestimated the effect,” said study author Andrew Phillips, PhD, professor of sleep health at Flinders University in Adelaide, Australia, “since they did not capture indoor light environments.”

Using data from 85,000 participants from the UK Biobank, the recent study is the largest to date linking diabetes risk to personal light exposure at night.

“This is really a phenomenal study,” said Courtney Peterson, PhD, a scientist at the University of Alabama at Birmingham’s Diabetes Research Center, who was not involved in the study. “This is the first large-scale study we have looking at people’s light exposure patterns and linking it to their long-term health.”
 

What the Study Showed

The participants wore the light sensors for a week, recording day and night light from all sources — whether from sunlight, lamps, streetlights, or digital screens. The researchers then tracked participants for 8 years.

“About half of the people that we looked at had very dim levels of light at night, so less than 1 lux — that basically means less than candlelight,” said Dr. Phillips. “They were the people who were protected against type 2 diabetes.”

Those exposed to more light at night — defined in the study as 12:30 a.m.–6 a.m. — had a higher risk for type 2 diabetes. The risk went up as a dose response, Phillips said: The brighter the light exposure, the higher the diabetes risk.

Participants in the top 10% of light exposure — who were exposed to about 48 lux , or the equivalent of relatively dim overhead lighting — were 1.5 times more likely to develop diabetes than those in the dark. That’s about the risk increase you’d get from having a family history of type 2 diabetes, the researchers said.

Even when they controlled for factors like socioeconomic status, smoking, diet, exercise, and shift work, “we still found there was this very strong relationship between light exposure and risk of type 2 diabetes,” said Dr. Phillips.
 

How Light at Night May Increase Diabetes Risk

The results are not entirely surprising, said endocrinologist Susanne Miedlich, MD, a professor at the University of Rochester Medical Center, Rochester, New York, who was not involved in the study.

Light at night can disrupt the circadian rhythm, or your body’s internal 24-hour cycle. And scientists have long known that circadian rhythm is important for all kinds of biologic processes, including how the body manages blood sugar.

One’s internal clock regulates food intake, sugar absorption, and the release of insulin. Dysregulation in the circadian rhythm is associated with insulin resistance, a precursor to type 2 diabetes.

Dr. Phillips speculated that the sleep hormone melatonin also plays a role.

“Melatonin does a lot of things, but one of the things that it does is it manages our glucose and our insulin responses,” Dr. Phillips said. “So if you’re chronically getting light exposure at night, that’s reducing a level of melatonin that, in the long term, could lead to poor metabolic outcomes.”

Previous studies have explored melatonin supplementation to help manage diabetes. “However, while melatonin clearly regulates circadian rhythms, its utility as a drug to prevent diabetes has not really panned out thus far,” Dr. Miedlich said.
 

Takeaways

Interventional studies are needed to confirm whether strategies like powering down screens, turning off lights, or using blackout curtains could reduce diabetes risk.

That said, “there’s no reason not to tell people to get healthy light exposure patterns and sleep, especially in the context of diabetes,” said Dr. Phillips.

Other known strategies for reducing diabetes risk include intensive lifestyle programs, which reduce risk by up to 58%, and GLP-1 agonists.

“Probably a GLP-1 agonist is going to be more effective,” Dr. Peterson said. “But this is still a fairly large effect without having to go through the expense of buying a GLP-1 or losing a lot of weight or making a big lifestyle change.”

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

Concerned about your patient’s type 2 diabetes risk? Along with the usual preventive strategies — like diet and exercise and, when appropriate, glucagon-like peptide 1 (GLP-1) agonists — there’s another simple, no-risk strategy that just might help: Turning off the light at night.

A study in The Lancet found that people who were exposed to the most light between 12:30 a.m. and 6 a.m. were 1.5 times more likely to develop diabetes than those who remained in darkness during that time frame.

The study builds on growing evidence linking nighttime light exposure to type 2 diabetes risk. But unlike previous large studies that relied on satellite data of outdoor light levels (an indirect measure of light exposure), the recent study looked at personal light exposure — that is, light measured directly on individuals — as recorded by a wrist-worn sensor.

“Those previous studies likely underestimated the effect,” said study author Andrew Phillips, PhD, professor of sleep health at Flinders University in Adelaide, Australia, “since they did not capture indoor light environments.”

Using data from 85,000 participants from the UK Biobank, the recent study is the largest to date linking diabetes risk to personal light exposure at night.

“This is really a phenomenal study,” said Courtney Peterson, PhD, a scientist at the University of Alabama at Birmingham’s Diabetes Research Center, who was not involved in the study. “This is the first large-scale study we have looking at people’s light exposure patterns and linking it to their long-term health.”
 

What the Study Showed

The participants wore the light sensors for a week, recording day and night light from all sources — whether from sunlight, lamps, streetlights, or digital screens. The researchers then tracked participants for 8 years.

“About half of the people that we looked at had very dim levels of light at night, so less than 1 lux — that basically means less than candlelight,” said Dr. Phillips. “They were the people who were protected against type 2 diabetes.”

Those exposed to more light at night — defined in the study as 12:30 a.m.–6 a.m. — had a higher risk for type 2 diabetes. The risk went up as a dose response, Phillips said: The brighter the light exposure, the higher the diabetes risk.

Participants in the top 10% of light exposure — who were exposed to about 48 lux , or the equivalent of relatively dim overhead lighting — were 1.5 times more likely to develop diabetes than those in the dark. That’s about the risk increase you’d get from having a family history of type 2 diabetes, the researchers said.

Even when they controlled for factors like socioeconomic status, smoking, diet, exercise, and shift work, “we still found there was this very strong relationship between light exposure and risk of type 2 diabetes,” said Dr. Phillips.
 

How Light at Night May Increase Diabetes Risk

The results are not entirely surprising, said endocrinologist Susanne Miedlich, MD, a professor at the University of Rochester Medical Center, Rochester, New York, who was not involved in the study.

Light at night can disrupt the circadian rhythm, or your body’s internal 24-hour cycle. And scientists have long known that circadian rhythm is important for all kinds of biologic processes, including how the body manages blood sugar.

One’s internal clock regulates food intake, sugar absorption, and the release of insulin. Dysregulation in the circadian rhythm is associated with insulin resistance, a precursor to type 2 diabetes.

Dr. Phillips speculated that the sleep hormone melatonin also plays a role.

“Melatonin does a lot of things, but one of the things that it does is it manages our glucose and our insulin responses,” Dr. Phillips said. “So if you’re chronically getting light exposure at night, that’s reducing a level of melatonin that, in the long term, could lead to poor metabolic outcomes.”

Previous studies have explored melatonin supplementation to help manage diabetes. “However, while melatonin clearly regulates circadian rhythms, its utility as a drug to prevent diabetes has not really panned out thus far,” Dr. Miedlich said.
 

Takeaways

Interventional studies are needed to confirm whether strategies like powering down screens, turning off lights, or using blackout curtains could reduce diabetes risk.

That said, “there’s no reason not to tell people to get healthy light exposure patterns and sleep, especially in the context of diabetes,” said Dr. Phillips.

Other known strategies for reducing diabetes risk include intensive lifestyle programs, which reduce risk by up to 58%, and GLP-1 agonists.

“Probably a GLP-1 agonist is going to be more effective,” Dr. Peterson said. “But this is still a fairly large effect without having to go through the expense of buying a GLP-1 or losing a lot of weight or making a big lifestyle change.”

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

Concerned about your patient’s type 2 diabetes risk? Along with the usual preventive strategies — like diet and exercise and, when appropriate, glucagon-like peptide 1 (GLP-1) agonists — there’s another simple, no-risk strategy that just might help: Turning off the light at night.

A study in The Lancet found that people who were exposed to the most light between 12:30 a.m. and 6 a.m. were 1.5 times more likely to develop diabetes than those who remained in darkness during that time frame.

The study builds on growing evidence linking nighttime light exposure to type 2 diabetes risk. But unlike previous large studies that relied on satellite data of outdoor light levels (an indirect measure of light exposure), the recent study looked at personal light exposure — that is, light measured directly on individuals — as recorded by a wrist-worn sensor.

“Those previous studies likely underestimated the effect,” said study author Andrew Phillips, PhD, professor of sleep health at Flinders University in Adelaide, Australia, “since they did not capture indoor light environments.”

Using data from 85,000 participants from the UK Biobank, the recent study is the largest to date linking diabetes risk to personal light exposure at night.

“This is really a phenomenal study,” said Courtney Peterson, PhD, a scientist at the University of Alabama at Birmingham’s Diabetes Research Center, who was not involved in the study. “This is the first large-scale study we have looking at people’s light exposure patterns and linking it to their long-term health.”
 

What the Study Showed

The participants wore the light sensors for a week, recording day and night light from all sources — whether from sunlight, lamps, streetlights, or digital screens. The researchers then tracked participants for 8 years.

“About half of the people that we looked at had very dim levels of light at night, so less than 1 lux — that basically means less than candlelight,” said Dr. Phillips. “They were the people who were protected against type 2 diabetes.”

Those exposed to more light at night — defined in the study as 12:30 a.m.–6 a.m. — had a higher risk for type 2 diabetes. The risk went up as a dose response, Phillips said: The brighter the light exposure, the higher the diabetes risk.

Participants in the top 10% of light exposure — who were exposed to about 48 lux , or the equivalent of relatively dim overhead lighting — were 1.5 times more likely to develop diabetes than those in the dark. That’s about the risk increase you’d get from having a family history of type 2 diabetes, the researchers said.

Even when they controlled for factors like socioeconomic status, smoking, diet, exercise, and shift work, “we still found there was this very strong relationship between light exposure and risk of type 2 diabetes,” said Dr. Phillips.
 

How Light at Night May Increase Diabetes Risk

The results are not entirely surprising, said endocrinologist Susanne Miedlich, MD, a professor at the University of Rochester Medical Center, Rochester, New York, who was not involved in the study.

Light at night can disrupt the circadian rhythm, or your body’s internal 24-hour cycle. And scientists have long known that circadian rhythm is important for all kinds of biologic processes, including how the body manages blood sugar.

One’s internal clock regulates food intake, sugar absorption, and the release of insulin. Dysregulation in the circadian rhythm is associated with insulin resistance, a precursor to type 2 diabetes.

Dr. Phillips speculated that the sleep hormone melatonin also plays a role.

“Melatonin does a lot of things, but one of the things that it does is it manages our glucose and our insulin responses,” Dr. Phillips said. “So if you’re chronically getting light exposure at night, that’s reducing a level of melatonin that, in the long term, could lead to poor metabolic outcomes.”

Previous studies have explored melatonin supplementation to help manage diabetes. “However, while melatonin clearly regulates circadian rhythms, its utility as a drug to prevent diabetes has not really panned out thus far,” Dr. Miedlich said.
 

Takeaways

Interventional studies are needed to confirm whether strategies like powering down screens, turning off lights, or using blackout curtains could reduce diabetes risk.

That said, “there’s no reason not to tell people to get healthy light exposure patterns and sleep, especially in the context of diabetes,” said Dr. Phillips.

Other known strategies for reducing diabetes risk include intensive lifestyle programs, which reduce risk by up to 58%, and GLP-1 agonists.

“Probably a GLP-1 agonist is going to be more effective,” Dr. Peterson said. “But this is still a fairly large effect without having to go through the expense of buying a GLP-1 or losing a lot of weight or making a big lifestyle change.”

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

Philips Respironics Inc. has issued updated instructions for the use of its OmniLab Advanced+ (OLA+) Ventilator because of its demonstrated failure in the ventilator inoperative alarm that can cause an interruption or loss of therapy, according to a recall statement from the US Food and Drug Administration (FDA).

The OLA+ Ventilator is designed for use by individuals with obstructive sleep apnea, breathing problems, and mixed apnea and is approved for children aged 7 years and older, as well as adults.

The recall does not involve removal of the devices from where they are used or sold but does update the instructions for use, and its use without following the updated instructions could result in serious injury or death, according to the statement.

Following an alarm failure, the device may fail in one of two ways: By entering a ventilator inoperative state after three reboots within 24 hours (with no therapy and audible and visual alarms present) or by entering a ventilator inoperative state without rebooting first.

According to the statement, the alarm issue may be corrected with a software patch, available from Philips, or the company will offer a replacement device for patients until the affected devices are repaired. The statement updates an April 1, 2024, urgent recall from Philips urging the immediate removal of a patient from an OLA+ Ventilator and connecting them to alternative ventilation if possible if the ventilator’s inoperative alarm occurs.

The device failures may cause interruption or loss of therapy with effects including anxiety, confusion/disorientation, changes in respiratory rate, dyspnea, tachycardia, respiratory failure, and even death in especially vulnerable individuals. One death and 15 injuries have been reported as a result of the alarm failure, according to the FDA.

US customers can contact Philips Respironics Inc. at 1-800-345-6443 or respironics.clinical@philips.com with questions, according to the FDA, and clinicians and patients may report adverse reactions or other problems with the devices to MedWatch: The FDA Safety Information and Adverse Event Reporting Program.

A version of this article appeared on Medscape.com.

Philips Respironics Inc. has issued updated instructions for the use of its OmniLab Advanced+ (OLA+) Ventilator because of its demonstrated failure in the ventilator inoperative alarm that can cause an interruption or loss of therapy, according to a recall statement from the US Food and Drug Administration (FDA).

The OLA+ Ventilator is designed for use by individuals with obstructive sleep apnea, breathing problems, and mixed apnea and is approved for children aged 7 years and older, as well as adults.

The recall does not involve removal of the devices from where they are used or sold but does update the instructions for use, and its use without following the updated instructions could result in serious injury or death, according to the statement.

Following an alarm failure, the device may fail in one of two ways: By entering a ventilator inoperative state after three reboots within 24 hours (with no therapy and audible and visual alarms present) or by entering a ventilator inoperative state without rebooting first.

According to the statement, the alarm issue may be corrected with a software patch, available from Philips, or the company will offer a replacement device for patients until the affected devices are repaired. The statement updates an April 1, 2024, urgent recall from Philips urging the immediate removal of a patient from an OLA+ Ventilator and connecting them to alternative ventilation if possible if the ventilator’s inoperative alarm occurs.

The device failures may cause interruption or loss of therapy with effects including anxiety, confusion/disorientation, changes in respiratory rate, dyspnea, tachycardia, respiratory failure, and even death in especially vulnerable individuals. One death and 15 injuries have been reported as a result of the alarm failure, according to the FDA.

US customers can contact Philips Respironics Inc. at 1-800-345-6443 or respironics.clinical@philips.com with questions, according to the FDA, and clinicians and patients may report adverse reactions or other problems with the devices to MedWatch: The FDA Safety Information and Adverse Event Reporting Program.

A version of this article appeared on Medscape.com.

Philips Respironics Inc. has issued updated instructions for the use of its OmniLab Advanced+ (OLA+) Ventilator because of its demonstrated failure in the ventilator inoperative alarm that can cause an interruption or loss of therapy, according to a recall statement from the US Food and Drug Administration (FDA).

The OLA+ Ventilator is designed for use by individuals with obstructive sleep apnea, breathing problems, and mixed apnea and is approved for children aged 7 years and older, as well as adults.

The recall does not involve removal of the devices from where they are used or sold but does update the instructions for use, and its use without following the updated instructions could result in serious injury or death, according to the statement.

Following an alarm failure, the device may fail in one of two ways: By entering a ventilator inoperative state after three reboots within 24 hours (with no therapy and audible and visual alarms present) or by entering a ventilator inoperative state without rebooting first.

According to the statement, the alarm issue may be corrected with a software patch, available from Philips, or the company will offer a replacement device for patients until the affected devices are repaired. The statement updates an April 1, 2024, urgent recall from Philips urging the immediate removal of a patient from an OLA+ Ventilator and connecting them to alternative ventilation if possible if the ventilator’s inoperative alarm occurs.

The device failures may cause interruption or loss of therapy with effects including anxiety, confusion/disorientation, changes in respiratory rate, dyspnea, tachycardia, respiratory failure, and even death in especially vulnerable individuals. One death and 15 injuries have been reported as a result of the alarm failure, according to the FDA.

US customers can contact Philips Respironics Inc. at 1-800-345-6443 or respironics.clinical@philips.com with questions, according to the FDA, and clinicians and patients may report adverse reactions or other problems with the devices to MedWatch: The FDA Safety Information and Adverse Event Reporting Program.

A version of this article appeared on Medscape.com.

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

New research supports current guidelines cautioning against long-term use of benzodiazepines.

The study of more than 5000 older adults found that benzodiazepine use was associated with an accelerated reduction in the volume of the hippocampus and amygdala — brain regions involved in memory and mood regulation. However, benzodiazepine use overall was not associated with an increased risk for dementia.

The findings suggest that benzodiazepine use “may have subtle, long-term impact on brain health,” lead investigator Frank Wolters, MD, PhD, with Erasmus University Medical Center, Rotterdam, the Netherlands, and colleagues wrote.

The study was published online in BMC Medicine.
 

Conflicting Evidence 

Benzodiazepines are commonly prescribed in older adults for anxiety and sleep disorders. Though the short-term cognitive side effects are well documented, the long-term impact on neurodegeneration and dementia risk remains unclear. Some studies have linked benzodiazepine use to an increased risk for dementia, whereas others have not.

Dr. Wolters and colleagues assessed the effect of benzodiazepine use on long-term dementia risk and on imaging markers of neurodegeneration in 5443 cognitively healthy adults (mean age, 71 years; 57% women) from the population-based Rotterdam Study. 

Benzodiazepine use between 1991 and 2008 was determined using pharmacy dispensing records, and dementia incidence was determined from medical records. 

Half of the participants had used benzodiazepines at any time in the 15 years before baseline (2005-2008); 47% used anxiolytics, 20% used sedative-hypnotics, 34% used both, and 13% were still using the drugs at the baseline assessment. 

During an average follow-up of 11 years, 13% of participants developed dementia. 

Overall, use of benzodiazepines was not associated with dementia risk, compared with never-use (hazard ratio [HR], 1.06), irrespective of cumulative dose. 

The risk for dementia was somewhat higher with any use of anxiolytics than with sedative-hypnotics (HR, 1.17 vs HR, 0.92), although neither was statistically significant. The highest risk estimates were observed for high cumulative dose of anxiolytics (HR, 1.33). 

Sensitivity analyses of the two most commonly used anxiolytics found no differences in risk between use of short half-life oxazepam and long half-life diazepam (HR, 1.01 and HR, 1.06, respectively, for ever-use, compared with never-use for oxazepam and diazepam).
 

Brain Atrophy

The researchers investigated potential associations between benzodiazepine use and brain volumes using brain MRI imaging from 4836 participants.

They found that current use of a benzodiazepine at baseline was significantly associated with lower total brain volume — as well as lower hippocampus, amygdala, and thalamus volume cross-sectionally — and with accelerated volume loss of the hippocampus and, to a lesser extent, amygdala longitudinally. 

Imaging findings did not differ by type of benzodiazepine used or cumulative dose. 

“Given the availability of effective alternative pharmacological and nonpharmacological treatments for anxiety and sleep problems, it is important to carefully consider the necessity of prolonged benzodiazepine use in light of potential detrimental effects on brain health,” the authors wrote. 
 

Risks Go Beyond the Brain

Commenting on the study, Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami, Florida, noted that “chronic benzodiazepine use may reduce neuroplasticity, potentially interfering with the brain’s ability to form new connections and adapt.

“Long-term use can lead to down-regulation of GABA receptors, altering the brain’s natural inhibitory mechanisms and potentially contributing to tolerance and withdrawal symptoms. Prolonged use can also disrupt the balance of various neurotransmitter systems beyond just GABA, potentially affecting mood, cognition, and overall brain function,” said Dr. Lakhan, who was not involved in the study. 

“While the literature is mixed on chronic benzodiazepine use and dementia risk, prolonged use has consistently been associated with accelerated volume loss in certain brain regions, particularly the hippocampus and amygdala,” which are responsible for memory, learning, and emotional regulation, he noted. 

“Beyond cognitive impairments and brain volume loss, chronic benzodiazepine use is associated with tolerance and dependence, potential for abuse, interactions with other drugs, and increased fall risk, especially in older adults,” Dr. Lakhan added.

Current guidelines discourage long-term use of benzodiazepines because of risk for psychological and physical dependence; falls; and cognitive impairment, especially in older adults. Nevertheless, research shows that 30%-40% of older benzodiazepine users stay on the medication beyond the recommended period of several weeks.

Donovan T. Maust, MD, Department of Psychiatry, University of Michigan Medical School, Ann Arbor, said in an interview these new findings are consistent with other recently published observational research that suggest benzodiazepine use is not linked to dementia risk. 

“I realize that such meta-analyses that find a positive relationship between benzodiazepines and dementia are out there, but they include older, less rigorous studies,” said Dr. Maust, who was not part of the new study. “In my opinion, the jury is not still out on this topic. However, there are plenty of other reasons to avoid them — and in particular, starting them — in older adults, most notably the increased risk of fall injury as well as increased overdose risk when taken along with opioids.”

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

New research supports current guidelines cautioning against long-term use of benzodiazepines.

The study of more than 5000 older adults found that benzodiazepine use was associated with an accelerated reduction in the volume of the hippocampus and amygdala — brain regions involved in memory and mood regulation. However, benzodiazepine use overall was not associated with an increased risk for dementia.

The findings suggest that benzodiazepine use “may have subtle, long-term impact on brain health,” lead investigator Frank Wolters, MD, PhD, with Erasmus University Medical Center, Rotterdam, the Netherlands, and colleagues wrote.

The study was published online in BMC Medicine.
 

Conflicting Evidence 

Benzodiazepines are commonly prescribed in older adults for anxiety and sleep disorders. Though the short-term cognitive side effects are well documented, the long-term impact on neurodegeneration and dementia risk remains unclear. Some studies have linked benzodiazepine use to an increased risk for dementia, whereas others have not.

Dr. Wolters and colleagues assessed the effect of benzodiazepine use on long-term dementia risk and on imaging markers of neurodegeneration in 5443 cognitively healthy adults (mean age, 71 years; 57% women) from the population-based Rotterdam Study. 

Benzodiazepine use between 1991 and 2008 was determined using pharmacy dispensing records, and dementia incidence was determined from medical records. 

Half of the participants had used benzodiazepines at any time in the 15 years before baseline (2005-2008); 47% used anxiolytics, 20% used sedative-hypnotics, 34% used both, and 13% were still using the drugs at the baseline assessment. 

During an average follow-up of 11 years, 13% of participants developed dementia. 

Overall, use of benzodiazepines was not associated with dementia risk, compared with never-use (hazard ratio [HR], 1.06), irrespective of cumulative dose. 

The risk for dementia was somewhat higher with any use of anxiolytics than with sedative-hypnotics (HR, 1.17 vs HR, 0.92), although neither was statistically significant. The highest risk estimates were observed for high cumulative dose of anxiolytics (HR, 1.33). 

Sensitivity analyses of the two most commonly used anxiolytics found no differences in risk between use of short half-life oxazepam and long half-life diazepam (HR, 1.01 and HR, 1.06, respectively, for ever-use, compared with never-use for oxazepam and diazepam).
 

Brain Atrophy

The researchers investigated potential associations between benzodiazepine use and brain volumes using brain MRI imaging from 4836 participants.

They found that current use of a benzodiazepine at baseline was significantly associated with lower total brain volume — as well as lower hippocampus, amygdala, and thalamus volume cross-sectionally — and with accelerated volume loss of the hippocampus and, to a lesser extent, amygdala longitudinally. 

Imaging findings did not differ by type of benzodiazepine used or cumulative dose. 

“Given the availability of effective alternative pharmacological and nonpharmacological treatments for anxiety and sleep problems, it is important to carefully consider the necessity of prolonged benzodiazepine use in light of potential detrimental effects on brain health,” the authors wrote. 
 

Risks Go Beyond the Brain

Commenting on the study, Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami, Florida, noted that “chronic benzodiazepine use may reduce neuroplasticity, potentially interfering with the brain’s ability to form new connections and adapt.

“Long-term use can lead to down-regulation of GABA receptors, altering the brain’s natural inhibitory mechanisms and potentially contributing to tolerance and withdrawal symptoms. Prolonged use can also disrupt the balance of various neurotransmitter systems beyond just GABA, potentially affecting mood, cognition, and overall brain function,” said Dr. Lakhan, who was not involved in the study. 

“While the literature is mixed on chronic benzodiazepine use and dementia risk, prolonged use has consistently been associated with accelerated volume loss in certain brain regions, particularly the hippocampus and amygdala,” which are responsible for memory, learning, and emotional regulation, he noted. 

“Beyond cognitive impairments and brain volume loss, chronic benzodiazepine use is associated with tolerance and dependence, potential for abuse, interactions with other drugs, and increased fall risk, especially in older adults,” Dr. Lakhan added.

Current guidelines discourage long-term use of benzodiazepines because of risk for psychological and physical dependence; falls; and cognitive impairment, especially in older adults. Nevertheless, research shows that 30%-40% of older benzodiazepine users stay on the medication beyond the recommended period of several weeks.

Donovan T. Maust, MD, Department of Psychiatry, University of Michigan Medical School, Ann Arbor, said in an interview these new findings are consistent with other recently published observational research that suggest benzodiazepine use is not linked to dementia risk. 

“I realize that such meta-analyses that find a positive relationship between benzodiazepines and dementia are out there, but they include older, less rigorous studies,” said Dr. Maust, who was not part of the new study. “In my opinion, the jury is not still out on this topic. However, there are plenty of other reasons to avoid them — and in particular, starting them — in older adults, most notably the increased risk of fall injury as well as increased overdose risk when taken along with opioids.”

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

New research supports current guidelines cautioning against long-term use of benzodiazepines.

The study of more than 5000 older adults found that benzodiazepine use was associated with an accelerated reduction in the volume of the hippocampus and amygdala — brain regions involved in memory and mood regulation. However, benzodiazepine use overall was not associated with an increased risk for dementia.

The findings suggest that benzodiazepine use “may have subtle, long-term impact on brain health,” lead investigator Frank Wolters, MD, PhD, with Erasmus University Medical Center, Rotterdam, the Netherlands, and colleagues wrote.

The study was published online in BMC Medicine.
 

Conflicting Evidence 

Benzodiazepines are commonly prescribed in older adults for anxiety and sleep disorders. Though the short-term cognitive side effects are well documented, the long-term impact on neurodegeneration and dementia risk remains unclear. Some studies have linked benzodiazepine use to an increased risk for dementia, whereas others have not.

Dr. Wolters and colleagues assessed the effect of benzodiazepine use on long-term dementia risk and on imaging markers of neurodegeneration in 5443 cognitively healthy adults (mean age, 71 years; 57% women) from the population-based Rotterdam Study. 

Benzodiazepine use between 1991 and 2008 was determined using pharmacy dispensing records, and dementia incidence was determined from medical records. 

Half of the participants had used benzodiazepines at any time in the 15 years before baseline (2005-2008); 47% used anxiolytics, 20% used sedative-hypnotics, 34% used both, and 13% were still using the drugs at the baseline assessment. 

During an average follow-up of 11 years, 13% of participants developed dementia. 

Overall, use of benzodiazepines was not associated with dementia risk, compared with never-use (hazard ratio [HR], 1.06), irrespective of cumulative dose. 

The risk for dementia was somewhat higher with any use of anxiolytics than with sedative-hypnotics (HR, 1.17 vs HR, 0.92), although neither was statistically significant. The highest risk estimates were observed for high cumulative dose of anxiolytics (HR, 1.33). 

Sensitivity analyses of the two most commonly used anxiolytics found no differences in risk between use of short half-life oxazepam and long half-life diazepam (HR, 1.01 and HR, 1.06, respectively, for ever-use, compared with never-use for oxazepam and diazepam).
 

Brain Atrophy

The researchers investigated potential associations between benzodiazepine use and brain volumes using brain MRI imaging from 4836 participants.

They found that current use of a benzodiazepine at baseline was significantly associated with lower total brain volume — as well as lower hippocampus, amygdala, and thalamus volume cross-sectionally — and with accelerated volume loss of the hippocampus and, to a lesser extent, amygdala longitudinally. 

Imaging findings did not differ by type of benzodiazepine used or cumulative dose. 

“Given the availability of effective alternative pharmacological and nonpharmacological treatments for anxiety and sleep problems, it is important to carefully consider the necessity of prolonged benzodiazepine use in light of potential detrimental effects on brain health,” the authors wrote. 
 

Risks Go Beyond the Brain

Commenting on the study, Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami, Florida, noted that “chronic benzodiazepine use may reduce neuroplasticity, potentially interfering with the brain’s ability to form new connections and adapt.

“Long-term use can lead to down-regulation of GABA receptors, altering the brain’s natural inhibitory mechanisms and potentially contributing to tolerance and withdrawal symptoms. Prolonged use can also disrupt the balance of various neurotransmitter systems beyond just GABA, potentially affecting mood, cognition, and overall brain function,” said Dr. Lakhan, who was not involved in the study. 

“While the literature is mixed on chronic benzodiazepine use and dementia risk, prolonged use has consistently been associated with accelerated volume loss in certain brain regions, particularly the hippocampus and amygdala,” which are responsible for memory, learning, and emotional regulation, he noted. 

“Beyond cognitive impairments and brain volume loss, chronic benzodiazepine use is associated with tolerance and dependence, potential for abuse, interactions with other drugs, and increased fall risk, especially in older adults,” Dr. Lakhan added.

Current guidelines discourage long-term use of benzodiazepines because of risk for psychological and physical dependence; falls; and cognitive impairment, especially in older adults. Nevertheless, research shows that 30%-40% of older benzodiazepine users stay on the medication beyond the recommended period of several weeks.

Donovan T. Maust, MD, Department of Psychiatry, University of Michigan Medical School, Ann Arbor, said in an interview these new findings are consistent with other recently published observational research that suggest benzodiazepine use is not linked to dementia risk. 

“I realize that such meta-analyses that find a positive relationship between benzodiazepines and dementia are out there, but they include older, less rigorous studies,” said Dr. Maust, who was not part of the new study. “In my opinion, the jury is not still out on this topic. However, there are plenty of other reasons to avoid them — and in particular, starting them — in older adults, most notably the increased risk of fall injury as well as increased overdose risk when taken along with opioids.”

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

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.¹ We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.² Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.³ When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.¹ We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.² Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.³ When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.¹ We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.² Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.³ When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

Posttraumatic stress disorder (PTSD) may enhance the risk for obstructive sleep apnea (OSA) in older male veterans, the results of a cross-sectional twin study suggested. However, additional high-quality research is needed and may yield important mechanistic insights into both conditions and improve treatment, experts said.

In the trial, increasing PTSD symptom severity was associated with increasing severity of OSA, even after controlling for multiple factors.

“The strength of the association was a bit surprising,” said study investigator Amit J. Shah, MD, MSCR, Emory University, Atlanta, Georgia. “Many physicians and scientists may otherwise assume that the relationship between PTSD and sleep apnea would be primarily mediated by obesity, but we did not find that obesity explained our findings.”

The study was published online in JAMA Network Open.
 

A More Rigorous Evaluation

“Prior studies have shown an association between PTSD and sleep apnea, but the size of the association was not as strong,” Dr. Shah said, possibly because many were based on symptomatic patients referred for clinical evaluation of OSA and some relied on self-report of a sleep apnea diagnosis.

The current study involved 181 male twins, aged 61-71 years, including 66 pairs discordant for PTSD symptoms and 15 pairs discordant for PTSD diagnosis, who were recruited from the Vietnam Era Twin Registry and underwent a formal psychiatric and polysomnography evaluation as follow-up of the Emory Twin Study.

PTSD symptom severity was assessed using the self-administered Posttraumatic Stress Disorder Checklist (PCL). OSA was mild in 74% of participants, moderate to severe in 40%, and severe in 18%.

The mean apnea-hypopnea index (AHI) was 17.7 events per hour, and the mean proportion of the night with SaO₂ less than 90% was 8.9%.

In fully adjusted models, each 15-point within-pair difference in PCL score was associated with a 4.6 events-per-hour higher AHI, a 6.4 events-per-hour higher oxygen desaturation index, and a 4.8% greater sleep duration with SaO₂ less than 90%.

A current PTSD diagnosis is associated with an approximate 10-unit higher adjusted AHI in separate models involving potential cardiovascular mediators (10.5-unit; 95% CI, 5.7-15.3) and sociodemographic and psychiatric confounders (10.7-unit; 95% CI, 4.0-17.4).

The investigators called for more research into the underlying mechanisms but speculated that pharyngeal collapsibility and exaggerated loop gain, among others, may play a role.

“Our findings broaden the concept of OSA as one that may involve stress pathways in addition to the traditional mechanisms involving airway collapse and obesity,” Dr. Shah said. “We should be more suspicious of OSA as an important comorbidity in PTSD, given the high OSA prevalence that we found in PTSD veterans.”
 

Questions Remain

In an accompanying editorial, Steven H. Woodward, PhD, and Ruth M. Benca, MD, PhD, VA Palo Alto Health Care Systems, Palo Alto, California, noted the study affirmatively answers the decades-old question of whether rates of OSA are elevated in PTSD and “eliminates many potential confounders that might cast doubt on the PTSD-OSA association.”

However, they noted, it’s difficult to ascertain the directionality of this association and point out that, in terms of potential mechanisms, the oft-cited 1994 study linking sleep fragmentation with upper airway collapsibility has never been replicated and that a recent study found no difference in airway collapsibility or evidence of differential loop gain in combat veterans with and without PTSD.

Dr. Woodward and Dr. Benca also highlighted the large body of evidence that psychiatric disorders such as bipolar disorder, schizophrenia, and, in particular, major depressive disorder, are strongly associated with higher rates of OSA.

“In sum, we do not believe that a fair reading of the current literature supports a conclusion that PTSD bears an association with OSA that does not overlap with those manifested by other psychiatric disorders,” they wrote.

“This commentary is not intended to discourage any specific line of inquiry. Rather, we seek to keep the door open as wide as possible to hypotheses and research designs aimed at elucidating the relationships between OSA and psychiatric disorders,” Dr. Woodward and Dr. Benca concluded.

In response, Dr. Shah said the editorialists’ “point about psychiatric conditions other than PTSD also being important in OSA is well taken. In our own cohort, we did not see such an association, but that does not mean that this does not exist.

“Autonomic physiology, which we plan to study next, may underlie not only the PTSD-OSA relationship but also the relationship between other psychiatric factors and OSA,” he added.

The study was funded by grants from the National Institutes of Health (NIH). One study author reported receiving personal fees from Idorsia, and another reported receiving personal fees from Clinilabs, Eisai, Ferring Pharmaceuticals, Huxley, Idorsia, and Merck Sharp & Dohme. Dr. Benca reported receiving grants from the NIH and Eisai and personal fees from Eisai, Idorsia, Haleon, and Sage Therapeutics. Dr. Woodward reported having no relevant conflicts of interest.

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

Posttraumatic stress disorder (PTSD) may enhance the risk for obstructive sleep apnea (OSA) in older male veterans, the results of a cross-sectional twin study suggested. However, additional high-quality research is needed and may yield important mechanistic insights into both conditions and improve treatment, experts said.

In the trial, increasing PTSD symptom severity was associated with increasing severity of OSA, even after controlling for multiple factors.

“The strength of the association was a bit surprising,” said study investigator Amit J. Shah, MD, MSCR, Emory University, Atlanta, Georgia. “Many physicians and scientists may otherwise assume that the relationship between PTSD and sleep apnea would be primarily mediated by obesity, but we did not find that obesity explained our findings.”

The study was published online in JAMA Network Open.
 

A More Rigorous Evaluation

“Prior studies have shown an association between PTSD and sleep apnea, but the size of the association was not as strong,” Dr. Shah said, possibly because many were based on symptomatic patients referred for clinical evaluation of OSA and some relied on self-report of a sleep apnea diagnosis.

The current study involved 181 male twins, aged 61-71 years, including 66 pairs discordant for PTSD symptoms and 15 pairs discordant for PTSD diagnosis, who were recruited from the Vietnam Era Twin Registry and underwent a formal psychiatric and polysomnography evaluation as follow-up of the Emory Twin Study.

PTSD symptom severity was assessed using the self-administered Posttraumatic Stress Disorder Checklist (PCL). OSA was mild in 74% of participants, moderate to severe in 40%, and severe in 18%.

The mean apnea-hypopnea index (AHI) was 17.7 events per hour, and the mean proportion of the night with SaO₂ less than 90% was 8.9%.

In fully adjusted models, each 15-point within-pair difference in PCL score was associated with a 4.6 events-per-hour higher AHI, a 6.4 events-per-hour higher oxygen desaturation index, and a 4.8% greater sleep duration with SaO₂ less than 90%.

A current PTSD diagnosis is associated with an approximate 10-unit higher adjusted AHI in separate models involving potential cardiovascular mediators (10.5-unit; 95% CI, 5.7-15.3) and sociodemographic and psychiatric confounders (10.7-unit; 95% CI, 4.0-17.4).

The investigators called for more research into the underlying mechanisms but speculated that pharyngeal collapsibility and exaggerated loop gain, among others, may play a role.

“Our findings broaden the concept of OSA as one that may involve stress pathways in addition to the traditional mechanisms involving airway collapse and obesity,” Dr. Shah said. “We should be more suspicious of OSA as an important comorbidity in PTSD, given the high OSA prevalence that we found in PTSD veterans.”
 

Questions Remain

In an accompanying editorial, Steven H. Woodward, PhD, and Ruth M. Benca, MD, PhD, VA Palo Alto Health Care Systems, Palo Alto, California, noted the study affirmatively answers the decades-old question of whether rates of OSA are elevated in PTSD and “eliminates many potential confounders that might cast doubt on the PTSD-OSA association.”

However, they noted, it’s difficult to ascertain the directionality of this association and point out that, in terms of potential mechanisms, the oft-cited 1994 study linking sleep fragmentation with upper airway collapsibility has never been replicated and that a recent study found no difference in airway collapsibility or evidence of differential loop gain in combat veterans with and without PTSD.

Dr. Woodward and Dr. Benca also highlighted the large body of evidence that psychiatric disorders such as bipolar disorder, schizophrenia, and, in particular, major depressive disorder, are strongly associated with higher rates of OSA.

“In sum, we do not believe that a fair reading of the current literature supports a conclusion that PTSD bears an association with OSA that does not overlap with those manifested by other psychiatric disorders,” they wrote.

“This commentary is not intended to discourage any specific line of inquiry. Rather, we seek to keep the door open as wide as possible to hypotheses and research designs aimed at elucidating the relationships between OSA and psychiatric disorders,” Dr. Woodward and Dr. Benca concluded.

In response, Dr. Shah said the editorialists’ “point about psychiatric conditions other than PTSD also being important in OSA is well taken. In our own cohort, we did not see such an association, but that does not mean that this does not exist.

“Autonomic physiology, which we plan to study next, may underlie not only the PTSD-OSA relationship but also the relationship between other psychiatric factors and OSA,” he added.

The study was funded by grants from the National Institutes of Health (NIH). One study author reported receiving personal fees from Idorsia, and another reported receiving personal fees from Clinilabs, Eisai, Ferring Pharmaceuticals, Huxley, Idorsia, and Merck Sharp & Dohme. Dr. Benca reported receiving grants from the NIH and Eisai and personal fees from Eisai, Idorsia, Haleon, and Sage Therapeutics. Dr. Woodward reported having no relevant conflicts of interest.

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

Posttraumatic stress disorder (PTSD) may enhance the risk for obstructive sleep apnea (OSA) in older male veterans, the results of a cross-sectional twin study suggested. However, additional high-quality research is needed and may yield important mechanistic insights into both conditions and improve treatment, experts said.

In the trial, increasing PTSD symptom severity was associated with increasing severity of OSA, even after controlling for multiple factors.

“The strength of the association was a bit surprising,” said study investigator Amit J. Shah, MD, MSCR, Emory University, Atlanta, Georgia. “Many physicians and scientists may otherwise assume that the relationship between PTSD and sleep apnea would be primarily mediated by obesity, but we did not find that obesity explained our findings.”

The study was published online in JAMA Network Open.
 

A More Rigorous Evaluation

“Prior studies have shown an association between PTSD and sleep apnea, but the size of the association was not as strong,” Dr. Shah said, possibly because many were based on symptomatic patients referred for clinical evaluation of OSA and some relied on self-report of a sleep apnea diagnosis.

The current study involved 181 male twins, aged 61-71 years, including 66 pairs discordant for PTSD symptoms and 15 pairs discordant for PTSD diagnosis, who were recruited from the Vietnam Era Twin Registry and underwent a formal psychiatric and polysomnography evaluation as follow-up of the Emory Twin Study.

PTSD symptom severity was assessed using the self-administered Posttraumatic Stress Disorder Checklist (PCL). OSA was mild in 74% of participants, moderate to severe in 40%, and severe in 18%.

The mean apnea-hypopnea index (AHI) was 17.7 events per hour, and the mean proportion of the night with SaO₂ less than 90% was 8.9%.

In fully adjusted models, each 15-point within-pair difference in PCL score was associated with a 4.6 events-per-hour higher AHI, a 6.4 events-per-hour higher oxygen desaturation index, and a 4.8% greater sleep duration with SaO₂ less than 90%.

A current PTSD diagnosis is associated with an approximate 10-unit higher adjusted AHI in separate models involving potential cardiovascular mediators (10.5-unit; 95% CI, 5.7-15.3) and sociodemographic and psychiatric confounders (10.7-unit; 95% CI, 4.0-17.4).

The investigators called for more research into the underlying mechanisms but speculated that pharyngeal collapsibility and exaggerated loop gain, among others, may play a role.

“Our findings broaden the concept of OSA as one that may involve stress pathways in addition to the traditional mechanisms involving airway collapse and obesity,” Dr. Shah said. “We should be more suspicious of OSA as an important comorbidity in PTSD, given the high OSA prevalence that we found in PTSD veterans.”
 

Questions Remain

In an accompanying editorial, Steven H. Woodward, PhD, and Ruth M. Benca, MD, PhD, VA Palo Alto Health Care Systems, Palo Alto, California, noted the study affirmatively answers the decades-old question of whether rates of OSA are elevated in PTSD and “eliminates many potential confounders that might cast doubt on the PTSD-OSA association.”

However, they noted, it’s difficult to ascertain the directionality of this association and point out that, in terms of potential mechanisms, the oft-cited 1994 study linking sleep fragmentation with upper airway collapsibility has never been replicated and that a recent study found no difference in airway collapsibility or evidence of differential loop gain in combat veterans with and without PTSD.

Dr. Woodward and Dr. Benca also highlighted the large body of evidence that psychiatric disorders such as bipolar disorder, schizophrenia, and, in particular, major depressive disorder, are strongly associated with higher rates of OSA.

“In sum, we do not believe that a fair reading of the current literature supports a conclusion that PTSD bears an association with OSA that does not overlap with those manifested by other psychiatric disorders,” they wrote.

“This commentary is not intended to discourage any specific line of inquiry. Rather, we seek to keep the door open as wide as possible to hypotheses and research designs aimed at elucidating the relationships between OSA and psychiatric disorders,” Dr. Woodward and Dr. Benca concluded.

In response, Dr. Shah said the editorialists’ “point about psychiatric conditions other than PTSD also being important in OSA is well taken. In our own cohort, we did not see such an association, but that does not mean that this does not exist.

“Autonomic physiology, which we plan to study next, may underlie not only the PTSD-OSA relationship but also the relationship between other psychiatric factors and OSA,” he added.

The study was funded by grants from the National Institutes of Health (NIH). One study author reported receiving personal fees from Idorsia, and another reported receiving personal fees from Clinilabs, Eisai, Ferring Pharmaceuticals, Huxley, Idorsia, and Merck Sharp & Dohme. Dr. Benca reported receiving grants from the NIH and Eisai and personal fees from Eisai, Idorsia, Haleon, and Sage Therapeutics. Dr. Woodward reported having no relevant conflicts of interest.

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

Despite their best efforts, 80% of people who lose weight regain it and many end up heavier within 5 years. Why? Our bodies fight back, revving up hunger while slowing metabolism after weight loss. In ongoing obesity discussions, ghrelin is in the spotlight as the “hunger hormone” playing a crucial role in driving appetite and facilitating weight gain. 

Weight loss interventions, such as diet or gastric bypass surgery, may trigger an increase in ghrelin levels, potentially fueling long-term weight gain. Consequently, ghrelin remains a focal point of research into innovative antiobesity treatments. 

Ghrelin, a hormone produced in the stomach, is often called the “hunger hormone.” Ghrelin is a circulating orexigenic gut hormone with growth hormone–releasing activity. In the intricate balance of energy, central and peripheral peptides such as ghrelin, leptin, adiponectin, and insulin play crucial roles. They regulate hunger, fullness, and metabolic rates, shaping our body weight outcomes. 

Since the discovery of ghrelin, in 1999, research in mice and people has focused on its effect on regulating appetite and implications for long-term weight control. When hunger strikes, ghrelin levels surge, sending signals to the brain that ramp up the appetite. Following a meal, ghrelin decreases, indicating fullness. 

Studies have found that people who were injected with subcutaneous ghrelin experienced a 46% increase in hunger and ate 28% more at their next meal than those who didn’t receive a ghrelin injection.

We might expect high levels of ghrelin in individuals with obesity, but this is not the case. In fact, ghrelin levels are typically lower in individuals with obesity than in leaner individuals. This finding might seem to contradict the idea that obesity is due to high levels of the hunger hormone. 

Excess weight could increase sensitivity to ghrelin, where more receptors lead to higher hunger stimulation with less ghrelin. Beyond hunger, ghrelin can also lead us to eat for comfort, as when stressed or anxious. Ghrelin and synthetic ghrelin mimetics increase body weight and fat mass by activating receptors in the arcuate nucleus of the hypothalamus (Müller et al.; Bany Bakar et al.). There, it also activates the brain’s reward pathways, making us crave food even when we are not hungry. This connection between ghrelin and emotional eating can contribute to stress-induced obesity. 

In my clinical practice, I have seen individuals gain maximum weight when they are under more stress and are sleep-deprived. This is because ghrelin levels increased in these scenarios. This elevation of ghrelin in high-stress, low-sleep situations affects weight gain in women during the postpartum period and menopause. 

Evidence also suggests that certain foods affect ghrelin levels. After a person eats carbohydrates, their ghrelin levels initially decrease quickly, but this is followed by a rise in ghrelin, leading them to become hungry again. In contrast, protein intake helps suppress ghrelin levels for longer. Hence, we advise patients to increase protein intake while reducing their carb intake, or to always eat protein along with carbs.

It makes sense that when individuals with obesity lose weight by fasting or caloric restriction and try to maintain that weight loss, their bodies tend to produce more ghrelin. This effect might explain why people who lose weight often find it hard to keep it off: Rising ghrelin levels after weight loss might drive them to eat more and regain weight. 

Two prominent weight loss surgeries, sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB), have opposite effects on ghrelin levels, reflecting their distinct mechanisms for weight loss. SG involves removal of the gastric fundus, where ghrelin is produced, resulting in a significant decrease in ghrelin levels; RYGB operates through malabsorption without directly affecting ghrelin production. Despite these differing approaches, both techniques demonstrate remarkable weight loss efficacy. Research comparing the two procedures reveals that SG leads to decreased fasting plasma ghrelin levels, whereas RYGB prompts an increase, highlighting the additional appetite-reducing mechanism of SG through ghrelin suppression. This contrast underscores the intricate role of ghrelin in appetite regulation and suggests that its manipulation can significantly influence weight loss outcomes.

With the effect of ghrelin in stimulating appetite being established, other studies have explored the relationship between ghrelin and insulin resistance. A meta-analysis by researchers at Qingdao University, Qingdao, China, found that circulating ghrelin levels were negatively correlated with insulin resistance in individuals with obesity and normal fasting glucose levels. The findings suggest that the role of ghrelin in obesity might extend beyond appetite regulation to influence metabolic pathways and that ghrelin may be a marker for predicting obesity.

Researchers are exploring potential therapeutic targets focusing on ghrelin modulation. Although selective neutralization of ghrelin has not yielded consistent results in rodent models, the interplay between ghrelin and LEAP2— a hormone that attaches to the same brain receptors — could be an area of interest for future obesity treatments.

Could ghrelin be the key to tackling obesity? Blocking ghrelin pharmacologically might be a strategy to keep weight off after weight loss, and it could help prevent the typical rebound effect seen with diets and withdrawal of medications. Considering the high rates of weight regain after diet-induced weight loss and withdrawal of weight loss medications, targeting ghrelin might be the missing link in long-term obesity treatment. It could be a valuable approach to improving long-term outcomes for obesity. However, these blockers might have significant side effects, given that ghrelin affects not only hunger but also the brain’s reward and pleasure centers. Therefore, caution will be needed in developing such medications owing to their potential impact on mood and mental health.

With ghrelin playing roles in hunger, reward pathways, and energy regulation, understanding this hormone is crucial in the fight against obesity. Stay tuned for future research that could shed light on the underlying mechanisms at play and hopefully results in clinical action steps.

Dimpi Desai, MD, is a professor in the Department of Medicine, Division of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, California, and has disclosed no relevant financial relationships. Ashni Dharia, MD, is a resident in the Department of Internal Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania.

A version of this article appeared on Medscape.com.

Despite their best efforts, 80% of people who lose weight regain it and many end up heavier within 5 years. Why? Our bodies fight back, revving up hunger while slowing metabolism after weight loss. In ongoing obesity discussions, ghrelin is in the spotlight as the “hunger hormone” playing a crucial role in driving appetite and facilitating weight gain. 

Weight loss interventions, such as diet or gastric bypass surgery, may trigger an increase in ghrelin levels, potentially fueling long-term weight gain. Consequently, ghrelin remains a focal point of research into innovative antiobesity treatments. 

Ghrelin, a hormone produced in the stomach, is often called the “hunger hormone.” Ghrelin is a circulating orexigenic gut hormone with growth hormone–releasing activity. In the intricate balance of energy, central and peripheral peptides such as ghrelin, leptin, adiponectin, and insulin play crucial roles. They regulate hunger, fullness, and metabolic rates, shaping our body weight outcomes. 

Since the discovery of ghrelin, in 1999, research in mice and people has focused on its effect on regulating appetite and implications for long-term weight control. When hunger strikes, ghrelin levels surge, sending signals to the brain that ramp up the appetite. Following a meal, ghrelin decreases, indicating fullness. 

Studies have found that people who were injected with subcutaneous ghrelin experienced a 46% increase in hunger and ate 28% more at their next meal than those who didn’t receive a ghrelin injection.

We might expect high levels of ghrelin in individuals with obesity, but this is not the case. In fact, ghrelin levels are typically lower in individuals with obesity than in leaner individuals. This finding might seem to contradict the idea that obesity is due to high levels of the hunger hormone. 

Excess weight could increase sensitivity to ghrelin, where more receptors lead to higher hunger stimulation with less ghrelin. Beyond hunger, ghrelin can also lead us to eat for comfort, as when stressed or anxious. Ghrelin and synthetic ghrelin mimetics increase body weight and fat mass by activating receptors in the arcuate nucleus of the hypothalamus (Müller et al.; Bany Bakar et al.). There, it also activates the brain’s reward pathways, making us crave food even when we are not hungry. This connection between ghrelin and emotional eating can contribute to stress-induced obesity. 

In my clinical practice, I have seen individuals gain maximum weight when they are under more stress and are sleep-deprived. This is because ghrelin levels increased in these scenarios. This elevation of ghrelin in high-stress, low-sleep situations affects weight gain in women during the postpartum period and menopause. 

Evidence also suggests that certain foods affect ghrelin levels. After a person eats carbohydrates, their ghrelin levels initially decrease quickly, but this is followed by a rise in ghrelin, leading them to become hungry again. In contrast, protein intake helps suppress ghrelin levels for longer. Hence, we advise patients to increase protein intake while reducing their carb intake, or to always eat protein along with carbs.

It makes sense that when individuals with obesity lose weight by fasting or caloric restriction and try to maintain that weight loss, their bodies tend to produce more ghrelin. This effect might explain why people who lose weight often find it hard to keep it off: Rising ghrelin levels after weight loss might drive them to eat more and regain weight. 

Two prominent weight loss surgeries, sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB), have opposite effects on ghrelin levels, reflecting their distinct mechanisms for weight loss. SG involves removal of the gastric fundus, where ghrelin is produced, resulting in a significant decrease in ghrelin levels; RYGB operates through malabsorption without directly affecting ghrelin production. Despite these differing approaches, both techniques demonstrate remarkable weight loss efficacy. Research comparing the two procedures reveals that SG leads to decreased fasting plasma ghrelin levels, whereas RYGB prompts an increase, highlighting the additional appetite-reducing mechanism of SG through ghrelin suppression. This contrast underscores the intricate role of ghrelin in appetite regulation and suggests that its manipulation can significantly influence weight loss outcomes.

With the effect of ghrelin in stimulating appetite being established, other studies have explored the relationship between ghrelin and insulin resistance. A meta-analysis by researchers at Qingdao University, Qingdao, China, found that circulating ghrelin levels were negatively correlated with insulin resistance in individuals with obesity and normal fasting glucose levels. The findings suggest that the role of ghrelin in obesity might extend beyond appetite regulation to influence metabolic pathways and that ghrelin may be a marker for predicting obesity.

Researchers are exploring potential therapeutic targets focusing on ghrelin modulation. Although selective neutralization of ghrelin has not yielded consistent results in rodent models, the interplay between ghrelin and LEAP2— a hormone that attaches to the same brain receptors — could be an area of interest for future obesity treatments.

Could ghrelin be the key to tackling obesity? Blocking ghrelin pharmacologically might be a strategy to keep weight off after weight loss, and it could help prevent the typical rebound effect seen with diets and withdrawal of medications. Considering the high rates of weight regain after diet-induced weight loss and withdrawal of weight loss medications, targeting ghrelin might be the missing link in long-term obesity treatment. It could be a valuable approach to improving long-term outcomes for obesity. However, these blockers might have significant side effects, given that ghrelin affects not only hunger but also the brain’s reward and pleasure centers. Therefore, caution will be needed in developing such medications owing to their potential impact on mood and mental health.

With ghrelin playing roles in hunger, reward pathways, and energy regulation, understanding this hormone is crucial in the fight against obesity. Stay tuned for future research that could shed light on the underlying mechanisms at play and hopefully results in clinical action steps.

Dimpi Desai, MD, is a professor in the Department of Medicine, Division of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, California, and has disclosed no relevant financial relationships. Ashni Dharia, MD, is a resident in the Department of Internal Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania.

A version of this article appeared on Medscape.com.

Despite their best efforts, 80% of people who lose weight regain it and many end up heavier within 5 years. Why? Our bodies fight back, revving up hunger while slowing metabolism after weight loss. In ongoing obesity discussions, ghrelin is in the spotlight as the “hunger hormone” playing a crucial role in driving appetite and facilitating weight gain. 

Weight loss interventions, such as diet or gastric bypass surgery, may trigger an increase in ghrelin levels, potentially fueling long-term weight gain. Consequently, ghrelin remains a focal point of research into innovative antiobesity treatments. 

Ghrelin, a hormone produced in the stomach, is often called the “hunger hormone.” Ghrelin is a circulating orexigenic gut hormone with growth hormone–releasing activity. In the intricate balance of energy, central and peripheral peptides such as ghrelin, leptin, adiponectin, and insulin play crucial roles. They regulate hunger, fullness, and metabolic rates, shaping our body weight outcomes. 

Since the discovery of ghrelin, in 1999, research in mice and people has focused on its effect on regulating appetite and implications for long-term weight control. When hunger strikes, ghrelin levels surge, sending signals to the brain that ramp up the appetite. Following a meal, ghrelin decreases, indicating fullness. 

Studies have found that people who were injected with subcutaneous ghrelin experienced a 46% increase in hunger and ate 28% more at their next meal than those who didn’t receive a ghrelin injection.

We might expect high levels of ghrelin in individuals with obesity, but this is not the case. In fact, ghrelin levels are typically lower in individuals with obesity than in leaner individuals. This finding might seem to contradict the idea that obesity is due to high levels of the hunger hormone. 

Excess weight could increase sensitivity to ghrelin, where more receptors lead to higher hunger stimulation with less ghrelin. Beyond hunger, ghrelin can also lead us to eat for comfort, as when stressed or anxious. Ghrelin and synthetic ghrelin mimetics increase body weight and fat mass by activating receptors in the arcuate nucleus of the hypothalamus (Müller et al.; Bany Bakar et al.). There, it also activates the brain’s reward pathways, making us crave food even when we are not hungry. This connection between ghrelin and emotional eating can contribute to stress-induced obesity. 

In my clinical practice, I have seen individuals gain maximum weight when they are under more stress and are sleep-deprived. This is because ghrelin levels increased in these scenarios. This elevation of ghrelin in high-stress, low-sleep situations affects weight gain in women during the postpartum period and menopause. 

Evidence also suggests that certain foods affect ghrelin levels. After a person eats carbohydrates, their ghrelin levels initially decrease quickly, but this is followed by a rise in ghrelin, leading them to become hungry again. In contrast, protein intake helps suppress ghrelin levels for longer. Hence, we advise patients to increase protein intake while reducing their carb intake, or to always eat protein along with carbs.

It makes sense that when individuals with obesity lose weight by fasting or caloric restriction and try to maintain that weight loss, their bodies tend to produce more ghrelin. This effect might explain why people who lose weight often find it hard to keep it off: Rising ghrelin levels after weight loss might drive them to eat more and regain weight. 

Two prominent weight loss surgeries, sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB), have opposite effects on ghrelin levels, reflecting their distinct mechanisms for weight loss. SG involves removal of the gastric fundus, where ghrelin is produced, resulting in a significant decrease in ghrelin levels; RYGB operates through malabsorption without directly affecting ghrelin production. Despite these differing approaches, both techniques demonstrate remarkable weight loss efficacy. Research comparing the two procedures reveals that SG leads to decreased fasting plasma ghrelin levels, whereas RYGB prompts an increase, highlighting the additional appetite-reducing mechanism of SG through ghrelin suppression. This contrast underscores the intricate role of ghrelin in appetite regulation and suggests that its manipulation can significantly influence weight loss outcomes.

With the effect of ghrelin in stimulating appetite being established, other studies have explored the relationship between ghrelin and insulin resistance. A meta-analysis by researchers at Qingdao University, Qingdao, China, found that circulating ghrelin levels were negatively correlated with insulin resistance in individuals with obesity and normal fasting glucose levels. The findings suggest that the role of ghrelin in obesity might extend beyond appetite regulation to influence metabolic pathways and that ghrelin may be a marker for predicting obesity.

Researchers are exploring potential therapeutic targets focusing on ghrelin modulation. Although selective neutralization of ghrelin has not yielded consistent results in rodent models, the interplay between ghrelin and LEAP2— a hormone that attaches to the same brain receptors — could be an area of interest for future obesity treatments.

Could ghrelin be the key to tackling obesity? Blocking ghrelin pharmacologically might be a strategy to keep weight off after weight loss, and it could help prevent the typical rebound effect seen with diets and withdrawal of medications. Considering the high rates of weight regain after diet-induced weight loss and withdrawal of weight loss medications, targeting ghrelin might be the missing link in long-term obesity treatment. It could be a valuable approach to improving long-term outcomes for obesity. However, these blockers might have significant side effects, given that ghrelin affects not only hunger but also the brain’s reward and pleasure centers. Therefore, caution will be needed in developing such medications owing to their potential impact on mood and mental health.

With ghrelin playing roles in hunger, reward pathways, and energy regulation, understanding this hormone is crucial in the fight against obesity. Stay tuned for future research that could shed light on the underlying mechanisms at play and hopefully results in clinical action steps.

Dimpi Desai, MD, is a professor in the Department of Medicine, Division of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, California, and has disclosed no relevant financial relationships. Ashni Dharia, MD, is a resident in the Department of Internal Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania.

A version of this article appeared on Medscape.com.

ORLANDO, FLA. — The diabetes and weight loss drug tirzepatide (Mounjaro for type 2 diabetes; Zepbound for obesity) was so effective at reducing sleep disruptions in patients with obesity and obstructive sleep apnea (OSA) that 40%-50% no longer needed to use a continuous positive airway pressure (CPAP) device, according to two new studies.

Tirzepatide, a long-acting glucose-dependent insulinotropic polypeptide (GIP) receptor agonist and glucagon-like peptide 1 (GLP-1) receptor agonist, also lowered C-reactive protein levels and systolic blood pressure. And patients taking the medication lost 18%-20% of their body weight. 

The SURMOUNT-OSA studies “mark a significant milestone in the treatment of OSA, offering a promising new therapeutic option that addresses both respiratory and metabolic complications,” said lead author Atul Malhotra, MD, professor of medicine at the University of California, San Diego, and director of sleep medicine at UC San Diego Health. 

The two double-blind, randomized, controlled trials in patients with obesity and moderate to severe OSA were conducted at 60 sites in nine countries. The results were presented at the American Diabetes Association (ADA) 84th Scientific Sessions and simultaneously published online in the New England Journal of Medicine.

OSA affects 1 billion people worldwide and 30 million American adults, many of whom are undiagnosed. Obesity is a common risk factor. According to the ADA, 40% of those with obesity have OSA and 70% of those with OSA have obesity. 

CPAP is an effective and the most-used intervention for OSA, but many patients refuse to use the device, stop using it, or cannot use it. Should tirzepatide eventually gain Food and Drug Administration approval for OSA, it would be the first drug approved for the condition.

“This new drug treatment offers a more accessible alternative for individuals who cannot tolerate or adhere to existing therapies,” said Dr. Malhotra.
 

Huge Reduction in Episodes, Severity

For the two studies, patients were enrolled who had moderate to severe OSA, defined as more than 15 events per hour (using the apnea-hypopnea index [AHI]) and a body mass index of 30 kg/m² or greater. Those not using a CPAP device were enrolled in study 1, and those using a CPAP device were enrolled in study 2. 

Participants received either the maximum tolerated dose of tirzepatide (10 or 15 mg by once-weekly injection) or placebo for 1 year. In study 1, 114 individuals received tirzepatide and 120 received placebo. For study 2, 119 patients received tirzepatide and 114 received placebo. All participants received regular lifestyle counseling sessions about nutrition and were instructed to reduce food intake by 500 kcal/day and to engage in at least 150 min/week of physical activity.

Enrollment was limited to 70% men to ensure adequate representation of women.

At baseline, 65%-70% of participants had severe OSA, with more than 30 events/hour on the AHI scale and a mean of 51.5 events/hour.

By 1 year, patients taking tirzepatide had 27-30 fewer events/hour, compared with 4-6 fewer events/hour for those taking placebo.

Up to half of those who received tirzepatide in both trials had less than 5 events/hour or 5-14 AHI events/hour and an Epworth Sleepiness Scale score of 10 or less. Those thresholds “represent a level at which CPAP therapy may not be recommended,” wrote the authors.

Patients in the tirzepatide group also had a decrease in systolic blood pressure from baseline of 9.7 mm Hg in study 1 and 7.6 mm Hg in study 2 at week 48.

The most common adverse events were diarrhea, nausea, and vomiting, which occurred in approximately a quarter of patients taking tirzepatide. There were two adjudicated-confirmed cases of acute pancreatitis in those taking tirzepatide in study 2. 

Patients who received tirzepatide also reported fewer daytime and nighttime disturbances, as measured using the Patient-Reported Outcomes Measurement Information System Short Form scale for Sleep-Related Impairment and Sleep Disturbance.
 

Tirzepatide Plus CPAP Are Best

Writing in an accompanying editorial, Sanjay R. Patel, MD, noted that, although clinical guidelines have recommended that weight loss strategies be incorporated as part of OSA treatment, “the integration of obesity management into the approaches to care for obstructive sleep apnea has lagged.”

As many as half of patients abandon CPAP therapy within 3 years, wrote Dr. Patel, who is professor of medicine and epidemiology at the University of Pittsburgh, Pittsburgh, Pennsylvania, and medical director of the UPMC Comprehensive Sleep Disorders program. “An effective medication to treat obesity is thus an obvious avenue to pursue.”

Dr. Patel noted the large reductions in the number of events on the AHI scale. He wrote that the improvement in systolic blood pressure “was substantially larger than effects seen with CPAP therapy alone and indicate that tirzepatide may be an attractive option for those patients who seek to reduce their cardiovascular risk.”

Dr. Patel raised concerns about whether patients outside of a trial would stick with therapy, noting studies have shown high rates of discontinuation of GLP-1 receptor agonists.

And, he wrote, “racial disparities in the use of GLP-1 receptor agonists among patients with diabetes arouse concern that the addition of tirzepatide as a treatment option for obstructive sleep apnea without directly addressing policies relative to coverage of care will only further exacerbate already pervasive disparities in clinical care for obstructive sleep apnea.”

Commenting on the study during the presentation of the results, Louis Aronne, MD, said he believes the trials demonstrate “the treatment of obesity with tirzepatide plus CPAP is really the optimal treatment for obstructive sleep apnea and obesity-related cardiometabolic risks.” Dr. Aronne is the Sanford I. Weill professor of metabolic research at Weill Cornell Medical College, New York City.

Dr. Aronne added there is still much to learn. It is still not clear whether tirzepatide had an independent effect in the OSA trial — as has been seen in other studies where the drug clearly reduced cardiovascular risk — or whether the positive results were primarily caused by weight loss.

“I believe that over time we’ll see that this particular effect in sleep apnea is related to weight,” he said. 

The study was supported by Eli Lilly. Dr. Malhotra has reported being a paid consultant for Lilly and ZOLL Medical and a cofounder of Healcisio. 

A version of this article appeared on Medscape.com.
 

ORLANDO, FLA. — The diabetes and weight loss drug tirzepatide (Mounjaro for type 2 diabetes; Zepbound for obesity) was so effective at reducing sleep disruptions in patients with obesity and obstructive sleep apnea (OSA) that 40%-50% no longer needed to use a continuous positive airway pressure (CPAP) device, according to two new studies.

Tirzepatide, a long-acting glucose-dependent insulinotropic polypeptide (GIP) receptor agonist and glucagon-like peptide 1 (GLP-1) receptor agonist, also lowered C-reactive protein levels and systolic blood pressure. And patients taking the medication lost 18%-20% of their body weight. 

The SURMOUNT-OSA studies “mark a significant milestone in the treatment of OSA, offering a promising new therapeutic option that addresses both respiratory and metabolic complications,” said lead author Atul Malhotra, MD, professor of medicine at the University of California, San Diego, and director of sleep medicine at UC San Diego Health. 

The two double-blind, randomized, controlled trials in patients with obesity and moderate to severe OSA were conducted at 60 sites in nine countries. The results were presented at the American Diabetes Association (ADA) 84th Scientific Sessions and simultaneously published online in the New England Journal of Medicine.

OSA affects 1 billion people worldwide and 30 million American adults, many of whom are undiagnosed. Obesity is a common risk factor. According to the ADA, 40% of those with obesity have OSA and 70% of those with OSA have obesity. 

CPAP is an effective and the most-used intervention for OSA, but many patients refuse to use the device, stop using it, or cannot use it. Should tirzepatide eventually gain Food and Drug Administration approval for OSA, it would be the first drug approved for the condition.

“This new drug treatment offers a more accessible alternative for individuals who cannot tolerate or adhere to existing therapies,” said Dr. Malhotra.
 

Huge Reduction in Episodes, Severity

For the two studies, patients were enrolled who had moderate to severe OSA, defined as more than 15 events per hour (using the apnea-hypopnea index [AHI]) and a body mass index of 30 kg/m² or greater. Those not using a CPAP device were enrolled in study 1, and those using a CPAP device were enrolled in study 2. 

Participants received either the maximum tolerated dose of tirzepatide (10 or 15 mg by once-weekly injection) or placebo for 1 year. In study 1, 114 individuals received tirzepatide and 120 received placebo. For study 2, 119 patients received tirzepatide and 114 received placebo. All participants received regular lifestyle counseling sessions about nutrition and were instructed to reduce food intake by 500 kcal/day and to engage in at least 150 min/week of physical activity.

Enrollment was limited to 70% men to ensure adequate representation of women.

At baseline, 65%-70% of participants had severe OSA, with more than 30 events/hour on the AHI scale and a mean of 51.5 events/hour.

By 1 year, patients taking tirzepatide had 27-30 fewer events/hour, compared with 4-6 fewer events/hour for those taking placebo.

Up to half of those who received tirzepatide in both trials had less than 5 events/hour or 5-14 AHI events/hour and an Epworth Sleepiness Scale score of 10 or less. Those thresholds “represent a level at which CPAP therapy may not be recommended,” wrote the authors.

Patients in the tirzepatide group also had a decrease in systolic blood pressure from baseline of 9.7 mm Hg in study 1 and 7.6 mm Hg in study 2 at week 48.

The most common adverse events were diarrhea, nausea, and vomiting, which occurred in approximately a quarter of patients taking tirzepatide. There were two adjudicated-confirmed cases of acute pancreatitis in those taking tirzepatide in study 2. 

Patients who received tirzepatide also reported fewer daytime and nighttime disturbances, as measured using the Patient-Reported Outcomes Measurement Information System Short Form scale for Sleep-Related Impairment and Sleep Disturbance.
 

Tirzepatide Plus CPAP Are Best

Writing in an accompanying editorial, Sanjay R. Patel, MD, noted that, although clinical guidelines have recommended that weight loss strategies be incorporated as part of OSA treatment, “the integration of obesity management into the approaches to care for obstructive sleep apnea has lagged.”

As many as half of patients abandon CPAP therapy within 3 years, wrote Dr. Patel, who is professor of medicine and epidemiology at the University of Pittsburgh, Pittsburgh, Pennsylvania, and medical director of the UPMC Comprehensive Sleep Disorders program. “An effective medication to treat obesity is thus an obvious avenue to pursue.”

Dr. Patel noted the large reductions in the number of events on the AHI scale. He wrote that the improvement in systolic blood pressure “was substantially larger than effects seen with CPAP therapy alone and indicate that tirzepatide may be an attractive option for those patients who seek to reduce their cardiovascular risk.”

Dr. Patel raised concerns about whether patients outside of a trial would stick with therapy, noting studies have shown high rates of discontinuation of GLP-1 receptor agonists.

And, he wrote, “racial disparities in the use of GLP-1 receptor agonists among patients with diabetes arouse concern that the addition of tirzepatide as a treatment option for obstructive sleep apnea without directly addressing policies relative to coverage of care will only further exacerbate already pervasive disparities in clinical care for obstructive sleep apnea.”

Commenting on the study during the presentation of the results, Louis Aronne, MD, said he believes the trials demonstrate “the treatment of obesity with tirzepatide plus CPAP is really the optimal treatment for obstructive sleep apnea and obesity-related cardiometabolic risks.” Dr. Aronne is the Sanford I. Weill professor of metabolic research at Weill Cornell Medical College, New York City.

Dr. Aronne added there is still much to learn. It is still not clear whether tirzepatide had an independent effect in the OSA trial — as has been seen in other studies where the drug clearly reduced cardiovascular risk — or whether the positive results were primarily caused by weight loss.

“I believe that over time we’ll see that this particular effect in sleep apnea is related to weight,” he said. 

The study was supported by Eli Lilly. Dr. Malhotra has reported being a paid consultant for Lilly and ZOLL Medical and a cofounder of Healcisio. 

A version of this article appeared on Medscape.com.
 

ORLANDO, FLA. — The diabetes and weight loss drug tirzepatide (Mounjaro for type 2 diabetes; Zepbound for obesity) was so effective at reducing sleep disruptions in patients with obesity and obstructive sleep apnea (OSA) that 40%-50% no longer needed to use a continuous positive airway pressure (CPAP) device, according to two new studies.

Tirzepatide, a long-acting glucose-dependent insulinotropic polypeptide (GIP) receptor agonist and glucagon-like peptide 1 (GLP-1) receptor agonist, also lowered C-reactive protein levels and systolic blood pressure. And patients taking the medication lost 18%-20% of their body weight. 

The SURMOUNT-OSA studies “mark a significant milestone in the treatment of OSA, offering a promising new therapeutic option that addresses both respiratory and metabolic complications,” said lead author Atul Malhotra, MD, professor of medicine at the University of California, San Diego, and director of sleep medicine at UC San Diego Health. 

The two double-blind, randomized, controlled trials in patients with obesity and moderate to severe OSA were conducted at 60 sites in nine countries. The results were presented at the American Diabetes Association (ADA) 84th Scientific Sessions and simultaneously published online in the New England Journal of Medicine.

OSA affects 1 billion people worldwide and 30 million American adults, many of whom are undiagnosed. Obesity is a common risk factor. According to the ADA, 40% of those with obesity have OSA and 70% of those with OSA have obesity. 

CPAP is an effective and the most-used intervention for OSA, but many patients refuse to use the device, stop using it, or cannot use it. Should tirzepatide eventually gain Food and Drug Administration approval for OSA, it would be the first drug approved for the condition.

“This new drug treatment offers a more accessible alternative for individuals who cannot tolerate or adhere to existing therapies,” said Dr. Malhotra.
 

Huge Reduction in Episodes, Severity

For the two studies, patients were enrolled who had moderate to severe OSA, defined as more than 15 events per hour (using the apnea-hypopnea index [AHI]) and a body mass index of 30 kg/m² or greater. Those not using a CPAP device were enrolled in study 1, and those using a CPAP device were enrolled in study 2. 

Participants received either the maximum tolerated dose of tirzepatide (10 or 15 mg by once-weekly injection) or placebo for 1 year. In study 1, 114 individuals received tirzepatide and 120 received placebo. For study 2, 119 patients received tirzepatide and 114 received placebo. All participants received regular lifestyle counseling sessions about nutrition and were instructed to reduce food intake by 500 kcal/day and to engage in at least 150 min/week of physical activity.

Enrollment was limited to 70% men to ensure adequate representation of women.

At baseline, 65%-70% of participants had severe OSA, with more than 30 events/hour on the AHI scale and a mean of 51.5 events/hour.

By 1 year, patients taking tirzepatide had 27-30 fewer events/hour, compared with 4-6 fewer events/hour for those taking placebo.

Up to half of those who received tirzepatide in both trials had less than 5 events/hour or 5-14 AHI events/hour and an Epworth Sleepiness Scale score of 10 or less. Those thresholds “represent a level at which CPAP therapy may not be recommended,” wrote the authors.

Patients in the tirzepatide group also had a decrease in systolic blood pressure from baseline of 9.7 mm Hg in study 1 and 7.6 mm Hg in study 2 at week 48.

The most common adverse events were diarrhea, nausea, and vomiting, which occurred in approximately a quarter of patients taking tirzepatide. There were two adjudicated-confirmed cases of acute pancreatitis in those taking tirzepatide in study 2. 

Patients who received tirzepatide also reported fewer daytime and nighttime disturbances, as measured using the Patient-Reported Outcomes Measurement Information System Short Form scale for Sleep-Related Impairment and Sleep Disturbance.
 

Tirzepatide Plus CPAP Are Best

Writing in an accompanying editorial, Sanjay R. Patel, MD, noted that, although clinical guidelines have recommended that weight loss strategies be incorporated as part of OSA treatment, “the integration of obesity management into the approaches to care for obstructive sleep apnea has lagged.”

As many as half of patients abandon CPAP therapy within 3 years, wrote Dr. Patel, who is professor of medicine and epidemiology at the University of Pittsburgh, Pittsburgh, Pennsylvania, and medical director of the UPMC Comprehensive Sleep Disorders program. “An effective medication to treat obesity is thus an obvious avenue to pursue.”

Dr. Patel noted the large reductions in the number of events on the AHI scale. He wrote that the improvement in systolic blood pressure “was substantially larger than effects seen with CPAP therapy alone and indicate that tirzepatide may be an attractive option for those patients who seek to reduce their cardiovascular risk.”

Dr. Patel raised concerns about whether patients outside of a trial would stick with therapy, noting studies have shown high rates of discontinuation of GLP-1 receptor agonists.

And, he wrote, “racial disparities in the use of GLP-1 receptor agonists among patients with diabetes arouse concern that the addition of tirzepatide as a treatment option for obstructive sleep apnea without directly addressing policies relative to coverage of care will only further exacerbate already pervasive disparities in clinical care for obstructive sleep apnea.”

Commenting on the study during the presentation of the results, Louis Aronne, MD, said he believes the trials demonstrate “the treatment of obesity with tirzepatide plus CPAP is really the optimal treatment for obstructive sleep apnea and obesity-related cardiometabolic risks.” Dr. Aronne is the Sanford I. Weill professor of metabolic research at Weill Cornell Medical College, New York City.

Dr. Aronne added there is still much to learn. It is still not clear whether tirzepatide had an independent effect in the OSA trial — as has been seen in other studies where the drug clearly reduced cardiovascular risk — or whether the positive results were primarily caused by weight loss.

“I believe that over time we’ll see that this particular effect in sleep apnea is related to weight,” he said. 

The study was supported by Eli Lilly. Dr. Malhotra has reported being a paid consultant for Lilly and ZOLL Medical and a cofounder of Healcisio. 

A version of this article appeared on Medscape.com.