MDedge Psychiatry

New research adds to a growing body of evidence suggesting that COVID-19 infection can be hard on mental health. 

The UK study of more than 18 million adults showed an elevated rate of mental illness, including depression and serious mental illness, for up to a year following a bout of COVID-19, particularly in those with severe COVID who had not been vaccinated. 

Importantly, vaccination appeared to mitigate the adverse effects of COVID-19 on mental health, the investigators found. 

“Our results highlight the importance COVID-19 vaccination in the general population and particularly among those with mental illnesses, who may be at higher risk of both SARS-CoV-2 infection and adverse outcomes following COVID-19,” first author Venexia Walker, PhD, with University of Bristol, United Kingdom, said in a news release. 

The study was published online on August 21 in JAMA Psychiatry.
 

Novel Data

“Before this study, a number of papers had looked at associations of COVID diagnosis with mental ill health, and broadly speaking, they had reported associations of different magnitudes,” study author Jonathan A. C. Sterne, PhD, with University of Bristol, noted in a journal podcast. 

“Some studies were restricted to patients who were hospitalized with COVID-19 and some not and the duration of follow-up varied. And importantly, the nature of COVID-19 changed profoundly as vaccination became available and there was little data on the impact of vaccination on associations of COVID-19 with subsequent mental ill health,” Dr. Sterne said. 

The UK study was conducted in three cohorts — a cohort of about 18.6 million people who were diagnosed with COVID-19 before a vaccine was available, a cohort of about 14 million adults who were vaccinated, and a cohort of about 3.2 million people who were unvaccinated.

The researchers compared rates of various mental illnesses after COVID-19 with rates before or without COVID-19 and by vaccination status.

Across all cohorts, rates of most mental illnesses examined were “markedly elevated” during the first month following a COVID-19 diagnosis compared with rates before or without COVID-19.

For example, the adjusted hazard ratios for depression (the most common illness) and serious mental illness in the month after COVID-19 were 1.93 and 1.49, respectively, in the prevaccination cohort and 1.79 and 1.45, respectively, in the unvaccinated cohort compared with 1.16 and 0.91 in the vaccinated cohort.

This elevation in the rate of mental illnesses was mainly seen after severe COVID-19 that led to hospitalization and remained higher for up to a year following severe COVID-19 in unvaccinated adults.

For severe COVID-19 with hospitalization, the adjusted hazard ratio for depression in the month following admission was 16.3 in the prevaccine cohort, 15.6 in the unvaccinated cohort, and 12.9 in the vaccinated cohort.

The adjusted hazard ratios for serious mental illness in the month after COVID hospitalization was 9.71 in the prevaccine cohort, 8.75 with no vaccination, and 6.52 with vaccination. 

“Incidences of other mental illnesses were broadly similar to those of depression and serious mental illness, both overall and for COVID-19 with and without hospitalization,” the authors report in their paper.

Consistent with prior research, subgroup analyzes found the association of COVID-19 and mental illness was stronger among older adults and men, with no marked differences by ethnic group.

“We should be concerned about continuing consequences in people who experienced severe COVID-19 early in the pandemic, and they may include a continuing higher incidence of mental ill health, such as depression and serious mental illness,” Dr. Sterne said in the podcast. 

In terms of ongoing booster vaccinations, “people who are advised that they are under vaccinated or recommended for further COVID-19 vaccination, should take those invitations seriously, because by preventing severe COVID-19, which is what vaccination does, you can prevent consequences such as mental illness,” Dr. Sterne added. 

The study was supported by the COVID-19 Longitudinal Health and Wellbeing National Core Study, which is funded by the Medical Research Council and National Institute for Health and Care Research. The authors had no relevant conflicts of interest.
 

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

New research adds to a growing body of evidence suggesting that COVID-19 infection can be hard on mental health. 

The UK study of more than 18 million adults showed an elevated rate of mental illness, including depression and serious mental illness, for up to a year following a bout of COVID-19, particularly in those with severe COVID who had not been vaccinated. 

Importantly, vaccination appeared to mitigate the adverse effects of COVID-19 on mental health, the investigators found. 

“Our results highlight the importance COVID-19 vaccination in the general population and particularly among those with mental illnesses, who may be at higher risk of both SARS-CoV-2 infection and adverse outcomes following COVID-19,” first author Venexia Walker, PhD, with University of Bristol, United Kingdom, said in a news release. 

The study was published online on August 21 in JAMA Psychiatry.
 

Novel Data

“Before this study, a number of papers had looked at associations of COVID diagnosis with mental ill health, and broadly speaking, they had reported associations of different magnitudes,” study author Jonathan A. C. Sterne, PhD, with University of Bristol, noted in a journal podcast. 

“Some studies were restricted to patients who were hospitalized with COVID-19 and some not and the duration of follow-up varied. And importantly, the nature of COVID-19 changed profoundly as vaccination became available and there was little data on the impact of vaccination on associations of COVID-19 with subsequent mental ill health,” Dr. Sterne said. 

The UK study was conducted in three cohorts — a cohort of about 18.6 million people who were diagnosed with COVID-19 before a vaccine was available, a cohort of about 14 million adults who were vaccinated, and a cohort of about 3.2 million people who were unvaccinated.

The researchers compared rates of various mental illnesses after COVID-19 with rates before or without COVID-19 and by vaccination status.

Across all cohorts, rates of most mental illnesses examined were “markedly elevated” during the first month following a COVID-19 diagnosis compared with rates before or without COVID-19.

For example, the adjusted hazard ratios for depression (the most common illness) and serious mental illness in the month after COVID-19 were 1.93 and 1.49, respectively, in the prevaccination cohort and 1.79 and 1.45, respectively, in the unvaccinated cohort compared with 1.16 and 0.91 in the vaccinated cohort.

This elevation in the rate of mental illnesses was mainly seen after severe COVID-19 that led to hospitalization and remained higher for up to a year following severe COVID-19 in unvaccinated adults.

For severe COVID-19 with hospitalization, the adjusted hazard ratio for depression in the month following admission was 16.3 in the prevaccine cohort, 15.6 in the unvaccinated cohort, and 12.9 in the vaccinated cohort.

The adjusted hazard ratios for serious mental illness in the month after COVID hospitalization was 9.71 in the prevaccine cohort, 8.75 with no vaccination, and 6.52 with vaccination. 

“Incidences of other mental illnesses were broadly similar to those of depression and serious mental illness, both overall and for COVID-19 with and without hospitalization,” the authors report in their paper.

Consistent with prior research, subgroup analyzes found the association of COVID-19 and mental illness was stronger among older adults and men, with no marked differences by ethnic group.

“We should be concerned about continuing consequences in people who experienced severe COVID-19 early in the pandemic, and they may include a continuing higher incidence of mental ill health, such as depression and serious mental illness,” Dr. Sterne said in the podcast. 

In terms of ongoing booster vaccinations, “people who are advised that they are under vaccinated or recommended for further COVID-19 vaccination, should take those invitations seriously, because by preventing severe COVID-19, which is what vaccination does, you can prevent consequences such as mental illness,” Dr. Sterne added. 

The study was supported by the COVID-19 Longitudinal Health and Wellbeing National Core Study, which is funded by the Medical Research Council and National Institute for Health and Care Research. The authors had no relevant conflicts of interest.
 

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

New research adds to a growing body of evidence suggesting that COVID-19 infection can be hard on mental health. 

The UK study of more than 18 million adults showed an elevated rate of mental illness, including depression and serious mental illness, for up to a year following a bout of COVID-19, particularly in those with severe COVID who had not been vaccinated. 

Importantly, vaccination appeared to mitigate the adverse effects of COVID-19 on mental health, the investigators found. 

“Our results highlight the importance COVID-19 vaccination in the general population and particularly among those with mental illnesses, who may be at higher risk of both SARS-CoV-2 infection and adverse outcomes following COVID-19,” first author Venexia Walker, PhD, with University of Bristol, United Kingdom, said in a news release. 

The study was published online on August 21 in JAMA Psychiatry.
 

Novel Data

“Before this study, a number of papers had looked at associations of COVID diagnosis with mental ill health, and broadly speaking, they had reported associations of different magnitudes,” study author Jonathan A. C. Sterne, PhD, with University of Bristol, noted in a journal podcast. 

“Some studies were restricted to patients who were hospitalized with COVID-19 and some not and the duration of follow-up varied. And importantly, the nature of COVID-19 changed profoundly as vaccination became available and there was little data on the impact of vaccination on associations of COVID-19 with subsequent mental ill health,” Dr. Sterne said. 

The UK study was conducted in three cohorts — a cohort of about 18.6 million people who were diagnosed with COVID-19 before a vaccine was available, a cohort of about 14 million adults who were vaccinated, and a cohort of about 3.2 million people who were unvaccinated.

The researchers compared rates of various mental illnesses after COVID-19 with rates before or without COVID-19 and by vaccination status.

Across all cohorts, rates of most mental illnesses examined were “markedly elevated” during the first month following a COVID-19 diagnosis compared with rates before or without COVID-19.

For example, the adjusted hazard ratios for depression (the most common illness) and serious mental illness in the month after COVID-19 were 1.93 and 1.49, respectively, in the prevaccination cohort and 1.79 and 1.45, respectively, in the unvaccinated cohort compared with 1.16 and 0.91 in the vaccinated cohort.

This elevation in the rate of mental illnesses was mainly seen after severe COVID-19 that led to hospitalization and remained higher for up to a year following severe COVID-19 in unvaccinated adults.

For severe COVID-19 with hospitalization, the adjusted hazard ratio for depression in the month following admission was 16.3 in the prevaccine cohort, 15.6 in the unvaccinated cohort, and 12.9 in the vaccinated cohort.

The adjusted hazard ratios for serious mental illness in the month after COVID hospitalization was 9.71 in the prevaccine cohort, 8.75 with no vaccination, and 6.52 with vaccination. 

“Incidences of other mental illnesses were broadly similar to those of depression and serious mental illness, both overall and for COVID-19 with and without hospitalization,” the authors report in their paper.

Consistent with prior research, subgroup analyzes found the association of COVID-19 and mental illness was stronger among older adults and men, with no marked differences by ethnic group.

“We should be concerned about continuing consequences in people who experienced severe COVID-19 early in the pandemic, and they may include a continuing higher incidence of mental ill health, such as depression and serious mental illness,” Dr. Sterne said in the podcast. 

In terms of ongoing booster vaccinations, “people who are advised that they are under vaccinated or recommended for further COVID-19 vaccination, should take those invitations seriously, because by preventing severe COVID-19, which is what vaccination does, you can prevent consequences such as mental illness,” Dr. Sterne added. 

The study was supported by the COVID-19 Longitudinal Health and Wellbeing National Core Study, which is funded by the Medical Research Council and National Institute for Health and Care Research. The authors had no relevant conflicts of interest.
 

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

Most physicians oppose the way standardized relative value units (RVUs) are used to determine performance and compensation, according to Medscape’s 2024 Physicians and RVUs Report. About 6 in 10 survey respondents were unhappy with how RVUs affected them financially, while 7 in 10 said RVUs were poor measures of productivity.

The report analyzed 2024 survey data from 1005 practicing physicians who earn RVUs.

“I’m already mad that the medical field is controlled by health insurers and what they pay and authorize,” said an anesthesiologist in New York. “Then [that approach] is transferred to medical offices and hospitals, where physicians are paid by RVUs.”

Most physicians surveyed produced between 4000 and 8000 RVUs per year. Roughly one in six were high RVU generators, generating more than 10,000 annually.

In most cases, the metric influences earning potential — 42% of doctors surveyed said RVUs affect their salaries to some degree. One quarter said their salary was based entirely on RVUs. More than three fourths of physicians who received performance bonuses said they must meet RVU targets to do so.

“The current RVU system encourages unnecessary procedures, hurting patients,” said an orthopedic surgeon in Maine.

Nearly three fourths of practitioners surveyed said they occasionally to frequently felt pressure to take on more patients as a result of this system.

“I know numerous primary care doctors and specialists who have been forced to increase patient volume to meet RVU goals, and none is happy about it,” said Alok Patel, MD, a pediatric hospitalist with Stanford Hospital in Palo Alto, California. “Plus, patients are definitely not happy about being rushed.”

More than half of respondents said they occasionally or frequently felt compelled by their employer to use higher-level coding, which interferes with a physician’s ethical responsibility to the patient, said Arthur L. Caplan, PhD, a bioethicist at NYU Langone Medical Center in New York City.

“Rather than rewarding excellence or good outcomes, you’re kind of rewarding procedures and volume,” said Dr. Caplan. “It’s more than pressure; it’s expected.”

Nearly 6 in 10 physicians said that the method for calculating reimbursements was unfair. Almost half said that they weren’t happy with how their workplace uses RVUs.

A few respondents said that their RVU model, which is often based on what Dr. Patel called an “overly complicated algorithm,” did not account for the time spent on tasks or the fact that some patients miss appointments. RVUs also rely on factors outside the control of a physician, such as location and patient volume, said one doctor.

The model can also lower the level of care patients receive, Dr. Patel said.

“I know primary care doctors who work in RVU-based systems and simply cannot take the necessary time — even if it’s 30-45 minutes — to thoroughly assess a patient, when the model forces them to take on 15-minute encounters.”

Finally, over half of clinicians said alternatives to the RVU system would be more effective, and 77% suggested including qualitative data. One respondent recommended incorporating time spent doing paperwork and communicating with patients, complexity of conditions, and medication management.

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

Most physicians oppose the way standardized relative value units (RVUs) are used to determine performance and compensation, according to Medscape’s 2024 Physicians and RVUs Report. About 6 in 10 survey respondents were unhappy with how RVUs affected them financially, while 7 in 10 said RVUs were poor measures of productivity.

The report analyzed 2024 survey data from 1005 practicing physicians who earn RVUs.

“I’m already mad that the medical field is controlled by health insurers and what they pay and authorize,” said an anesthesiologist in New York. “Then [that approach] is transferred to medical offices and hospitals, where physicians are paid by RVUs.”

Most physicians surveyed produced between 4000 and 8000 RVUs per year. Roughly one in six were high RVU generators, generating more than 10,000 annually.

In most cases, the metric influences earning potential — 42% of doctors surveyed said RVUs affect their salaries to some degree. One quarter said their salary was based entirely on RVUs. More than three fourths of physicians who received performance bonuses said they must meet RVU targets to do so.

“The current RVU system encourages unnecessary procedures, hurting patients,” said an orthopedic surgeon in Maine.

Nearly three fourths of practitioners surveyed said they occasionally to frequently felt pressure to take on more patients as a result of this system.

“I know numerous primary care doctors and specialists who have been forced to increase patient volume to meet RVU goals, and none is happy about it,” said Alok Patel, MD, a pediatric hospitalist with Stanford Hospital in Palo Alto, California. “Plus, patients are definitely not happy about being rushed.”

More than half of respondents said they occasionally or frequently felt compelled by their employer to use higher-level coding, which interferes with a physician’s ethical responsibility to the patient, said Arthur L. Caplan, PhD, a bioethicist at NYU Langone Medical Center in New York City.

“Rather than rewarding excellence or good outcomes, you’re kind of rewarding procedures and volume,” said Dr. Caplan. “It’s more than pressure; it’s expected.”

Nearly 6 in 10 physicians said that the method for calculating reimbursements was unfair. Almost half said that they weren’t happy with how their workplace uses RVUs.

A few respondents said that their RVU model, which is often based on what Dr. Patel called an “overly complicated algorithm,” did not account for the time spent on tasks or the fact that some patients miss appointments. RVUs also rely on factors outside the control of a physician, such as location and patient volume, said one doctor.

The model can also lower the level of care patients receive, Dr. Patel said.

“I know primary care doctors who work in RVU-based systems and simply cannot take the necessary time — even if it’s 30-45 minutes — to thoroughly assess a patient, when the model forces them to take on 15-minute encounters.”

Finally, over half of clinicians said alternatives to the RVU system would be more effective, and 77% suggested including qualitative data. One respondent recommended incorporating time spent doing paperwork and communicating with patients, complexity of conditions, and medication management.

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

Most physicians oppose the way standardized relative value units (RVUs) are used to determine performance and compensation, according to Medscape’s 2024 Physicians and RVUs Report. About 6 in 10 survey respondents were unhappy with how RVUs affected them financially, while 7 in 10 said RVUs were poor measures of productivity.

The report analyzed 2024 survey data from 1005 practicing physicians who earn RVUs.

“I’m already mad that the medical field is controlled by health insurers and what they pay and authorize,” said an anesthesiologist in New York. “Then [that approach] is transferred to medical offices and hospitals, where physicians are paid by RVUs.”

Most physicians surveyed produced between 4000 and 8000 RVUs per year. Roughly one in six were high RVU generators, generating more than 10,000 annually.

In most cases, the metric influences earning potential — 42% of doctors surveyed said RVUs affect their salaries to some degree. One quarter said their salary was based entirely on RVUs. More than three fourths of physicians who received performance bonuses said they must meet RVU targets to do so.

“The current RVU system encourages unnecessary procedures, hurting patients,” said an orthopedic surgeon in Maine.

Nearly three fourths of practitioners surveyed said they occasionally to frequently felt pressure to take on more patients as a result of this system.

“I know numerous primary care doctors and specialists who have been forced to increase patient volume to meet RVU goals, and none is happy about it,” said Alok Patel, MD, a pediatric hospitalist with Stanford Hospital in Palo Alto, California. “Plus, patients are definitely not happy about being rushed.”

More than half of respondents said they occasionally or frequently felt compelled by their employer to use higher-level coding, which interferes with a physician’s ethical responsibility to the patient, said Arthur L. Caplan, PhD, a bioethicist at NYU Langone Medical Center in New York City.

“Rather than rewarding excellence or good outcomes, you’re kind of rewarding procedures and volume,” said Dr. Caplan. “It’s more than pressure; it’s expected.”

Nearly 6 in 10 physicians said that the method for calculating reimbursements was unfair. Almost half said that they weren’t happy with how their workplace uses RVUs.

A few respondents said that their RVU model, which is often based on what Dr. Patel called an “overly complicated algorithm,” did not account for the time spent on tasks or the fact that some patients miss appointments. RVUs also rely on factors outside the control of a physician, such as location and patient volume, said one doctor.

The model can also lower the level of care patients receive, Dr. Patel said.

“I know primary care doctors who work in RVU-based systems and simply cannot take the necessary time — even if it’s 30-45 minutes — to thoroughly assess a patient, when the model forces them to take on 15-minute encounters.”

Finally, over half of clinicians said alternatives to the RVU system would be more effective, and 77% suggested including qualitative data. One respondent recommended incorporating time spent doing paperwork and communicating with patients, complexity of conditions, and medication management.

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

A growing body of research has increasingly connected hearing loss with a higher risk for dementia. In addition, some studies suggest that wearing hearing aids may help prevent dementia, though one study was recently voluntarily retracted due to methodological errors.

Given the overall evidence, how robust are these associations? And what guidance should clinicians provide to their patients?

Frank Lin, MD, PhD, a clinician and professor of otolaryngology and epidemiology at Johns Hopkins University School of Medicine, Baltimore, emphasized that the evidence from the past 10-15 years strongly links hearing loss to cognitive decline.

While quantifying the exact increase in risk is challenging, Dr. Lin said, “there’s no doubt about it; it’s not trivial.”

With respect to the potential link between hearing aids and dementia prevention, Dr. Lin is involved in the ongoing ACHIEVE randomized trial. Results presented at the 2023 Alzheimer’s Association International Conference and simultaneously published in The Lancet revealed participants who used hearing aids experienced a significant slowing of cognitive decline compared with those who received health education.

“It’s a no-risk intervention that can benefit social function, and for people at risk for cognitive decline, it can actually benefit cognitive health,” Dr. Lin said.
 

Potential Mechanisms

Dr. Lin pointed out that the Lancet Commission on Dementia identifies hearing impairment as one of the most significant risk factors for dementia. Overall, the consensus from most studies is that hearing loss definitely increases the risk for cognitive decline and dementia, he said.

Several hypotheses may explain this connection, and Dr. Lin believes that a combination of three key mechanisms is likely to be central to understanding this link.

The first theory focuses on cognitive load. As people experience age-related hearing changes, “the inner ear is no longer sending signals clearly to the brain,” Dr. Lin explained. This forces the brain to work harder, increasing its cognitive load as it reallocates resources to assist with hearing.

Dr. Lin emphasized that this is a hypothesis and does not prove hearing loss directly causes cognitive decline or dementia. Rather, it suggests that hearing loss accelerates the “unmasking” of cognitive issues. Brain resources that might otherwise buffer against dementia’s pathologic triggers are consumed earlier due to the demands of managing hearing loss.

The second potential mechanism suggests that hearing loss may have detrimental effects on brain structure and function over time — a theory supported by several recent studies.

These studies show that individuals with more severe hearing loss experience faster rates of brain atrophy. The reduced stimulation from poor auditory signals accelerates brain atrophy, Dr. Lin explained.

The third hypothesis focuses on social isolation. Individuals with hearing loss may engage less in social activities, reducing cognitive stimulation and overall social interaction. It’s well-known that social engagement and cognitive stimulation are crucial for maintaining cognitive health over time, Dr. Lin said.

Overall, Dr. Lin believes that the association between hearing loss and an increased risk for cognitive decline likely involves a combination of all three potential mechanisms. It’s not a matter of one theory being right and the others being wrong, he said.
 

The Role of Hearing Aids

However, the jury is out on the role of hearing aids in preventing dementia.

A large observational study published in 2023 in Lancet Public Health was hailed by its investigators as providing “the best evidence to date” that hearing aids could mitigate the impact of hearing loss on dementia (Lancet Public Health. 2023 May;8[5]:e329-e338. doi: 10.1016/S2468-2667[23]00048-8). However, the authors voluntarily retracted the paper in December 2023 due to a coding error.

Despite this, a large meta-analysis published in JAMA Neurology suggested that hearing aids might reduce cognitive decline and dementia risk and even enhance short-term cognitive function.

Additionally, the ACHIEVE study, the first randomized trial to investigate these issues, included nearly 1000 older participants from two populations — those from the ARIC study and healthy volunteers. Participants were randomly assigned to receive either a hearing intervention or education on healthy aging.

Although the primary endpoint of change in standardized neurocognitive scores at year 3 showed no significant difference between the hearing intervention and health education groups, the ARIC cohort experienced a notable 48% reduction in cognitive decline with hearing aids compared with education.

Dr. Lin explained that, due to the study’s design, the control group was healthier than the ARIC cohort, which was at higher risk for cognitive decline due to factors such as age and diabetes. This is where they observed a strong effect of hearing intervention in reducing cognitive decline within just 3 years, Dr. Lin said.

Conversely, the hearing aids had minimal impact on the healthy controls, likely because they had not experienced cognitive decline to begin with. Essentially, the benefits of hearing aids were more apparent once cognitive issues were already present.

“It seems sort of obvious. In a group of people who aren’t at risk for cognitive decline, a hearing intervention isn’t going to benefit their cognition” in the short term, Dr. Lin noted. That said, the investigators are continuing to follow the healthy controls to determine whether hearing aids lower dementia risk over the long term.
 

Which Comes First?

Some experts have questioned the directionality of the link between hearing aids and dementia — do hearing aids reduce dementia risk or are individuals with dementia simply less likely to use them?

Dr. Lin noted that observational studies often have confounders. For instance, people who use hearing aids are often healthier and better educated. This makes it difficult to distinguish the effect of the intervention from the factors that led people to use it, he said.

In contrast, the ACHIEVE trial, a randomized study, was designed to separate these factors from the hearing intervention, Dr. Lin explained.

However, he added that ACHIEVE was not specifically powered to assess dementia development, focusing instead on cognitive decline. The investigators plan long-term follow-up of participants to evaluate the impact on dementia in the future.

So, given the current evidence, what should clinicians tell their patients?

Because all people experience some degree of hearing changes as they age, which can gradually affect communication and social engagement, it’s important for everyone to be aware of their hearing health, Dr. Lin said.

He noted there are apps available that allow individuals to measure their hearing with their phones, including determining their “hearing number.”

With respect to hearing aids, Dr. Lin noted that if individuals have trouble participating in everyday activities, addressing hearing issues and considering a hearing intervention is crucial.

There’s no medical risk associated with hearing aids, he said. Even if they only improve social activities and engagement, that’s a benefit. If they also have potential positive effects on cognitive health, “even better,” he added.

Dr. Lin noted that as of 2022, hearing aids are now available over the counter, a move that has improved accessibility. In addition, new technologies, such as stylish “hearing aid glasses,” are being developed to offer more appealing options and reduce the stigma associated with traditional devices.

People often view hearing loss as a significant life event and are reluctant to admit they need hearing aids. However, focusing on “what’s your hearing?” as a neutral tracking metric could make it easier to adopt new technologies in the future, Lin said.
 

Alzheimer’s Association Weighs in

Heather Snyder, PhD, vice president, Medical & Scientific Relations at the Alzheimer’s Association, echoed Dr. Lin, noting that there has been substantial research showing a link between hearing loss and cognitive decline.

“This association is something that we have seen repeated and replicated in a number of different studies. What we don’t know is the cause and effect,” Dr. Snyder said.

She noted it is unknown whether there is a causal link between hearing loss and cognitive decline and/or whether cognitive decline may contribute to hearing loss. These are some of the “big questions” that remain, said Dr. Snyder.

Still, she noted that hearing health is an important part of quality of life and overall brain health and “should be part of the conversation” between clinicians and their patients.

Discussing the results of the ACHIEVE study, Dr. Snyder highlighted that while the subgroup at higher risk for cognitive decline did experience significant improvement, the overall population did not show a benefit from the intervention.

The brain “is complex,” and it’s unlikely that a single intervention or target will provide all the benefits, Dr. Snyder said.

She emphasized that addressing hearing loss with hearing aids, combined with managing other modifiable risk factors — such as heart and metabolic health, physical activity, and a balanced diet — appears to offer the greatest potential for synergy and preserving cognition.

Drs. Lin and Snyder reported no relevant conflicts of interest.
 

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

A growing body of research has increasingly connected hearing loss with a higher risk for dementia. In addition, some studies suggest that wearing hearing aids may help prevent dementia, though one study was recently voluntarily retracted due to methodological errors.

Given the overall evidence, how robust are these associations? And what guidance should clinicians provide to their patients?

Frank Lin, MD, PhD, a clinician and professor of otolaryngology and epidemiology at Johns Hopkins University School of Medicine, Baltimore, emphasized that the evidence from the past 10-15 years strongly links hearing loss to cognitive decline.

While quantifying the exact increase in risk is challenging, Dr. Lin said, “there’s no doubt about it; it’s not trivial.”

With respect to the potential link between hearing aids and dementia prevention, Dr. Lin is involved in the ongoing ACHIEVE randomized trial. Results presented at the 2023 Alzheimer’s Association International Conference and simultaneously published in The Lancet revealed participants who used hearing aids experienced a significant slowing of cognitive decline compared with those who received health education.

“It’s a no-risk intervention that can benefit social function, and for people at risk for cognitive decline, it can actually benefit cognitive health,” Dr. Lin said.
 

Potential Mechanisms

Dr. Lin pointed out that the Lancet Commission on Dementia identifies hearing impairment as one of the most significant risk factors for dementia. Overall, the consensus from most studies is that hearing loss definitely increases the risk for cognitive decline and dementia, he said.

Several hypotheses may explain this connection, and Dr. Lin believes that a combination of three key mechanisms is likely to be central to understanding this link.

The first theory focuses on cognitive load. As people experience age-related hearing changes, “the inner ear is no longer sending signals clearly to the brain,” Dr. Lin explained. This forces the brain to work harder, increasing its cognitive load as it reallocates resources to assist with hearing.

Dr. Lin emphasized that this is a hypothesis and does not prove hearing loss directly causes cognitive decline or dementia. Rather, it suggests that hearing loss accelerates the “unmasking” of cognitive issues. Brain resources that might otherwise buffer against dementia’s pathologic triggers are consumed earlier due to the demands of managing hearing loss.

The second potential mechanism suggests that hearing loss may have detrimental effects on brain structure and function over time — a theory supported by several recent studies.

These studies show that individuals with more severe hearing loss experience faster rates of brain atrophy. The reduced stimulation from poor auditory signals accelerates brain atrophy, Dr. Lin explained.

The third hypothesis focuses on social isolation. Individuals with hearing loss may engage less in social activities, reducing cognitive stimulation and overall social interaction. It’s well-known that social engagement and cognitive stimulation are crucial for maintaining cognitive health over time, Dr. Lin said.

Overall, Dr. Lin believes that the association between hearing loss and an increased risk for cognitive decline likely involves a combination of all three potential mechanisms. It’s not a matter of one theory being right and the others being wrong, he said.
 

The Role of Hearing Aids

However, the jury is out on the role of hearing aids in preventing dementia.

A large observational study published in 2023 in Lancet Public Health was hailed by its investigators as providing “the best evidence to date” that hearing aids could mitigate the impact of hearing loss on dementia (Lancet Public Health. 2023 May;8[5]:e329-e338. doi: 10.1016/S2468-2667[23]00048-8). However, the authors voluntarily retracted the paper in December 2023 due to a coding error.

Despite this, a large meta-analysis published in JAMA Neurology suggested that hearing aids might reduce cognitive decline and dementia risk and even enhance short-term cognitive function.

Additionally, the ACHIEVE study, the first randomized trial to investigate these issues, included nearly 1000 older participants from two populations — those from the ARIC study and healthy volunteers. Participants were randomly assigned to receive either a hearing intervention or education on healthy aging.

Although the primary endpoint of change in standardized neurocognitive scores at year 3 showed no significant difference between the hearing intervention and health education groups, the ARIC cohort experienced a notable 48% reduction in cognitive decline with hearing aids compared with education.

Dr. Lin explained that, due to the study’s design, the control group was healthier than the ARIC cohort, which was at higher risk for cognitive decline due to factors such as age and diabetes. This is where they observed a strong effect of hearing intervention in reducing cognitive decline within just 3 years, Dr. Lin said.

Conversely, the hearing aids had minimal impact on the healthy controls, likely because they had not experienced cognitive decline to begin with. Essentially, the benefits of hearing aids were more apparent once cognitive issues were already present.

“It seems sort of obvious. In a group of people who aren’t at risk for cognitive decline, a hearing intervention isn’t going to benefit their cognition” in the short term, Dr. Lin noted. That said, the investigators are continuing to follow the healthy controls to determine whether hearing aids lower dementia risk over the long term.
 

Which Comes First?

Some experts have questioned the directionality of the link between hearing aids and dementia — do hearing aids reduce dementia risk or are individuals with dementia simply less likely to use them?

Dr. Lin noted that observational studies often have confounders. For instance, people who use hearing aids are often healthier and better educated. This makes it difficult to distinguish the effect of the intervention from the factors that led people to use it, he said.

In contrast, the ACHIEVE trial, a randomized study, was designed to separate these factors from the hearing intervention, Dr. Lin explained.

However, he added that ACHIEVE was not specifically powered to assess dementia development, focusing instead on cognitive decline. The investigators plan long-term follow-up of participants to evaluate the impact on dementia in the future.

So, given the current evidence, what should clinicians tell their patients?

Because all people experience some degree of hearing changes as they age, which can gradually affect communication and social engagement, it’s important for everyone to be aware of their hearing health, Dr. Lin said.

He noted there are apps available that allow individuals to measure their hearing with their phones, including determining their “hearing number.”

With respect to hearing aids, Dr. Lin noted that if individuals have trouble participating in everyday activities, addressing hearing issues and considering a hearing intervention is crucial.

There’s no medical risk associated with hearing aids, he said. Even if they only improve social activities and engagement, that’s a benefit. If they also have potential positive effects on cognitive health, “even better,” he added.

Dr. Lin noted that as of 2022, hearing aids are now available over the counter, a move that has improved accessibility. In addition, new technologies, such as stylish “hearing aid glasses,” are being developed to offer more appealing options and reduce the stigma associated with traditional devices.

People often view hearing loss as a significant life event and are reluctant to admit they need hearing aids. However, focusing on “what’s your hearing?” as a neutral tracking metric could make it easier to adopt new technologies in the future, Lin said.
 

Alzheimer’s Association Weighs in

Heather Snyder, PhD, vice president, Medical & Scientific Relations at the Alzheimer’s Association, echoed Dr. Lin, noting that there has been substantial research showing a link between hearing loss and cognitive decline.

“This association is something that we have seen repeated and replicated in a number of different studies. What we don’t know is the cause and effect,” Dr. Snyder said.

She noted it is unknown whether there is a causal link between hearing loss and cognitive decline and/or whether cognitive decline may contribute to hearing loss. These are some of the “big questions” that remain, said Dr. Snyder.

Still, she noted that hearing health is an important part of quality of life and overall brain health and “should be part of the conversation” between clinicians and their patients.

Discussing the results of the ACHIEVE study, Dr. Snyder highlighted that while the subgroup at higher risk for cognitive decline did experience significant improvement, the overall population did not show a benefit from the intervention.

The brain “is complex,” and it’s unlikely that a single intervention or target will provide all the benefits, Dr. Snyder said.

She emphasized that addressing hearing loss with hearing aids, combined with managing other modifiable risk factors — such as heart and metabolic health, physical activity, and a balanced diet — appears to offer the greatest potential for synergy and preserving cognition.

Drs. Lin and Snyder reported no relevant conflicts of interest.
 

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

A growing body of research has increasingly connected hearing loss with a higher risk for dementia. In addition, some studies suggest that wearing hearing aids may help prevent dementia, though one study was recently voluntarily retracted due to methodological errors.

Given the overall evidence, how robust are these associations? And what guidance should clinicians provide to their patients?

Frank Lin, MD, PhD, a clinician and professor of otolaryngology and epidemiology at Johns Hopkins University School of Medicine, Baltimore, emphasized that the evidence from the past 10-15 years strongly links hearing loss to cognitive decline.

While quantifying the exact increase in risk is challenging, Dr. Lin said, “there’s no doubt about it; it’s not trivial.”

With respect to the potential link between hearing aids and dementia prevention, Dr. Lin is involved in the ongoing ACHIEVE randomized trial. Results presented at the 2023 Alzheimer’s Association International Conference and simultaneously published in The Lancet revealed participants who used hearing aids experienced a significant slowing of cognitive decline compared with those who received health education.

“It’s a no-risk intervention that can benefit social function, and for people at risk for cognitive decline, it can actually benefit cognitive health,” Dr. Lin said.
 

Potential Mechanisms

Dr. Lin pointed out that the Lancet Commission on Dementia identifies hearing impairment as one of the most significant risk factors for dementia. Overall, the consensus from most studies is that hearing loss definitely increases the risk for cognitive decline and dementia, he said.

Several hypotheses may explain this connection, and Dr. Lin believes that a combination of three key mechanisms is likely to be central to understanding this link.

The first theory focuses on cognitive load. As people experience age-related hearing changes, “the inner ear is no longer sending signals clearly to the brain,” Dr. Lin explained. This forces the brain to work harder, increasing its cognitive load as it reallocates resources to assist with hearing.

Dr. Lin emphasized that this is a hypothesis and does not prove hearing loss directly causes cognitive decline or dementia. Rather, it suggests that hearing loss accelerates the “unmasking” of cognitive issues. Brain resources that might otherwise buffer against dementia’s pathologic triggers are consumed earlier due to the demands of managing hearing loss.

The second potential mechanism suggests that hearing loss may have detrimental effects on brain structure and function over time — a theory supported by several recent studies.

These studies show that individuals with more severe hearing loss experience faster rates of brain atrophy. The reduced stimulation from poor auditory signals accelerates brain atrophy, Dr. Lin explained.

The third hypothesis focuses on social isolation. Individuals with hearing loss may engage less in social activities, reducing cognitive stimulation and overall social interaction. It’s well-known that social engagement and cognitive stimulation are crucial for maintaining cognitive health over time, Dr. Lin said.

Overall, Dr. Lin believes that the association between hearing loss and an increased risk for cognitive decline likely involves a combination of all three potential mechanisms. It’s not a matter of one theory being right and the others being wrong, he said.
 

The Role of Hearing Aids

However, the jury is out on the role of hearing aids in preventing dementia.

A large observational study published in 2023 in Lancet Public Health was hailed by its investigators as providing “the best evidence to date” that hearing aids could mitigate the impact of hearing loss on dementia (Lancet Public Health. 2023 May;8[5]:e329-e338. doi: 10.1016/S2468-2667[23]00048-8). However, the authors voluntarily retracted the paper in December 2023 due to a coding error.

Despite this, a large meta-analysis published in JAMA Neurology suggested that hearing aids might reduce cognitive decline and dementia risk and even enhance short-term cognitive function.

Additionally, the ACHIEVE study, the first randomized trial to investigate these issues, included nearly 1000 older participants from two populations — those from the ARIC study and healthy volunteers. Participants were randomly assigned to receive either a hearing intervention or education on healthy aging.

Although the primary endpoint of change in standardized neurocognitive scores at year 3 showed no significant difference between the hearing intervention and health education groups, the ARIC cohort experienced a notable 48% reduction in cognitive decline with hearing aids compared with education.

Dr. Lin explained that, due to the study’s design, the control group was healthier than the ARIC cohort, which was at higher risk for cognitive decline due to factors such as age and diabetes. This is where they observed a strong effect of hearing intervention in reducing cognitive decline within just 3 years, Dr. Lin said.

Conversely, the hearing aids had minimal impact on the healthy controls, likely because they had not experienced cognitive decline to begin with. Essentially, the benefits of hearing aids were more apparent once cognitive issues were already present.

“It seems sort of obvious. In a group of people who aren’t at risk for cognitive decline, a hearing intervention isn’t going to benefit their cognition” in the short term, Dr. Lin noted. That said, the investigators are continuing to follow the healthy controls to determine whether hearing aids lower dementia risk over the long term.
 

Which Comes First?

Some experts have questioned the directionality of the link between hearing aids and dementia — do hearing aids reduce dementia risk or are individuals with dementia simply less likely to use them?

Dr. Lin noted that observational studies often have confounders. For instance, people who use hearing aids are often healthier and better educated. This makes it difficult to distinguish the effect of the intervention from the factors that led people to use it, he said.

In contrast, the ACHIEVE trial, a randomized study, was designed to separate these factors from the hearing intervention, Dr. Lin explained.

However, he added that ACHIEVE was not specifically powered to assess dementia development, focusing instead on cognitive decline. The investigators plan long-term follow-up of participants to evaluate the impact on dementia in the future.

So, given the current evidence, what should clinicians tell their patients?

Because all people experience some degree of hearing changes as they age, which can gradually affect communication and social engagement, it’s important for everyone to be aware of their hearing health, Dr. Lin said.

He noted there are apps available that allow individuals to measure their hearing with their phones, including determining their “hearing number.”

With respect to hearing aids, Dr. Lin noted that if individuals have trouble participating in everyday activities, addressing hearing issues and considering a hearing intervention is crucial.

There’s no medical risk associated with hearing aids, he said. Even if they only improve social activities and engagement, that’s a benefit. If they also have potential positive effects on cognitive health, “even better,” he added.

Dr. Lin noted that as of 2022, hearing aids are now available over the counter, a move that has improved accessibility. In addition, new technologies, such as stylish “hearing aid glasses,” are being developed to offer more appealing options and reduce the stigma associated with traditional devices.

People often view hearing loss as a significant life event and are reluctant to admit they need hearing aids. However, focusing on “what’s your hearing?” as a neutral tracking metric could make it easier to adopt new technologies in the future, Lin said.
 

Alzheimer’s Association Weighs in

Heather Snyder, PhD, vice president, Medical & Scientific Relations at the Alzheimer’s Association, echoed Dr. Lin, noting that there has been substantial research showing a link between hearing loss and cognitive decline.

“This association is something that we have seen repeated and replicated in a number of different studies. What we don’t know is the cause and effect,” Dr. Snyder said.

She noted it is unknown whether there is a causal link between hearing loss and cognitive decline and/or whether cognitive decline may contribute to hearing loss. These are some of the “big questions” that remain, said Dr. Snyder.

Still, she noted that hearing health is an important part of quality of life and overall brain health and “should be part of the conversation” between clinicians and their patients.

Discussing the results of the ACHIEVE study, Dr. Snyder highlighted that while the subgroup at higher risk for cognitive decline did experience significant improvement, the overall population did not show a benefit from the intervention.

The brain “is complex,” and it’s unlikely that a single intervention or target will provide all the benefits, Dr. Snyder said.

She emphasized that addressing hearing loss with hearing aids, combined with managing other modifiable risk factors — such as heart and metabolic health, physical activity, and a balanced diet — appears to offer the greatest potential for synergy and preserving cognition.

Drs. Lin and Snyder reported no relevant conflicts of interest.
 

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

Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.

This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.

Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.

Sexual dysfunction is a common and significant late effect among CCS. The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
 

Characteristics and Mechanisms

Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.

As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.

Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.

Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects. 
 

Sexual Function in CCS

A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.

The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.

Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.

In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.

The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
 

Factors Influencing Sexual Function

The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.

Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.

Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.

Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.

The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.

Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.

Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.

Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
 

This story was translated from Univadis Italy using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.

This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.

Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.

Sexual dysfunction is a common and significant late effect among CCS. The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
 

Characteristics and Mechanisms

Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.

As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.

Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.

Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects. 
 

Sexual Function in CCS

A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.

The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.

Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.

In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.

The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
 

Factors Influencing Sexual Function

The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.

Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.

Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.

Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.

The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.

Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.

Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.

Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
 

This story was translated from Univadis Italy using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.

This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.

Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.

Sexual dysfunction is a common and significant late effect among CCS. The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
 

Characteristics and Mechanisms

Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.

As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.

Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.

Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects. 
 

Sexual Function in CCS

A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.

The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.

Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.

In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.

The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
 

Factors Influencing Sexual Function

The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.

Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.

Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.

Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.

The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.

Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.

Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.

Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
 

This story was translated from Univadis Italy using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Edema in the feet and legs is a common complaint in our practices. It can cause pain, weakness, heaviness, discomfort, limited movement, and a negative body image. Medications can contribute to edema, either alone or in combination with other health issues.

Edema is also associated with advanced age, female sex, obesity, diabetes, hypertension, pain, lack of physical activity, and mobility limitations. These factors often necessitate medication prescriptions, which can aggravate the problem. Therefore, it is important to know how to treat or prevent medication-induced edema.

There are four main causes of edema, and all can facilitate medication-induced edema.

• Increased capillary pressure. Conditions such as heart failure, renal dysfunction, venous insufficiency, deep vein thrombosis, and cirrhosis can increase capillary pressure, leading to edema.
• Decreased oncotic pressure. Hypoalbuminemia, a primary cause of reduced colloid oncotic pressure, can result from nephrotic syndrome, diabetic nephropathy, lupus nephropathy, amyloidosis, nephropathies, cirrhosis, chronic liver disease, and malabsorption or malnutrition.
• Increased capillary permeability. Vascular injury, often associated with diabetes, can increase capillary permeability and contribute to edema.
• Impaired lymphatic drainage. Lymphatic obstruction is common in patients with lymphedema, tumors, inflammation, fibrosis, certain infections, surgery, and congenital anomalies. Conditions such as thyroid disorders can also cause an increase in interstitial albumin and other proteins without a corresponding increase in lymphatic flow, leading to lymphedema.

Medications That Can Cause Edema

• Calcium channel blockers (CCBs). Drugs such as nifedipine and amlodipine can increase hydrostatic pressure by causing selective vasodilation of precapillary vessels, leading to increased intracapillary pressures. Newer lipophilic CCBs (eg, levamlodipine) exhibit lower rates of edema. Reducing the dose is often effective. Diuretics are not very effective for vasodilation-induced edema. Combining CCBs with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), which induce postcapillary dilation and normalize intracapillary pressure, may reduce fluid leakage into the interstitial space. This combination may be more beneficial than high-dose CCB monotherapy.
• Thiazolidinedione (eg, pioglitazone). These increase vascular permeability and hydrostatic pressure. They work by stimulating the peroxisome proliferator–activated gamma receptor, increasing vascular endothelial permeability, vascular endothelial growth factor secretion, and renal retention of sodium and fluids. Because of other adverse effects, their use is now limited.
• Agents for neuropathic pain (gabapentin and pregabalin). These drugs can induce selective vasodilation of arterioles through a mechanism similar to that of CCBs, causing increased intracapillary pressures. Edema usually begins within the first month of treatment or dose increase and often regresses after dose reduction or drug discontinuation.
• Antiparkinsonian dopamine agonists. These increase hydrostatic pressure by reducing sympathetic tone and dilating arterioles through alpha-2 adrenergic receptor activity.
• New antipsychotics. Drugs like clozapine, iloperidone, lurasidone, olanzapine, quetiapine, risperidone, and ziprasidone can increase hydrostatic pressure through antagonistic effects on alpha-1 adrenergic receptors, causing vasodilation.
• Nitrates. These drugs increase hydrostatic pressure by causing preferential venous dilation, leading to increased venous pooling.
• Nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs can increase hydrostatic pressure by inhibiting vasodilation of afferent renal arterioles, decreasing the glomerular filtration rate, and stimulating the renin-angiotensin-aldosterone system, which leads to sodium and water retention. These adverse effects warrant cautious use of these agents.
• ACE inhibitors. Drugs such as enalapril and ramipril can increase vascular permeability. They reduce the metabolism and accumulation of bradykinin, which increases vascular permeability and fluid leakage. These effects are rare and are usually related to allergic responses.
• Insulin. Insulin decreases capillary oncotic pressure and increases vascular permeability. Rapid correction of hyperglycemia can cause a loss of oncotic pressure, while chronic hyperglycemia can damage vascular membranes, increasing permeability. These effects are generally benign and can be managed with careful dose titration, sodium restriction, or diuretics.
• Steroids. Steroids with mineralocorticoid activity can increase renal sodium and water retention, leading to increased blood volume. Fludrocortisone has the highest mineralocorticoid activity, while dexamethasone and methylprednisolone have negligible activity.

Implications

Understanding how these medications cause edema is important for effective management. For example, in the case of those causing edema due to reduced oncotic pressure, like insulin, slow dose titrations can help adapt to osmolarity changes. For drugs causing edema due to increased hydrostatic pressure, diuretics are more effective in acute management.

The key takeaways from this review are:

• Awareness of drug-induced edema. Many drugs besides CCBs can cause edema.
• Combination therapy. Combining ACE inhibitors or ARBs with CCBs can prevent or reduce CCB-induced edema.
• Edema management strategies. Strategies to manage or prevent edema should include dose reductions or replacement of the problematic medication, especially in severe or refractory cases.

Dr. Wajngarten, professor of cardiology, University of São Paulo, Brazil, has disclosed no relevant financial relationships.

This story was translated from the Medscape Portuguese edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Edema in the feet and legs is a common complaint in our practices. It can cause pain, weakness, heaviness, discomfort, limited movement, and a negative body image. Medications can contribute to edema, either alone or in combination with other health issues.

Edema is also associated with advanced age, female sex, obesity, diabetes, hypertension, pain, lack of physical activity, and mobility limitations. These factors often necessitate medication prescriptions, which can aggravate the problem. Therefore, it is important to know how to treat or prevent medication-induced edema.

There are four main causes of edema, and all can facilitate medication-induced edema.

• Increased capillary pressure. Conditions such as heart failure, renal dysfunction, venous insufficiency, deep vein thrombosis, and cirrhosis can increase capillary pressure, leading to edema.
• Decreased oncotic pressure. Hypoalbuminemia, a primary cause of reduced colloid oncotic pressure, can result from nephrotic syndrome, diabetic nephropathy, lupus nephropathy, amyloidosis, nephropathies, cirrhosis, chronic liver disease, and malabsorption or malnutrition.
• Increased capillary permeability. Vascular injury, often associated with diabetes, can increase capillary permeability and contribute to edema.
• Impaired lymphatic drainage. Lymphatic obstruction is common in patients with lymphedema, tumors, inflammation, fibrosis, certain infections, surgery, and congenital anomalies. Conditions such as thyroid disorders can also cause an increase in interstitial albumin and other proteins without a corresponding increase in lymphatic flow, leading to lymphedema.

Medications That Can Cause Edema

• Calcium channel blockers (CCBs). Drugs such as nifedipine and amlodipine can increase hydrostatic pressure by causing selective vasodilation of precapillary vessels, leading to increased intracapillary pressures. Newer lipophilic CCBs (eg, levamlodipine) exhibit lower rates of edema. Reducing the dose is often effective. Diuretics are not very effective for vasodilation-induced edema. Combining CCBs with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), which induce postcapillary dilation and normalize intracapillary pressure, may reduce fluid leakage into the interstitial space. This combination may be more beneficial than high-dose CCB monotherapy.
• Thiazolidinedione (eg, pioglitazone). These increase vascular permeability and hydrostatic pressure. They work by stimulating the peroxisome proliferator–activated gamma receptor, increasing vascular endothelial permeability, vascular endothelial growth factor secretion, and renal retention of sodium and fluids. Because of other adverse effects, their use is now limited.
• Agents for neuropathic pain (gabapentin and pregabalin). These drugs can induce selective vasodilation of arterioles through a mechanism similar to that of CCBs, causing increased intracapillary pressures. Edema usually begins within the first month of treatment or dose increase and often regresses after dose reduction or drug discontinuation.
• Antiparkinsonian dopamine agonists. These increase hydrostatic pressure by reducing sympathetic tone and dilating arterioles through alpha-2 adrenergic receptor activity.
• New antipsychotics. Drugs like clozapine, iloperidone, lurasidone, olanzapine, quetiapine, risperidone, and ziprasidone can increase hydrostatic pressure through antagonistic effects on alpha-1 adrenergic receptors, causing vasodilation.
• Nitrates. These drugs increase hydrostatic pressure by causing preferential venous dilation, leading to increased venous pooling.
• Nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs can increase hydrostatic pressure by inhibiting vasodilation of afferent renal arterioles, decreasing the glomerular filtration rate, and stimulating the renin-angiotensin-aldosterone system, which leads to sodium and water retention. These adverse effects warrant cautious use of these agents.
• ACE inhibitors. Drugs such as enalapril and ramipril can increase vascular permeability. They reduce the metabolism and accumulation of bradykinin, which increases vascular permeability and fluid leakage. These effects are rare and are usually related to allergic responses.
• Insulin. Insulin decreases capillary oncotic pressure and increases vascular permeability. Rapid correction of hyperglycemia can cause a loss of oncotic pressure, while chronic hyperglycemia can damage vascular membranes, increasing permeability. These effects are generally benign and can be managed with careful dose titration, sodium restriction, or diuretics.
• Steroids. Steroids with mineralocorticoid activity can increase renal sodium and water retention, leading to increased blood volume. Fludrocortisone has the highest mineralocorticoid activity, while dexamethasone and methylprednisolone have negligible activity.

Implications

Understanding how these medications cause edema is important for effective management. For example, in the case of those causing edema due to reduced oncotic pressure, like insulin, slow dose titrations can help adapt to osmolarity changes. For drugs causing edema due to increased hydrostatic pressure, diuretics are more effective in acute management.

The key takeaways from this review are:

• Awareness of drug-induced edema. Many drugs besides CCBs can cause edema.
• Combination therapy. Combining ACE inhibitors or ARBs with CCBs can prevent or reduce CCB-induced edema.
• Edema management strategies. Strategies to manage or prevent edema should include dose reductions or replacement of the problematic medication, especially in severe or refractory cases.

Dr. Wajngarten, professor of cardiology, University of São Paulo, Brazil, has disclosed no relevant financial relationships.

This story was translated from the Medscape Portuguese edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Edema in the feet and legs is a common complaint in our practices. It can cause pain, weakness, heaviness, discomfort, limited movement, and a negative body image. Medications can contribute to edema, either alone or in combination with other health issues.

Edema is also associated with advanced age, female sex, obesity, diabetes, hypertension, pain, lack of physical activity, and mobility limitations. These factors often necessitate medication prescriptions, which can aggravate the problem. Therefore, it is important to know how to treat or prevent medication-induced edema.

There are four main causes of edema, and all can facilitate medication-induced edema.

• Increased capillary pressure. Conditions such as heart failure, renal dysfunction, venous insufficiency, deep vein thrombosis, and cirrhosis can increase capillary pressure, leading to edema.
• Decreased oncotic pressure. Hypoalbuminemia, a primary cause of reduced colloid oncotic pressure, can result from nephrotic syndrome, diabetic nephropathy, lupus nephropathy, amyloidosis, nephropathies, cirrhosis, chronic liver disease, and malabsorption or malnutrition.
• Increased capillary permeability. Vascular injury, often associated with diabetes, can increase capillary permeability and contribute to edema.
• Impaired lymphatic drainage. Lymphatic obstruction is common in patients with lymphedema, tumors, inflammation, fibrosis, certain infections, surgery, and congenital anomalies. Conditions such as thyroid disorders can also cause an increase in interstitial albumin and other proteins without a corresponding increase in lymphatic flow, leading to lymphedema.

Medications That Can Cause Edema

• Calcium channel blockers (CCBs). Drugs such as nifedipine and amlodipine can increase hydrostatic pressure by causing selective vasodilation of precapillary vessels, leading to increased intracapillary pressures. Newer lipophilic CCBs (eg, levamlodipine) exhibit lower rates of edema. Reducing the dose is often effective. Diuretics are not very effective for vasodilation-induced edema. Combining CCBs with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), which induce postcapillary dilation and normalize intracapillary pressure, may reduce fluid leakage into the interstitial space. This combination may be more beneficial than high-dose CCB monotherapy.
• Thiazolidinedione (eg, pioglitazone). These increase vascular permeability and hydrostatic pressure. They work by stimulating the peroxisome proliferator–activated gamma receptor, increasing vascular endothelial permeability, vascular endothelial growth factor secretion, and renal retention of sodium and fluids. Because of other adverse effects, their use is now limited.
• Agents for neuropathic pain (gabapentin and pregabalin). These drugs can induce selective vasodilation of arterioles through a mechanism similar to that of CCBs, causing increased intracapillary pressures. Edema usually begins within the first month of treatment or dose increase and often regresses after dose reduction or drug discontinuation.
• Antiparkinsonian dopamine agonists. These increase hydrostatic pressure by reducing sympathetic tone and dilating arterioles through alpha-2 adrenergic receptor activity.
• New antipsychotics. Drugs like clozapine, iloperidone, lurasidone, olanzapine, quetiapine, risperidone, and ziprasidone can increase hydrostatic pressure through antagonistic effects on alpha-1 adrenergic receptors, causing vasodilation.
• Nitrates. These drugs increase hydrostatic pressure by causing preferential venous dilation, leading to increased venous pooling.
• Nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs can increase hydrostatic pressure by inhibiting vasodilation of afferent renal arterioles, decreasing the glomerular filtration rate, and stimulating the renin-angiotensin-aldosterone system, which leads to sodium and water retention. These adverse effects warrant cautious use of these agents.
• ACE inhibitors. Drugs such as enalapril and ramipril can increase vascular permeability. They reduce the metabolism and accumulation of bradykinin, which increases vascular permeability and fluid leakage. These effects are rare and are usually related to allergic responses.
• Insulin. Insulin decreases capillary oncotic pressure and increases vascular permeability. Rapid correction of hyperglycemia can cause a loss of oncotic pressure, while chronic hyperglycemia can damage vascular membranes, increasing permeability. These effects are generally benign and can be managed with careful dose titration, sodium restriction, or diuretics.
• Steroids. Steroids with mineralocorticoid activity can increase renal sodium and water retention, leading to increased blood volume. Fludrocortisone has the highest mineralocorticoid activity, while dexamethasone and methylprednisolone have negligible activity.

Implications

Understanding how these medications cause edema is important for effective management. For example, in the case of those causing edema due to reduced oncotic pressure, like insulin, slow dose titrations can help adapt to osmolarity changes. For drugs causing edema due to increased hydrostatic pressure, diuretics are more effective in acute management.

The key takeaways from this review are:

• Awareness of drug-induced edema. Many drugs besides CCBs can cause edema.
• Combination therapy. Combining ACE inhibitors or ARBs with CCBs can prevent or reduce CCB-induced edema.
• Edema management strategies. Strategies to manage or prevent edema should include dose reductions or replacement of the problematic medication, especially in severe or refractory cases.

Dr. Wajngarten, professor of cardiology, University of São Paulo, Brazil, has disclosed no relevant financial relationships.

This story was translated from the Medscape Portuguese edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Since the COVID-19 pandemic, alcoholic hand sanitizers have become widely accessible nationwide. They can pose a problem, especially for emergency departments, when alcohol-dependent patients start drinking them. One example that demonstrates the challenge of diagnosing alcohol abuse is the medical history of a young man, as reported by Mahmoud El Hussein, MD, and colleagues from Hôpital Lariboisière in Paris, France.

Presentation and History

A 26-year-old man presented with severe abdominal pain at the emergency department. Upon arrival, he was hemodynamically stable but nervous and verbally aggressive at times. The patient reported no relevant preexisting conditions and was not taking any medications.

Findings

Upon initial physical examination, the patient had a soft, diffusely tender abdomen; tachycardia; and notably poor hygiene. The patient was afebrile. An ECG confirmed the tachycardia but showed no signs of ischemia. Blood work, except for slightly elevated liver values, did not reveal any abnormalities, particularly ruling out bleeding or kidney disease.

A urease rapid test to rule out kidney stones also showed no pathologic findings. In consultation with the surgical department, a CT scan of the abdomen was performed to rule out organ perforation, volvulus, or mesenteric ischemia. Only signs of fatty liver were found.
 

A Neighbor’s Tip

During all examinations, the patient’s abdomen was repeatedly palpated to promptly detect signs of an acute abdomen. However, there was never any defense tension at any point.

Intravenous analgesics and proton pump inhibitors (ie, paracetamol, phloroglucin, and pantoprazole) did not relieve the patient’s symptoms. Morphine was administered intravenously for sedation.

Only after a frustrating diagnostic process did a neighbor of the patient inform a nurse that he suspected the patient of stealing and consuming hand sanitizer. With the patient’s consent, a blood alcohol test was performed, revealing a blood alcohol concentration of 0.2% (2 g/L). A urine test, also conducted with the patient’s consent, tested positive for tetrahydrocannabinol. Additional tests showed the following results:

• Venous pH: 7.29 (normal, 7.32-7.38)
• Anion gap (mEq/L): 14 (normal, 3-9)
• Ketone bodies (mmol/L): 0.2 (normal, < 0.6)
• Calculated serum osmolality (mOsm/kg): 292 (normal, 285-295)
• Measured serum osmolality (mOsm/kg): 320 (normal, 285-295)
• Osmolality gap (mOsm/kg): 2 (normal, < 10)

The patient was informed of the test results and confessed to feigning abdominal pain. He was dependent on alcohol and experiencing withdrawal symptoms. The patient had stolen seven 475-mL bottles of hand sanitizer and consumed one and a half in the past 4-6 hours. According to the authors, the sanitizer consisted of 80% ethanol, 1.45% glycerol, and 0.13% hydrogen peroxide.
 

Discussion

In Germany, alcohol consumption results in approximately €57 billion in direct economic costs annually, according to data from the Federal Ministry of Health. In 2021, about 7.9 million people aged 18-64 years consumed alcohol in a risky manner (approximately 9.6% of the German population). About 9 million people (approximately 11%) were classified as alcoholics.

The authors of the case report pointed out that those in the advanced stages of alcohol addiction often consume any alcoholic liquid they can access. This includes alcoholic hand sanitizers commonly used in hospitals. Therefore, staff in emergency departments, where potential abusers encounter a wide range of potential abuse items, should exercise caution.

Although hand sanitizers are mainly composed of ethanol, they may also contain isopropanol, methanol, or acetone. Methanol poisoning can cause abdominal pain, visual disturbances, central nervous system damage, and death. Other alcohols such as ethylene glycol, commonly found in antifreeze, can distort blood values (lactate) and complicate a correct diagnosis.

Physicians working in emergency departments should proceed with caution when suspecting alcohol abuse. Questioning the patient’s environment and determining additional laboratory parameters (such as osmolality gap in the case report) can help unmask substance abuse if it is in doubt.

This story was translated from Univadis Germany, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Since the COVID-19 pandemic, alcoholic hand sanitizers have become widely accessible nationwide. They can pose a problem, especially for emergency departments, when alcohol-dependent patients start drinking them. One example that demonstrates the challenge of diagnosing alcohol abuse is the medical history of a young man, as reported by Mahmoud El Hussein, MD, and colleagues from Hôpital Lariboisière in Paris, France.

Presentation and History

A 26-year-old man presented with severe abdominal pain at the emergency department. Upon arrival, he was hemodynamically stable but nervous and verbally aggressive at times. The patient reported no relevant preexisting conditions and was not taking any medications.

Findings

Upon initial physical examination, the patient had a soft, diffusely tender abdomen; tachycardia; and notably poor hygiene. The patient was afebrile. An ECG confirmed the tachycardia but showed no signs of ischemia. Blood work, except for slightly elevated liver values, did not reveal any abnormalities, particularly ruling out bleeding or kidney disease.

A urease rapid test to rule out kidney stones also showed no pathologic findings. In consultation with the surgical department, a CT scan of the abdomen was performed to rule out organ perforation, volvulus, or mesenteric ischemia. Only signs of fatty liver were found.
 

A Neighbor’s Tip

During all examinations, the patient’s abdomen was repeatedly palpated to promptly detect signs of an acute abdomen. However, there was never any defense tension at any point.

Intravenous analgesics and proton pump inhibitors (ie, paracetamol, phloroglucin, and pantoprazole) did not relieve the patient’s symptoms. Morphine was administered intravenously for sedation.

Only after a frustrating diagnostic process did a neighbor of the patient inform a nurse that he suspected the patient of stealing and consuming hand sanitizer. With the patient’s consent, a blood alcohol test was performed, revealing a blood alcohol concentration of 0.2% (2 g/L). A urine test, also conducted with the patient’s consent, tested positive for tetrahydrocannabinol. Additional tests showed the following results:

• Venous pH: 7.29 (normal, 7.32-7.38)
• Anion gap (mEq/L): 14 (normal, 3-9)
• Ketone bodies (mmol/L): 0.2 (normal, < 0.6)
• Calculated serum osmolality (mOsm/kg): 292 (normal, 285-295)
• Measured serum osmolality (mOsm/kg): 320 (normal, 285-295)
• Osmolality gap (mOsm/kg): 2 (normal, < 10)

The patient was informed of the test results and confessed to feigning abdominal pain. He was dependent on alcohol and experiencing withdrawal symptoms. The patient had stolen seven 475-mL bottles of hand sanitizer and consumed one and a half in the past 4-6 hours. According to the authors, the sanitizer consisted of 80% ethanol, 1.45% glycerol, and 0.13% hydrogen peroxide.
 

Discussion

In Germany, alcohol consumption results in approximately €57 billion in direct economic costs annually, according to data from the Federal Ministry of Health. In 2021, about 7.9 million people aged 18-64 years consumed alcohol in a risky manner (approximately 9.6% of the German population). About 9 million people (approximately 11%) were classified as alcoholics.

The authors of the case report pointed out that those in the advanced stages of alcohol addiction often consume any alcoholic liquid they can access. This includes alcoholic hand sanitizers commonly used in hospitals. Therefore, staff in emergency departments, where potential abusers encounter a wide range of potential abuse items, should exercise caution.

Although hand sanitizers are mainly composed of ethanol, they may also contain isopropanol, methanol, or acetone. Methanol poisoning can cause abdominal pain, visual disturbances, central nervous system damage, and death. Other alcohols such as ethylene glycol, commonly found in antifreeze, can distort blood values (lactate) and complicate a correct diagnosis.

Physicians working in emergency departments should proceed with caution when suspecting alcohol abuse. Questioning the patient’s environment and determining additional laboratory parameters (such as osmolality gap in the case report) can help unmask substance abuse if it is in doubt.

This story was translated from Univadis Germany, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Since the COVID-19 pandemic, alcoholic hand sanitizers have become widely accessible nationwide. They can pose a problem, especially for emergency departments, when alcohol-dependent patients start drinking them. One example that demonstrates the challenge of diagnosing alcohol abuse is the medical history of a young man, as reported by Mahmoud El Hussein, MD, and colleagues from Hôpital Lariboisière in Paris, France.

Presentation and History

A 26-year-old man presented with severe abdominal pain at the emergency department. Upon arrival, he was hemodynamically stable but nervous and verbally aggressive at times. The patient reported no relevant preexisting conditions and was not taking any medications.

Findings

Upon initial physical examination, the patient had a soft, diffusely tender abdomen; tachycardia; and notably poor hygiene. The patient was afebrile. An ECG confirmed the tachycardia but showed no signs of ischemia. Blood work, except for slightly elevated liver values, did not reveal any abnormalities, particularly ruling out bleeding or kidney disease.

A urease rapid test to rule out kidney stones also showed no pathologic findings. In consultation with the surgical department, a CT scan of the abdomen was performed to rule out organ perforation, volvulus, or mesenteric ischemia. Only signs of fatty liver were found.
 

A Neighbor’s Tip

During all examinations, the patient’s abdomen was repeatedly palpated to promptly detect signs of an acute abdomen. However, there was never any defense tension at any point.

Intravenous analgesics and proton pump inhibitors (ie, paracetamol, phloroglucin, and pantoprazole) did not relieve the patient’s symptoms. Morphine was administered intravenously for sedation.

Only after a frustrating diagnostic process did a neighbor of the patient inform a nurse that he suspected the patient of stealing and consuming hand sanitizer. With the patient’s consent, a blood alcohol test was performed, revealing a blood alcohol concentration of 0.2% (2 g/L). A urine test, also conducted with the patient’s consent, tested positive for tetrahydrocannabinol. Additional tests showed the following results:

• Venous pH: 7.29 (normal, 7.32-7.38)
• Anion gap (mEq/L): 14 (normal, 3-9)
• Ketone bodies (mmol/L): 0.2 (normal, < 0.6)
• Calculated serum osmolality (mOsm/kg): 292 (normal, 285-295)
• Measured serum osmolality (mOsm/kg): 320 (normal, 285-295)
• Osmolality gap (mOsm/kg): 2 (normal, < 10)

The patient was informed of the test results and confessed to feigning abdominal pain. He was dependent on alcohol and experiencing withdrawal symptoms. The patient had stolen seven 475-mL bottles of hand sanitizer and consumed one and a half in the past 4-6 hours. According to the authors, the sanitizer consisted of 80% ethanol, 1.45% glycerol, and 0.13% hydrogen peroxide.
 

Discussion

In Germany, alcohol consumption results in approximately €57 billion in direct economic costs annually, according to data from the Federal Ministry of Health. In 2021, about 7.9 million people aged 18-64 years consumed alcohol in a risky manner (approximately 9.6% of the German population). About 9 million people (approximately 11%) were classified as alcoholics.

The authors of the case report pointed out that those in the advanced stages of alcohol addiction often consume any alcoholic liquid they can access. This includes alcoholic hand sanitizers commonly used in hospitals. Therefore, staff in emergency departments, where potential abusers encounter a wide range of potential abuse items, should exercise caution.

Although hand sanitizers are mainly composed of ethanol, they may also contain isopropanol, methanol, or acetone. Methanol poisoning can cause abdominal pain, visual disturbances, central nervous system damage, and death. Other alcohols such as ethylene glycol, commonly found in antifreeze, can distort blood values (lactate) and complicate a correct diagnosis.

Physicians working in emergency departments should proceed with caution when suspecting alcohol abuse. Questioning the patient’s environment and determining additional laboratory parameters (such as osmolality gap in the case report) can help unmask substance abuse if it is in doubt.

This story was translated from Univadis Germany, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In the case of a hip fracture, operating on a patient with dementia can be a difficult decision to make. Indeed, surgery exposes patients with dementia to a higher mortality rate, more delirium and postoperative complications, and a greater loss of mobility than patients of the same age without cognitive impairments. For patients with dementia in institutional settings, survival is better for those who undergo surgery than for those who do not. But what about the prognosis of surgery vs no surgery for patients with dementia who live at home?

To answer this question, researchers in the United States conducted a cohort study using Medicare data. This retrospective study included patients aged 66 years and older with dementia who were living at home and not placed in institutions and who had a hip fracture between January 2017 and June 2018. Patients with incomplete observations, particularly regarding the location and type of residence (home/institution), were excluded from the analysis. Fractures were categorized as (i) fractures of the head and neck, (ii) pertrochanteric, (iii) subtrochanteric, and (iv) multiple/complex. The type and severity (mild, moderate, or severe) of dementia were identified using the diagnostic code list in the International Statistical Classification of Diseases, Tenth Revision.
 

Examining Mortality

The primary outcome was mortality at 30, 90, and 180 days. Secondary outcomes included hospital delirium; the need for subsequent hospitalization (within 6 months) or home health services (within 10 days); and intensive care interventions such as dialysis, intubation, resuscitation maneuvers, mechanical ventilation, or the insertion of a feeding tube.

Postoperative medical facility admissions were distinguished according to whether there was a plan to return home. To compare the surgery and nonsurgery groups, an inverse propensity score analysis was conducted within subgroups determined by fracture type, comorbidities (using the Elixhauser score), the person or entity responsible for admission (ie, physician, clinic, hospital, etc.), dual eligibility (Medicare and Medicaid), place of residence (ie, urban or rural), race, and sex. Dementia severity was estimated using a frailty index on the basis of evaluation tests that were systematically collected in the Medicare database.
 

Results Favored Surgery

Among 56,209 patients with dementia who were admitted for a hip fracture (73.0% women; mean age, 86.4 ± 7.0 years), 33,142 (59.0%) underwent surgery and 23,067 (41.0%) did not. Among surgically treated patients, 73.3% had fractures of the head or neck of the femur, and 40.2% had moderate to severe dementia. The nonsurgically treated fractures were 78.5% pertrochanteric. Comorbidities were evenly distributed between the two groups.

At 180 days, mortality was 31.8% in the surgery group compared with 45.7% in the nonsurgery group, resulting in a significant reduction in the unadjusted relative risk (RR) for death in favor of surgery (RR, 0.67; 95% CI, 0.60-0.76; P < .001). Among patients with mild dementia and a fracture of the head or neck of the femur, mortality at 180 days was 26.5% among surgical patients and 34.9% among nonsurgical patients (RR, 0.67; 95% CI, 0.60-0.76; P < .001). After the investigators adjusted for risk according to propensity score, the benefit of surgery remained significant at 30, 90, and 180 days, regardless of dementia severity. There was no significant difference in mortality for other types of hip fractures between the surgery and nonsurgery groups, however.

The adjusted RR for in-hospital delirium was 1.23 (P = .008), which was significant for the surgery group, but only for those with moderate to severe dementia. There were also fewer permanent placements (P < .001) among the surgically treated patients, and fewer patients with mild dementia required nurse care at home. There was no difference in resuscitation maneuvers between surgery and nonsurgery patients, whether the dementia was mild or not. For patients with a fracture of the head or neck of the femur, there was no difference in the likelihood of rehabilitation admission within 180 days, whether they were operated on or not.
 

Ethical Considerations

This study can inform discussions among healthcare professionals, patients, and patients’ families about which goals to set and which strategy to choose. The main interest of this study lies in its comparison of outcomes between patients with dementia who were operated on and those who were not, rather than comparing patients with and without dementia. Among patients with dementia living at home with a fracture of the head or neck of the femur, those who underwent surgery had a lower risk for death than those who did not, regardless of the severity of dementia.

It is noteworthy that less than two thirds of patients with dementia underwent surgery, which contradicts recommendations for almost routine surgery for patients with dementia. This observation raises questions about respecting patient wishes and advance directives when known, possible detrimental delays in referrals, and legal-medical issues.

Furthermore, the treatment choices of American surgeons are clearly influenced by the type of hip fracture. Fractures of the head and neck of the femur are typically treated with prosthetic arthroplasty, which simplifies postoperative care, compared with osteosynthesis. The latter procedure is more often used for extra-articular hip fractures but entails higher risks. While survival is an apparently more easily achievable goal through surgery, ethical considerations about other treatment objectives such as pain control, functional recovery, and treatment adequacy cannot be overlooked. It is worth noting that the French National Authority for Health issued recommendations in 2018 regarding the care pathway for patients hospitalized for a hip fracture within an orthogeriatric organization.

This story was translated from JIM, which is part of the Medscape Medical News professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In the case of a hip fracture, operating on a patient with dementia can be a difficult decision to make. Indeed, surgery exposes patients with dementia to a higher mortality rate, more delirium and postoperative complications, and a greater loss of mobility than patients of the same age without cognitive impairments. For patients with dementia in institutional settings, survival is better for those who undergo surgery than for those who do not. But what about the prognosis of surgery vs no surgery for patients with dementia who live at home?

To answer this question, researchers in the United States conducted a cohort study using Medicare data. This retrospective study included patients aged 66 years and older with dementia who were living at home and not placed in institutions and who had a hip fracture between January 2017 and June 2018. Patients with incomplete observations, particularly regarding the location and type of residence (home/institution), were excluded from the analysis. Fractures were categorized as (i) fractures of the head and neck, (ii) pertrochanteric, (iii) subtrochanteric, and (iv) multiple/complex. The type and severity (mild, moderate, or severe) of dementia were identified using the diagnostic code list in the International Statistical Classification of Diseases, Tenth Revision.
 

Examining Mortality

The primary outcome was mortality at 30, 90, and 180 days. Secondary outcomes included hospital delirium; the need for subsequent hospitalization (within 6 months) or home health services (within 10 days); and intensive care interventions such as dialysis, intubation, resuscitation maneuvers, mechanical ventilation, or the insertion of a feeding tube.

Postoperative medical facility admissions were distinguished according to whether there was a plan to return home. To compare the surgery and nonsurgery groups, an inverse propensity score analysis was conducted within subgroups determined by fracture type, comorbidities (using the Elixhauser score), the person or entity responsible for admission (ie, physician, clinic, hospital, etc.), dual eligibility (Medicare and Medicaid), place of residence (ie, urban or rural), race, and sex. Dementia severity was estimated using a frailty index on the basis of evaluation tests that were systematically collected in the Medicare database.
 

Results Favored Surgery

Among 56,209 patients with dementia who were admitted for a hip fracture (73.0% women; mean age, 86.4 ± 7.0 years), 33,142 (59.0%) underwent surgery and 23,067 (41.0%) did not. Among surgically treated patients, 73.3% had fractures of the head or neck of the femur, and 40.2% had moderate to severe dementia. The nonsurgically treated fractures were 78.5% pertrochanteric. Comorbidities were evenly distributed between the two groups.

At 180 days, mortality was 31.8% in the surgery group compared with 45.7% in the nonsurgery group, resulting in a significant reduction in the unadjusted relative risk (RR) for death in favor of surgery (RR, 0.67; 95% CI, 0.60-0.76; P < .001). Among patients with mild dementia and a fracture of the head or neck of the femur, mortality at 180 days was 26.5% among surgical patients and 34.9% among nonsurgical patients (RR, 0.67; 95% CI, 0.60-0.76; P < .001). After the investigators adjusted for risk according to propensity score, the benefit of surgery remained significant at 30, 90, and 180 days, regardless of dementia severity. There was no significant difference in mortality for other types of hip fractures between the surgery and nonsurgery groups, however.

The adjusted RR for in-hospital delirium was 1.23 (P = .008), which was significant for the surgery group, but only for those with moderate to severe dementia. There were also fewer permanent placements (P < .001) among the surgically treated patients, and fewer patients with mild dementia required nurse care at home. There was no difference in resuscitation maneuvers between surgery and nonsurgery patients, whether the dementia was mild or not. For patients with a fracture of the head or neck of the femur, there was no difference in the likelihood of rehabilitation admission within 180 days, whether they were operated on or not.
 

Ethical Considerations

This study can inform discussions among healthcare professionals, patients, and patients’ families about which goals to set and which strategy to choose. The main interest of this study lies in its comparison of outcomes between patients with dementia who were operated on and those who were not, rather than comparing patients with and without dementia. Among patients with dementia living at home with a fracture of the head or neck of the femur, those who underwent surgery had a lower risk for death than those who did not, regardless of the severity of dementia.

It is noteworthy that less than two thirds of patients with dementia underwent surgery, which contradicts recommendations for almost routine surgery for patients with dementia. This observation raises questions about respecting patient wishes and advance directives when known, possible detrimental delays in referrals, and legal-medical issues.

Furthermore, the treatment choices of American surgeons are clearly influenced by the type of hip fracture. Fractures of the head and neck of the femur are typically treated with prosthetic arthroplasty, which simplifies postoperative care, compared with osteosynthesis. The latter procedure is more often used for extra-articular hip fractures but entails higher risks. While survival is an apparently more easily achievable goal through surgery, ethical considerations about other treatment objectives such as pain control, functional recovery, and treatment adequacy cannot be overlooked. It is worth noting that the French National Authority for Health issued recommendations in 2018 regarding the care pathway for patients hospitalized for a hip fracture within an orthogeriatric organization.

This story was translated from JIM, which is part of the Medscape Medical News professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In the case of a hip fracture, operating on a patient with dementia can be a difficult decision to make. Indeed, surgery exposes patients with dementia to a higher mortality rate, more delirium and postoperative complications, and a greater loss of mobility than patients of the same age without cognitive impairments. For patients with dementia in institutional settings, survival is better for those who undergo surgery than for those who do not. But what about the prognosis of surgery vs no surgery for patients with dementia who live at home?

To answer this question, researchers in the United States conducted a cohort study using Medicare data. This retrospective study included patients aged 66 years and older with dementia who were living at home and not placed in institutions and who had a hip fracture between January 2017 and June 2018. Patients with incomplete observations, particularly regarding the location and type of residence (home/institution), were excluded from the analysis. Fractures were categorized as (i) fractures of the head and neck, (ii) pertrochanteric, (iii) subtrochanteric, and (iv) multiple/complex. The type and severity (mild, moderate, or severe) of dementia were identified using the diagnostic code list in the International Statistical Classification of Diseases, Tenth Revision.
 

Examining Mortality

The primary outcome was mortality at 30, 90, and 180 days. Secondary outcomes included hospital delirium; the need for subsequent hospitalization (within 6 months) or home health services (within 10 days); and intensive care interventions such as dialysis, intubation, resuscitation maneuvers, mechanical ventilation, or the insertion of a feeding tube.

Postoperative medical facility admissions were distinguished according to whether there was a plan to return home. To compare the surgery and nonsurgery groups, an inverse propensity score analysis was conducted within subgroups determined by fracture type, comorbidities (using the Elixhauser score), the person or entity responsible for admission (ie, physician, clinic, hospital, etc.), dual eligibility (Medicare and Medicaid), place of residence (ie, urban or rural), race, and sex. Dementia severity was estimated using a frailty index on the basis of evaluation tests that were systematically collected in the Medicare database.
 

Results Favored Surgery

Among 56,209 patients with dementia who were admitted for a hip fracture (73.0% women; mean age, 86.4 ± 7.0 years), 33,142 (59.0%) underwent surgery and 23,067 (41.0%) did not. Among surgically treated patients, 73.3% had fractures of the head or neck of the femur, and 40.2% had moderate to severe dementia. The nonsurgically treated fractures were 78.5% pertrochanteric. Comorbidities were evenly distributed between the two groups.

At 180 days, mortality was 31.8% in the surgery group compared with 45.7% in the nonsurgery group, resulting in a significant reduction in the unadjusted relative risk (RR) for death in favor of surgery (RR, 0.67; 95% CI, 0.60-0.76; P < .001). Among patients with mild dementia and a fracture of the head or neck of the femur, mortality at 180 days was 26.5% among surgical patients and 34.9% among nonsurgical patients (RR, 0.67; 95% CI, 0.60-0.76; P < .001). After the investigators adjusted for risk according to propensity score, the benefit of surgery remained significant at 30, 90, and 180 days, regardless of dementia severity. There was no significant difference in mortality for other types of hip fractures between the surgery and nonsurgery groups, however.

The adjusted RR for in-hospital delirium was 1.23 (P = .008), which was significant for the surgery group, but only for those with moderate to severe dementia. There were also fewer permanent placements (P < .001) among the surgically treated patients, and fewer patients with mild dementia required nurse care at home. There was no difference in resuscitation maneuvers between surgery and nonsurgery patients, whether the dementia was mild or not. For patients with a fracture of the head or neck of the femur, there was no difference in the likelihood of rehabilitation admission within 180 days, whether they were operated on or not.
 

Ethical Considerations

This study can inform discussions among healthcare professionals, patients, and patients’ families about which goals to set and which strategy to choose. The main interest of this study lies in its comparison of outcomes between patients with dementia who were operated on and those who were not, rather than comparing patients with and without dementia. Among patients with dementia living at home with a fracture of the head or neck of the femur, those who underwent surgery had a lower risk for death than those who did not, regardless of the severity of dementia.

It is noteworthy that less than two thirds of patients with dementia underwent surgery, which contradicts recommendations for almost routine surgery for patients with dementia. This observation raises questions about respecting patient wishes and advance directives when known, possible detrimental delays in referrals, and legal-medical issues.

Furthermore, the treatment choices of American surgeons are clearly influenced by the type of hip fracture. Fractures of the head and neck of the femur are typically treated with prosthetic arthroplasty, which simplifies postoperative care, compared with osteosynthesis. The latter procedure is more often used for extra-articular hip fractures but entails higher risks. While survival is an apparently more easily achievable goal through surgery, ethical considerations about other treatment objectives such as pain control, functional recovery, and treatment adequacy cannot be overlooked. It is worth noting that the French National Authority for Health issued recommendations in 2018 regarding the care pathway for patients hospitalized for a hip fracture within an orthogeriatric organization.

This story was translated from JIM, which is part of the Medscape Medical News professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In 2019, 57 million people worldwide were living with dementia, a figure expected to soar to 153 million by 2050. A recent Lancet Commission report suggests that nearly half of dementia cases could be prevented or delayed by addressing 14 modifiable risk factors, including impaired vision. 

The report’s authors recommend that vision-loss screening and treatment be universally available. But are these recommendations warranted? What is the evidence? What is the potential mechanism? And what are the potential implications for clinical practice? 

Worldwide, the prevalence of avoidable vision loss and blindness in adults aged 50 years or older is estimated to hover around 13%.

“There is now overwhelming evidence that vision impairment in later life is associated with more rapid cognitive decline and an increased risk of dementia,” said Joshua Ehrlich, MD, MPH, associate professor in ophthalmology and visual sciences, the Institute for Social Research at the University of Michigan, Ann Arbor. 

The evidence includes a meta-analysis of 14 prospective cohort studies with roughly 6.2 million older adults who were cognitively intact at baseline. Over the course of up to 14 years, 171,888 developed dementia. Vision loss was associated with a pooled relative risk (RR) for dementia of 1.47. 

A separate meta-analysis also identified an increased risk for dementia (RR, 1.38) with visual loss. When broken down into different eye conditions, an increased dementia risk was associated with cataracts and diabetic retinopathy but not with glaucoma or age-related macular degeneration.

A US study that followed roughly 3000 older adults with cataracts and normal cognition at baseline for more than 20 years found that those who had cataract extraction had significantly reduced risk for dementia compared with those who did not have cataract extraction (hazard ratio, 0.71), after controlling for age, race, APOE genotype, education, smoking, and an extensive list of comorbidities. 
 

Causation or Coincidence?

The mechanisms behind these associations might be related to underlying illness, such as diabetes, which is a risk factor for dementia; vision loss itself, as might be suggested by a possible effect of cataract surgery; or shared neuropathologic processes in the retina and the brain. 

A longitudinal study from Korea that included roughly 6 million adults showed that dementia risk increased with severity of visual loss, which supports the hypothesis that vision loss in itself might be causal or that there is a dose-response effect to a shared causal factor. 

“Work is still needed to sort out” exactly how visual deficits may raise dementia risk, although several hypotheses exist, Dr. Ehrlich said. 

For example, “decreased input to the brain via the visual pathways may directly induce brain changes. Also, consequences of vision loss, like social isolation, physical inactivity, and depression, are themselves risk factors for dementia and may explain the pathways through which vision impairment increases risk,” he said. 

Is the link causal? “We’ll never know definitively because we can’t randomize people to not get cataract surgery versus getting cataract surgery, because we know that improving vision improves quality of life, so we’d never want to do that. But the new evidence that’s come in over the last 5 years or so is pretty promising,” said Esme Fuller-Thomson, PhD, director of the Institute for Life Course and Aging and professor, Department of Family and Community Medicine and Faculty of Nursing, at the University of Toronto, Ontario, Canada.

She noted that results of two studies that have looked at this “seem to indicate that those who have cataract surgery are not nearly at as high risk of dementia as those who have cataracts but don’t have the surgery. That’s leaning towards causality.”

A study published in July suggests that cataracts increase dementia risk through vascular and non–Alzheimer’s disease mechanisms. 
 

Clear Clinical Implications 

Dr. Ehrlich said that evidence for an association between untreated vision loss and dementia risk and potential modification by treatment has clear implications for care. 

“Loss of vision impacts so many aspects of people’s lives beyond just how they see the world and losing vision in later life is not a normal part of aging. Thus, when older adults experience vision loss, this should be a cause for concern and prompt an immediate referral to an eye care professional,” he noted. 

Dr. Fuller-Thomson agrees. “Addressing vision loss will certainly help people see better and function at a higher level and improve quality of life, and it seems probable that it might decrease dementia risk so it’s a win-win,” she said.

In her own research, Dr. Fuller-Thomson has found that the combination of hearing loss and vision loss is linked to an eightfold increased risk for cognitive impairment.

“The idea is that vision and/or hearing loss makes it harder for you to be physically active, to be socially engaged, to be mentally stimulated. They are equally important in terms of social isolation, which could lead to loneliness, and we know that loneliness is not good for dementia,” she said.

“With dual sensory impairment, you don’t have as much information coming in — your brain is not engaged as much — and having an engaged brain, doing hobbies, having intellectually stimulating conversation, all of those are factors are associated with lowering risk of dementia,” Dr. Fuller-Thomson said.

The latest Lancet Commission report noted that treatment for visual loss is “effective and cost-effective” for an estimated 90% of people. However, across the world, particularly in low- and middle-income countries, visual loss often goes untreated. 

“A clear opportunity for dementia prevention exists with treatment of visual loss,” the report concluded.

Dr. Ehrlich and Dr. Fuller-Thomson have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

In 2019, 57 million people worldwide were living with dementia, a figure expected to soar to 153 million by 2050. A recent Lancet Commission report suggests that nearly half of dementia cases could be prevented or delayed by addressing 14 modifiable risk factors, including impaired vision. 

The report’s authors recommend that vision-loss screening and treatment be universally available. But are these recommendations warranted? What is the evidence? What is the potential mechanism? And what are the potential implications for clinical practice? 

Worldwide, the prevalence of avoidable vision loss and blindness in adults aged 50 years or older is estimated to hover around 13%.

“There is now overwhelming evidence that vision impairment in later life is associated with more rapid cognitive decline and an increased risk of dementia,” said Joshua Ehrlich, MD, MPH, associate professor in ophthalmology and visual sciences, the Institute for Social Research at the University of Michigan, Ann Arbor. 

The evidence includes a meta-analysis of 14 prospective cohort studies with roughly 6.2 million older adults who were cognitively intact at baseline. Over the course of up to 14 years, 171,888 developed dementia. Vision loss was associated with a pooled relative risk (RR) for dementia of 1.47. 

A separate meta-analysis also identified an increased risk for dementia (RR, 1.38) with visual loss. When broken down into different eye conditions, an increased dementia risk was associated with cataracts and diabetic retinopathy but not with glaucoma or age-related macular degeneration.

A US study that followed roughly 3000 older adults with cataracts and normal cognition at baseline for more than 20 years found that those who had cataract extraction had significantly reduced risk for dementia compared with those who did not have cataract extraction (hazard ratio, 0.71), after controlling for age, race, APOE genotype, education, smoking, and an extensive list of comorbidities. 
 

Causation or Coincidence?

The mechanisms behind these associations might be related to underlying illness, such as diabetes, which is a risk factor for dementia; vision loss itself, as might be suggested by a possible effect of cataract surgery; or shared neuropathologic processes in the retina and the brain. 

A longitudinal study from Korea that included roughly 6 million adults showed that dementia risk increased with severity of visual loss, which supports the hypothesis that vision loss in itself might be causal or that there is a dose-response effect to a shared causal factor. 

“Work is still needed to sort out” exactly how visual deficits may raise dementia risk, although several hypotheses exist, Dr. Ehrlich said. 

For example, “decreased input to the brain via the visual pathways may directly induce brain changes. Also, consequences of vision loss, like social isolation, physical inactivity, and depression, are themselves risk factors for dementia and may explain the pathways through which vision impairment increases risk,” he said. 

Is the link causal? “We’ll never know definitively because we can’t randomize people to not get cataract surgery versus getting cataract surgery, because we know that improving vision improves quality of life, so we’d never want to do that. But the new evidence that’s come in over the last 5 years or so is pretty promising,” said Esme Fuller-Thomson, PhD, director of the Institute for Life Course and Aging and professor, Department of Family and Community Medicine and Faculty of Nursing, at the University of Toronto, Ontario, Canada.

She noted that results of two studies that have looked at this “seem to indicate that those who have cataract surgery are not nearly at as high risk of dementia as those who have cataracts but don’t have the surgery. That’s leaning towards causality.”

A study published in July suggests that cataracts increase dementia risk through vascular and non–Alzheimer’s disease mechanisms. 
 

Clear Clinical Implications 

Dr. Ehrlich said that evidence for an association between untreated vision loss and dementia risk and potential modification by treatment has clear implications for care. 

“Loss of vision impacts so many aspects of people’s lives beyond just how they see the world and losing vision in later life is not a normal part of aging. Thus, when older adults experience vision loss, this should be a cause for concern and prompt an immediate referral to an eye care professional,” he noted. 

Dr. Fuller-Thomson agrees. “Addressing vision loss will certainly help people see better and function at a higher level and improve quality of life, and it seems probable that it might decrease dementia risk so it’s a win-win,” she said.

In her own research, Dr. Fuller-Thomson has found that the combination of hearing loss and vision loss is linked to an eightfold increased risk for cognitive impairment.

“The idea is that vision and/or hearing loss makes it harder for you to be physically active, to be socially engaged, to be mentally stimulated. They are equally important in terms of social isolation, which could lead to loneliness, and we know that loneliness is not good for dementia,” she said.

“With dual sensory impairment, you don’t have as much information coming in — your brain is not engaged as much — and having an engaged brain, doing hobbies, having intellectually stimulating conversation, all of those are factors are associated with lowering risk of dementia,” Dr. Fuller-Thomson said.

The latest Lancet Commission report noted that treatment for visual loss is “effective and cost-effective” for an estimated 90% of people. However, across the world, particularly in low- and middle-income countries, visual loss often goes untreated. 

“A clear opportunity for dementia prevention exists with treatment of visual loss,” the report concluded.

Dr. Ehrlich and Dr. Fuller-Thomson have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

In 2019, 57 million people worldwide were living with dementia, a figure expected to soar to 153 million by 2050. A recent Lancet Commission report suggests that nearly half of dementia cases could be prevented or delayed by addressing 14 modifiable risk factors, including impaired vision. 

The report’s authors recommend that vision-loss screening and treatment be universally available. But are these recommendations warranted? What is the evidence? What is the potential mechanism? And what are the potential implications for clinical practice? 

Worldwide, the prevalence of avoidable vision loss and blindness in adults aged 50 years or older is estimated to hover around 13%.

“There is now overwhelming evidence that vision impairment in later life is associated with more rapid cognitive decline and an increased risk of dementia,” said Joshua Ehrlich, MD, MPH, associate professor in ophthalmology and visual sciences, the Institute for Social Research at the University of Michigan, Ann Arbor. 

The evidence includes a meta-analysis of 14 prospective cohort studies with roughly 6.2 million older adults who were cognitively intact at baseline. Over the course of up to 14 years, 171,888 developed dementia. Vision loss was associated with a pooled relative risk (RR) for dementia of 1.47. 

A separate meta-analysis also identified an increased risk for dementia (RR, 1.38) with visual loss. When broken down into different eye conditions, an increased dementia risk was associated with cataracts and diabetic retinopathy but not with glaucoma or age-related macular degeneration.

A US study that followed roughly 3000 older adults with cataracts and normal cognition at baseline for more than 20 years found that those who had cataract extraction had significantly reduced risk for dementia compared with those who did not have cataract extraction (hazard ratio, 0.71), after controlling for age, race, APOE genotype, education, smoking, and an extensive list of comorbidities. 
 

Causation or Coincidence?

The mechanisms behind these associations might be related to underlying illness, such as diabetes, which is a risk factor for dementia; vision loss itself, as might be suggested by a possible effect of cataract surgery; or shared neuropathologic processes in the retina and the brain. 

A longitudinal study from Korea that included roughly 6 million adults showed that dementia risk increased with severity of visual loss, which supports the hypothesis that vision loss in itself might be causal or that there is a dose-response effect to a shared causal factor. 

“Work is still needed to sort out” exactly how visual deficits may raise dementia risk, although several hypotheses exist, Dr. Ehrlich said. 

For example, “decreased input to the brain via the visual pathways may directly induce brain changes. Also, consequences of vision loss, like social isolation, physical inactivity, and depression, are themselves risk factors for dementia and may explain the pathways through which vision impairment increases risk,” he said. 

Is the link causal? “We’ll never know definitively because we can’t randomize people to not get cataract surgery versus getting cataract surgery, because we know that improving vision improves quality of life, so we’d never want to do that. But the new evidence that’s come in over the last 5 years or so is pretty promising,” said Esme Fuller-Thomson, PhD, director of the Institute for Life Course and Aging and professor, Department of Family and Community Medicine and Faculty of Nursing, at the University of Toronto, Ontario, Canada.

She noted that results of two studies that have looked at this “seem to indicate that those who have cataract surgery are not nearly at as high risk of dementia as those who have cataracts but don’t have the surgery. That’s leaning towards causality.”

A study published in July suggests that cataracts increase dementia risk through vascular and non–Alzheimer’s disease mechanisms. 
 

Clear Clinical Implications 

Dr. Ehrlich said that evidence for an association between untreated vision loss and dementia risk and potential modification by treatment has clear implications for care. 

“Loss of vision impacts so many aspects of people’s lives beyond just how they see the world and losing vision in later life is not a normal part of aging. Thus, when older adults experience vision loss, this should be a cause for concern and prompt an immediate referral to an eye care professional,” he noted. 

Dr. Fuller-Thomson agrees. “Addressing vision loss will certainly help people see better and function at a higher level and improve quality of life, and it seems probable that it might decrease dementia risk so it’s a win-win,” she said.

In her own research, Dr. Fuller-Thomson has found that the combination of hearing loss and vision loss is linked to an eightfold increased risk for cognitive impairment.

“The idea is that vision and/or hearing loss makes it harder for you to be physically active, to be socially engaged, to be mentally stimulated. They are equally important in terms of social isolation, which could lead to loneliness, and we know that loneliness is not good for dementia,” she said.

“With dual sensory impairment, you don’t have as much information coming in — your brain is not engaged as much — and having an engaged brain, doing hobbies, having intellectually stimulating conversation, all of those are factors are associated with lowering risk of dementia,” Dr. Fuller-Thomson said.

The latest Lancet Commission report noted that treatment for visual loss is “effective and cost-effective” for an estimated 90% of people. However, across the world, particularly in low- and middle-income countries, visual loss often goes untreated. 

“A clear opportunity for dementia prevention exists with treatment of visual loss,” the report concluded.

Dr. Ehrlich and Dr. Fuller-Thomson have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

When Andrea Austin, MD, an emergency medicine specialist, left the military in 2020, she knew the adjustment to civilian life and practice might be difficult. To help smooth the transition, she reached out to a physician mentor who also had a professional coaching certificate. After a conversation, Dr. Austin signed up for 6 months of career coaching. 

It was time well spent, according to Dr. Austin, who today is a coach herself. “It was really the first time I had the ability to choose what I wanted to do, and that required a mindset shift,” she explains. “A big part of coaching is helping physicians discover their agency so that they can make the best career choices.” 

courtesy Dr. Andrea Austin

Physicians have long lacked the coaching resources typically made available to corporate executives. But that’s changing. In today’s high-pressure environment, where doctors are burning out at a rapid pace, coaching can sometimes be an avenue to staying in the field, especially if that coach is a fellow physician who understands what you’re facing. 

With a physician shortage that the Association of American Medical Colleges expects to hit 86,000 in the next decade or so, coaching could be a stone worth turning over. A 2024 report in JAMA Network Open found that coaching provided by physician peers led to a significant reduction in interpersonal disengagement and burnout. 

“What I think is exciting about coaching is that it allows you to better understand yourself and know your strengths and weaknesses,” said Dr. Austin. “It might seem simple, but many ‘soft skills’ aren’t considered mainstream in medicine. Coaching allows us to understand them and ourselves better.” 
 

Why Are Doctors Using Coaches?

Although it’s hard to put a number on how many physicians are turning to coaches, the number of coaches available for doctors is growing rapidly. The American Medical Women’s Association maintains a database of physician coaches. According to deputy director Jodi Godfrey, MS, RDN, the number of members who have added coaching to their skill set has tripled in the past 4 years. “Many cite burnout as the reason they sought coaching support, and then they decided to go on to get certified in coaching.”

courtesy Michael Hanlon

The pandemic is one reason physician coaching has grown, said Elizabeth Esparaz, MD, an ophthalmologist and physician coach. “Since the pandemic, the word ‘burnout’ is thrown around a good deal.” And the causes are clear. “Doctors are facing longer hours, they must make split-second decisions, they’re multitasking, and they have less support staff.”

Among her coaching clients, Dr. Austin has noticed other common struggles: fears of litigation, time scarcity with patients, declining reimbursement that hasn’t kept up with inflation, and loss of autonomy because of the corporatization of healthcare. 

Coaching, Dr. Esparaz believes, can be an antidote to many of these issues. “Coaches help doctors see their strengths and find better ways of applying them,” she said. “We help them move forward, and also see their blind spots.”
 

Clarity, Goals, and Making the Right Choices

Physician coaching comes in a variety of flavors — some one on one, and others in the form of group sessions. All, however, serve the purpose of helping physicians gain career clarity. “Sometimes clients realize their job may not be working for them, but that there are things they can do to change that without having to leave the field,” said Jattu Senesie, MD, a former ob.gyn. who is now a physician coach. 

Dr. Esparaz works with doctors to establish SMART goals: specific, measurable, attainable, realistic, and time based. She gave the example of learning how to set boundaries. “If a physician is asked to create a presentation for work, I encourage them to ask for compensation or administrative time before committing to unpaid tasks.”

Another big issue: charting. It’s increasingly burdensome, and many doctors find it encroaching on their home lives. “If we can identify a problem like that, we can come up with a strategy for mitigating it,” Dr. Esparaz said. This might include setting a goal of getting 80% of charting completed immediately after the patient encounter on the busiest clinic day of the week. The client tests the experiment and then revisits it with the coach to discuss what worked and what didn’t, refining the process until it has freed up the physician’s home life. 

courtesy Dr. Jattu Senesie

The younger generation of doctors often struggles with career choices, too, because it’s the first time they are without structure, said Dr. Senesie. There’s med school and residency, which puts a framework around every move a doctor makes. But once they become attending physicians, the choices are endless. “Coaching can help them find a new structure and systems that will allow them to thrive.”

Although mentoring has been a well-embraced concept for decades, it “hits a wall,” at some point in terms of what it can offer, Dr. Austin said. That’s where coaching can take over. “There’s a point where a mentor cannot help someone self-actualize. As a coach, you don’t need to know everything about a doctor’s life, but you can help them learn to ask themselves the right questions to solve problems.”
 

Should You Stay or Should You Go?

Dr. Austin’s approach begins with the premise that healthcare today is challenging and dysfunctional — but doctors still have agency. She has worked with clients on the verge of leaving the field and helped them find their way back. 

“They have a light bulb moment and open up to the idea that they have much to give still,” she said. “We take an inventory to help them better communicate their needs and make changes, and I help them connect to their values. Sometimes that exercise allows them to reframe their current work environment.” 

Not every doctor who goes through coaching remains in the field. But “that’s the exception, not the rule,” Dr. Austin said. And that’s okay. “If that’s the outcome, coaching probably helped them get to that point faster, and with an informed decision.” 

Dr. Senesie has been coaching for about a decade, and in that time, she’s seen a shift that goes beyond figuring out career goals. “Doctors are more aware of the need for well-being today. The pandemic made it impossible to ignore what doesn’t work for us. When I work with clients, we look for ways to make the job more tenable.” 

According to Dr. Senesie, younger doctors are looking for that balance at the outset. “They want to be physicians, but they also want a life,” she said. “It’s a challenge for them because in addition to that mindset, they’re also coming out with more debt than older generations. They want out from underneath that.”
 

When It’s Time to Find a Physician Coach

Wondering whether coaching is right for you? Consider these symptoms:

• You need help setting boundaries at work.
• You feel like you’re sacrificing your own well-being for your job.
• You’re using maladaptive strategies to cope with the stress at work.
• You’ve reached a point where you are considering leaving the field.

If you’re interested in finding a physician coach, there are several places to begin your search, word of mouth being one of them. “Conferences and social media can also expose you to coaches,” suggested Dr. Esparaz. There are different methods and approaches to coaching. So, as you research, “make sure the coach you choose has techniques and a framework that fit what you’re after.” 

Dr. Austin warned that it is an unregulated industry, so buyer beware. To ensure you’re getting an accredited physician coach, look for people who have obtained an International Coach Federation (ICF) accreditation. These coaches will hold an associate certified coach credential, which requires at least 60 hours of coaching-specific training approved by the ICF, in addition to other assessments and education. 

Ensure that the coach you choose is within your budget. “There are some people charging astronomical rates out there,” Dr. Austin said. “If you’re burned out or struggling, it can be easy to reach for your credit card.”

Dr. Austin also cautioned doctors seeking a coach to avoid promises that sound too good to be true. Some coaching can have a gaslighting quality to it, she warned, “suggesting it can allow you to endure any environment.” But positive self-talk alone won’t cure an abusive or discriminatory situation. “If a client describes a toxic work environment,” the coach has an “ethical imperative” to help that person protect themselves. 
 

A Side Gig or a New Career Path

After Dr. Austin’s experience with her coach, she made the choice to continue as an emergency physician part-time while starting her own coaching business. “It’s important for me personally to keep in touch with what’s happening on the ground, but I have no judgment for anyone who chooses to leave clinical practice to become a coach.”

When Dr. Senesie looks back on her own struggles as a clinician, she recognizes the state of burnout she was in 10 years ago. “I knew there was an issue, but I didn’t have the mindset to find a way to make it work,” she said. “I left the field when I was at my depths of burnout, which is generally not the best way to go about it.” 

Guidance might have allowed her to take into account other avenues and helped her remain in the field, said Dr. Senesie. She has since learned that “there are many ways to practice medicine, and the way we’ve gone about it traditionally has worked for some, but not necessarily for everyone.” 

There may be more possibilities than you think. By helping you assess your path and make meaningful changes, a physician coach might be the key to remaining in the field you love.

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

When Andrea Austin, MD, an emergency medicine specialist, left the military in 2020, she knew the adjustment to civilian life and practice might be difficult. To help smooth the transition, she reached out to a physician mentor who also had a professional coaching certificate. After a conversation, Dr. Austin signed up for 6 months of career coaching. 

It was time well spent, according to Dr. Austin, who today is a coach herself. “It was really the first time I had the ability to choose what I wanted to do, and that required a mindset shift,” she explains. “A big part of coaching is helping physicians discover their agency so that they can make the best career choices.” 

courtesy Dr. Andrea Austin

Physicians have long lacked the coaching resources typically made available to corporate executives. But that’s changing. In today’s high-pressure environment, where doctors are burning out at a rapid pace, coaching can sometimes be an avenue to staying in the field, especially if that coach is a fellow physician who understands what you’re facing. 

With a physician shortage that the Association of American Medical Colleges expects to hit 86,000 in the next decade or so, coaching could be a stone worth turning over. A 2024 report in JAMA Network Open found that coaching provided by physician peers led to a significant reduction in interpersonal disengagement and burnout. 

“What I think is exciting about coaching is that it allows you to better understand yourself and know your strengths and weaknesses,” said Dr. Austin. “It might seem simple, but many ‘soft skills’ aren’t considered mainstream in medicine. Coaching allows us to understand them and ourselves better.” 
 

Why Are Doctors Using Coaches?

Although it’s hard to put a number on how many physicians are turning to coaches, the number of coaches available for doctors is growing rapidly. The American Medical Women’s Association maintains a database of physician coaches. According to deputy director Jodi Godfrey, MS, RDN, the number of members who have added coaching to their skill set has tripled in the past 4 years. “Many cite burnout as the reason they sought coaching support, and then they decided to go on to get certified in coaching.”

courtesy Michael Hanlon

The pandemic is one reason physician coaching has grown, said Elizabeth Esparaz, MD, an ophthalmologist and physician coach. “Since the pandemic, the word ‘burnout’ is thrown around a good deal.” And the causes are clear. “Doctors are facing longer hours, they must make split-second decisions, they’re multitasking, and they have less support staff.”

Among her coaching clients, Dr. Austin has noticed other common struggles: fears of litigation, time scarcity with patients, declining reimbursement that hasn’t kept up with inflation, and loss of autonomy because of the corporatization of healthcare. 

Coaching, Dr. Esparaz believes, can be an antidote to many of these issues. “Coaches help doctors see their strengths and find better ways of applying them,” she said. “We help them move forward, and also see their blind spots.”
 

Clarity, Goals, and Making the Right Choices

Physician coaching comes in a variety of flavors — some one on one, and others in the form of group sessions. All, however, serve the purpose of helping physicians gain career clarity. “Sometimes clients realize their job may not be working for them, but that there are things they can do to change that without having to leave the field,” said Jattu Senesie, MD, a former ob.gyn. who is now a physician coach. 

Dr. Esparaz works with doctors to establish SMART goals: specific, measurable, attainable, realistic, and time based. She gave the example of learning how to set boundaries. “If a physician is asked to create a presentation for work, I encourage them to ask for compensation or administrative time before committing to unpaid tasks.”

Another big issue: charting. It’s increasingly burdensome, and many doctors find it encroaching on their home lives. “If we can identify a problem like that, we can come up with a strategy for mitigating it,” Dr. Esparaz said. This might include setting a goal of getting 80% of charting completed immediately after the patient encounter on the busiest clinic day of the week. The client tests the experiment and then revisits it with the coach to discuss what worked and what didn’t, refining the process until it has freed up the physician’s home life. 

courtesy Dr. Jattu Senesie

The younger generation of doctors often struggles with career choices, too, because it’s the first time they are without structure, said Dr. Senesie. There’s med school and residency, which puts a framework around every move a doctor makes. But once they become attending physicians, the choices are endless. “Coaching can help them find a new structure and systems that will allow them to thrive.”

Although mentoring has been a well-embraced concept for decades, it “hits a wall,” at some point in terms of what it can offer, Dr. Austin said. That’s where coaching can take over. “There’s a point where a mentor cannot help someone self-actualize. As a coach, you don’t need to know everything about a doctor’s life, but you can help them learn to ask themselves the right questions to solve problems.”
 

Should You Stay or Should You Go?

Dr. Austin’s approach begins with the premise that healthcare today is challenging and dysfunctional — but doctors still have agency. She has worked with clients on the verge of leaving the field and helped them find their way back. 

“They have a light bulb moment and open up to the idea that they have much to give still,” she said. “We take an inventory to help them better communicate their needs and make changes, and I help them connect to their values. Sometimes that exercise allows them to reframe their current work environment.” 

Not every doctor who goes through coaching remains in the field. But “that’s the exception, not the rule,” Dr. Austin said. And that’s okay. “If that’s the outcome, coaching probably helped them get to that point faster, and with an informed decision.” 

Dr. Senesie has been coaching for about a decade, and in that time, she’s seen a shift that goes beyond figuring out career goals. “Doctors are more aware of the need for well-being today. The pandemic made it impossible to ignore what doesn’t work for us. When I work with clients, we look for ways to make the job more tenable.” 

According to Dr. Senesie, younger doctors are looking for that balance at the outset. “They want to be physicians, but they also want a life,” she said. “It’s a challenge for them because in addition to that mindset, they’re also coming out with more debt than older generations. They want out from underneath that.”
 

When It’s Time to Find a Physician Coach

Wondering whether coaching is right for you? Consider these symptoms:

• You need help setting boundaries at work.
• You feel like you’re sacrificing your own well-being for your job.
• You’re using maladaptive strategies to cope with the stress at work.
• You’ve reached a point where you are considering leaving the field.

If you’re interested in finding a physician coach, there are several places to begin your search, word of mouth being one of them. “Conferences and social media can also expose you to coaches,” suggested Dr. Esparaz. There are different methods and approaches to coaching. So, as you research, “make sure the coach you choose has techniques and a framework that fit what you’re after.” 

Dr. Austin warned that it is an unregulated industry, so buyer beware. To ensure you’re getting an accredited physician coach, look for people who have obtained an International Coach Federation (ICF) accreditation. These coaches will hold an associate certified coach credential, which requires at least 60 hours of coaching-specific training approved by the ICF, in addition to other assessments and education. 

Ensure that the coach you choose is within your budget. “There are some people charging astronomical rates out there,” Dr. Austin said. “If you’re burned out or struggling, it can be easy to reach for your credit card.”

Dr. Austin also cautioned doctors seeking a coach to avoid promises that sound too good to be true. Some coaching can have a gaslighting quality to it, she warned, “suggesting it can allow you to endure any environment.” But positive self-talk alone won’t cure an abusive or discriminatory situation. “If a client describes a toxic work environment,” the coach has an “ethical imperative” to help that person protect themselves. 
 

A Side Gig or a New Career Path

After Dr. Austin’s experience with her coach, she made the choice to continue as an emergency physician part-time while starting her own coaching business. “It’s important for me personally to keep in touch with what’s happening on the ground, but I have no judgment for anyone who chooses to leave clinical practice to become a coach.”

When Dr. Senesie looks back on her own struggles as a clinician, she recognizes the state of burnout she was in 10 years ago. “I knew there was an issue, but I didn’t have the mindset to find a way to make it work,” she said. “I left the field when I was at my depths of burnout, which is generally not the best way to go about it.” 

Guidance might have allowed her to take into account other avenues and helped her remain in the field, said Dr. Senesie. She has since learned that “there are many ways to practice medicine, and the way we’ve gone about it traditionally has worked for some, but not necessarily for everyone.” 

There may be more possibilities than you think. By helping you assess your path and make meaningful changes, a physician coach might be the key to remaining in the field you love.

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

When Andrea Austin, MD, an emergency medicine specialist, left the military in 2020, she knew the adjustment to civilian life and practice might be difficult. To help smooth the transition, she reached out to a physician mentor who also had a professional coaching certificate. After a conversation, Dr. Austin signed up for 6 months of career coaching. 

It was time well spent, according to Dr. Austin, who today is a coach herself. “It was really the first time I had the ability to choose what I wanted to do, and that required a mindset shift,” she explains. “A big part of coaching is helping physicians discover their agency so that they can make the best career choices.” 

courtesy Dr. Andrea Austin

Physicians have long lacked the coaching resources typically made available to corporate executives. But that’s changing. In today’s high-pressure environment, where doctors are burning out at a rapid pace, coaching can sometimes be an avenue to staying in the field, especially if that coach is a fellow physician who understands what you’re facing. 

With a physician shortage that the Association of American Medical Colleges expects to hit 86,000 in the next decade or so, coaching could be a stone worth turning over. A 2024 report in JAMA Network Open found that coaching provided by physician peers led to a significant reduction in interpersonal disengagement and burnout. 

“What I think is exciting about coaching is that it allows you to better understand yourself and know your strengths and weaknesses,” said Dr. Austin. “It might seem simple, but many ‘soft skills’ aren’t considered mainstream in medicine. Coaching allows us to understand them and ourselves better.” 
 

Why Are Doctors Using Coaches?

Although it’s hard to put a number on how many physicians are turning to coaches, the number of coaches available for doctors is growing rapidly. The American Medical Women’s Association maintains a database of physician coaches. According to deputy director Jodi Godfrey, MS, RDN, the number of members who have added coaching to their skill set has tripled in the past 4 years. “Many cite burnout as the reason they sought coaching support, and then they decided to go on to get certified in coaching.”

courtesy Michael Hanlon

The pandemic is one reason physician coaching has grown, said Elizabeth Esparaz, MD, an ophthalmologist and physician coach. “Since the pandemic, the word ‘burnout’ is thrown around a good deal.” And the causes are clear. “Doctors are facing longer hours, they must make split-second decisions, they’re multitasking, and they have less support staff.”

Among her coaching clients, Dr. Austin has noticed other common struggles: fears of litigation, time scarcity with patients, declining reimbursement that hasn’t kept up with inflation, and loss of autonomy because of the corporatization of healthcare. 

Coaching, Dr. Esparaz believes, can be an antidote to many of these issues. “Coaches help doctors see their strengths and find better ways of applying them,” she said. “We help them move forward, and also see their blind spots.”
 

Clarity, Goals, and Making the Right Choices

Physician coaching comes in a variety of flavors — some one on one, and others in the form of group sessions. All, however, serve the purpose of helping physicians gain career clarity. “Sometimes clients realize their job may not be working for them, but that there are things they can do to change that without having to leave the field,” said Jattu Senesie, MD, a former ob.gyn. who is now a physician coach. 

Dr. Esparaz works with doctors to establish SMART goals: specific, measurable, attainable, realistic, and time based. She gave the example of learning how to set boundaries. “If a physician is asked to create a presentation for work, I encourage them to ask for compensation or administrative time before committing to unpaid tasks.”

Another big issue: charting. It’s increasingly burdensome, and many doctors find it encroaching on their home lives. “If we can identify a problem like that, we can come up with a strategy for mitigating it,” Dr. Esparaz said. This might include setting a goal of getting 80% of charting completed immediately after the patient encounter on the busiest clinic day of the week. The client tests the experiment and then revisits it with the coach to discuss what worked and what didn’t, refining the process until it has freed up the physician’s home life. 

courtesy Dr. Jattu Senesie

The younger generation of doctors often struggles with career choices, too, because it’s the first time they are without structure, said Dr. Senesie. There’s med school and residency, which puts a framework around every move a doctor makes. But once they become attending physicians, the choices are endless. “Coaching can help them find a new structure and systems that will allow them to thrive.”

Although mentoring has been a well-embraced concept for decades, it “hits a wall,” at some point in terms of what it can offer, Dr. Austin said. That’s where coaching can take over. “There’s a point where a mentor cannot help someone self-actualize. As a coach, you don’t need to know everything about a doctor’s life, but you can help them learn to ask themselves the right questions to solve problems.”
 

Should You Stay or Should You Go?

Dr. Austin’s approach begins with the premise that healthcare today is challenging and dysfunctional — but doctors still have agency. She has worked with clients on the verge of leaving the field and helped them find their way back. 

“They have a light bulb moment and open up to the idea that they have much to give still,” she said. “We take an inventory to help them better communicate their needs and make changes, and I help them connect to their values. Sometimes that exercise allows them to reframe their current work environment.” 

Not every doctor who goes through coaching remains in the field. But “that’s the exception, not the rule,” Dr. Austin said. And that’s okay. “If that’s the outcome, coaching probably helped them get to that point faster, and with an informed decision.” 

Dr. Senesie has been coaching for about a decade, and in that time, she’s seen a shift that goes beyond figuring out career goals. “Doctors are more aware of the need for well-being today. The pandemic made it impossible to ignore what doesn’t work for us. When I work with clients, we look for ways to make the job more tenable.” 

According to Dr. Senesie, younger doctors are looking for that balance at the outset. “They want to be physicians, but they also want a life,” she said. “It’s a challenge for them because in addition to that mindset, they’re also coming out with more debt than older generations. They want out from underneath that.”
 

When It’s Time to Find a Physician Coach

Wondering whether coaching is right for you? Consider these symptoms:

• You need help setting boundaries at work.
• You feel like you’re sacrificing your own well-being for your job.
• You’re using maladaptive strategies to cope with the stress at work.
• You’ve reached a point where you are considering leaving the field.

If you’re interested in finding a physician coach, there are several places to begin your search, word of mouth being one of them. “Conferences and social media can also expose you to coaches,” suggested Dr. Esparaz. There are different methods and approaches to coaching. So, as you research, “make sure the coach you choose has techniques and a framework that fit what you’re after.” 

Dr. Austin warned that it is an unregulated industry, so buyer beware. To ensure you’re getting an accredited physician coach, look for people who have obtained an International Coach Federation (ICF) accreditation. These coaches will hold an associate certified coach credential, which requires at least 60 hours of coaching-specific training approved by the ICF, in addition to other assessments and education. 

Ensure that the coach you choose is within your budget. “There are some people charging astronomical rates out there,” Dr. Austin said. “If you’re burned out or struggling, it can be easy to reach for your credit card.”

Dr. Austin also cautioned doctors seeking a coach to avoid promises that sound too good to be true. Some coaching can have a gaslighting quality to it, she warned, “suggesting it can allow you to endure any environment.” But positive self-talk alone won’t cure an abusive or discriminatory situation. “If a client describes a toxic work environment,” the coach has an “ethical imperative” to help that person protect themselves. 
 

A Side Gig or a New Career Path

After Dr. Austin’s experience with her coach, she made the choice to continue as an emergency physician part-time while starting her own coaching business. “It’s important for me personally to keep in touch with what’s happening on the ground, but I have no judgment for anyone who chooses to leave clinical practice to become a coach.”

When Dr. Senesie looks back on her own struggles as a clinician, she recognizes the state of burnout she was in 10 years ago. “I knew there was an issue, but I didn’t have the mindset to find a way to make it work,” she said. “I left the field when I was at my depths of burnout, which is generally not the best way to go about it.” 

Guidance might have allowed her to take into account other avenues and helped her remain in the field, said Dr. Senesie. She has since learned that “there are many ways to practice medicine, and the way we’ve gone about it traditionally has worked for some, but not necessarily for everyone.” 

There may be more possibilities than you think. By helping you assess your path and make meaningful changes, a physician coach might be the key to remaining in the field you love.

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

This transcript has been edited for clarity. 

I usually report five or six studies in the field of neurology that were published in the last months, but July was a vacation month.

I decided to cover another topic, which is the role of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptor agonists beyond diabetes and obesity, and in particular, for the field of neurology and psychiatry. Until a few years ago, the treatment of diabetes with traditional antidiabetic drugs was frustrating for vascular neurologists.

These drugs would lower glucose and had an impact on small-vessel disease, but they had no impact on large-vessel disease, stroke, and vascular mortality. This changed with the sodium-glucose cotransporter 2 antagonists because these drugs were not only effective for diabetes, but they also lowered cardiac mortality, in particular, in patients with cardiac failure.

The next generation of antidiabetic drugs were the GLP-1 receptor agonists and the combined GIP/GLP-1 receptor agonists. These two polypeptides and their receptors play a very important role in diabetes and in obesity. The receptors are found not only in the pancreas but also in the intestinal system, the liver, and the central nervous system.

We have a number of preclinical models, mostly in transgenic mice, which show that these drugs are not effective only in diabetes and obesity, but also in liver disease, kidney failure, and neurodegenerative diseases. GLP-1 receptor agonists also have powerful anti-inflammatory properties. These drugs reduce body weight, and they have positive effects on blood pressure and lipid metabolism. 

In the studies on the use of GLP-1 receptor agonists in diabetes, a meta-analysis with more than 58,000 patients showed a significant risk reduction for stroke compared with placebo, and this risk reduction was in the range of 80%.
 

Stroke, Smoking, and Alcohol

A meta-analysis on the use of GLP-1 receptor agonists in over 30,000 nondiabetic patients with obesity found a significant reduction in blood pressure, mortality, and the risk of myocardial infarction. There was no significant decrease in the risk of stroke, but most probably this is due to the fact that strokes are much less frequent in obesity than in diabetes.

You all know that obesity is also a major risk factor for sleep apnea syndrome. Recently, two large studies with the GIP/GLP-1 receptor agonist tirzepatide found a significant improvement in sleep apnea syndrome compared to placebo, regardless of whether patients needed continuous positive airway pressure therapy or not.

In the therapy studies on diabetes and obesity, there were indications that some smokers in the studies stopped their nicotine consumption. A small pilot study with exenatide in 84 overweight patients who were smokers showed that 46% of patients on exenatide stopped smoking compared with 27% in the placebo group. This could be an indication that GLP-1 receptor agonists have activity on the reward system in the brain. Currently, there are a number of larger placebo-controlled trials ongoing. 

Another aspect is alcohol consumption. An epidemiologic study in Denmark using data from the National Health Registry showed that the incidence of alcohol-related events decreased significantly in almost 40,000 patients with diabetes when they were treated with GLP-1 receptor agonists compared with other antidiabetic drugs.

A retrospective cohort study from the United States with over 80,000 patients with obesity showed that treatment with GLP-1 receptor agonists was associated with a 50%-60% lower risk for occurrence or recurrence of high alcohol consumption. There is only one small study with exenatide, which was not really informative.

There are a number of studies underway for GLP-1 receptor agonists compared with placebo in patients with alcohol dependence or alcohol consumption. Preclinical models also indicate that these drugs might be effective in cocaine abuse, and there is one placebo-controlled study ongoing. 
 

Parkinson’s Disease

Let’s come to neurology. Preclinical models of Parkinson’s disease have shown neuroprotective activities of GLP-1. Until now, we have three randomized placebo-controlled trials with exenatide, NLY01, and lixisenatide. Two of these studies were positive, showing that the symptoms of Parkinson’s disease were stable over time and deteriorated with placebo. One study was neutral. This means we need more large-scale placebo-controlled studies in the early phases of Parkinson’s disease. 

Another potential use of GIP/GLP-1 receptor agonists is in dementia. These substances, as you know, have positive effects on high blood pressure and vascular risk factors. 

A working group in China analyzed 27 studies on the treatment of diabetes. A small number of randomized studies and a large number of cohort studies showed that modern antidiabetic drugs reduce the risk for dementia. The risk reduction for dementia for the GLP-1 receptor agonists was 75%. At the moment, there are only small prospective studies and they are not conclusive. Again, we need large-scale placebo-controlled studies.

The most important limitation at the moment beyond the cost is the other adverse drug reactions with the GLP-1 receptor agonists; these include nausea, vomiting, diarrhea, and constipation. There might be a slightly increased risk for pancreatitis. The US Food and Drug Administration recently reported there is no increased risk for suicide. Another potential adverse drug reaction is nonatherosclerotic anterior optic neuropathy. 

These drugs, GLP-1 receptor agonists and GIP agonists, are also investigated in a variety of other non-neurologic diseases. The focus here is on metabolic liver disease, such as fatty liver and kidney diseases. Smaller, positive studies have been conducted in this area, and large placebo-controlled trials for both indications are currently underway.

If these diverse therapeutic properties would turn out to be really the case with GLP-1 receptor agonists, this would lead to a significant expansion of the range of indications. If we consider cost, this would be the end of our healthcare systems because we cannot afford this. In addition, the new antidiabetic drugs and the treatment of obesity are available only to a limited extent.

Finally, at least for neurology, it’s unclear whether the impact of these diseases is in the brain or whether it’s indirect, due to the effectiveness on vascular risk factors and concomitant diseases. In the next 5 years, we will learn whether GLP-1 or GIP/GLP-1 receptor agonists are the new wonder drugs in medicine.
 

Dr. Diener is Professor in the Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen, Essen, Germany; he has disclosed conflicts of interest with numerous pharmaceutical companies.
 

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

This transcript has been edited for clarity. 

I usually report five or six studies in the field of neurology that were published in the last months, but July was a vacation month.

I decided to cover another topic, which is the role of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptor agonists beyond diabetes and obesity, and in particular, for the field of neurology and psychiatry. Until a few years ago, the treatment of diabetes with traditional antidiabetic drugs was frustrating for vascular neurologists.

These drugs would lower glucose and had an impact on small-vessel disease, but they had no impact on large-vessel disease, stroke, and vascular mortality. This changed with the sodium-glucose cotransporter 2 antagonists because these drugs were not only effective for diabetes, but they also lowered cardiac mortality, in particular, in patients with cardiac failure.

The next generation of antidiabetic drugs were the GLP-1 receptor agonists and the combined GIP/GLP-1 receptor agonists. These two polypeptides and their receptors play a very important role in diabetes and in obesity. The receptors are found not only in the pancreas but also in the intestinal system, the liver, and the central nervous system.

We have a number of preclinical models, mostly in transgenic mice, which show that these drugs are not effective only in diabetes and obesity, but also in liver disease, kidney failure, and neurodegenerative diseases. GLP-1 receptor agonists also have powerful anti-inflammatory properties. These drugs reduce body weight, and they have positive effects on blood pressure and lipid metabolism. 

In the studies on the use of GLP-1 receptor agonists in diabetes, a meta-analysis with more than 58,000 patients showed a significant risk reduction for stroke compared with placebo, and this risk reduction was in the range of 80%.
 

Stroke, Smoking, and Alcohol

A meta-analysis on the use of GLP-1 receptor agonists in over 30,000 nondiabetic patients with obesity found a significant reduction in blood pressure, mortality, and the risk of myocardial infarction. There was no significant decrease in the risk of stroke, but most probably this is due to the fact that strokes are much less frequent in obesity than in diabetes.

You all know that obesity is also a major risk factor for sleep apnea syndrome. Recently, two large studies with the GIP/GLP-1 receptor agonist tirzepatide found a significant improvement in sleep apnea syndrome compared to placebo, regardless of whether patients needed continuous positive airway pressure therapy or not.

In the therapy studies on diabetes and obesity, there were indications that some smokers in the studies stopped their nicotine consumption. A small pilot study with exenatide in 84 overweight patients who were smokers showed that 46% of patients on exenatide stopped smoking compared with 27% in the placebo group. This could be an indication that GLP-1 receptor agonists have activity on the reward system in the brain. Currently, there are a number of larger placebo-controlled trials ongoing. 

Another aspect is alcohol consumption. An epidemiologic study in Denmark using data from the National Health Registry showed that the incidence of alcohol-related events decreased significantly in almost 40,000 patients with diabetes when they were treated with GLP-1 receptor agonists compared with other antidiabetic drugs.

A retrospective cohort study from the United States with over 80,000 patients with obesity showed that treatment with GLP-1 receptor agonists was associated with a 50%-60% lower risk for occurrence or recurrence of high alcohol consumption. There is only one small study with exenatide, which was not really informative.

There are a number of studies underway for GLP-1 receptor agonists compared with placebo in patients with alcohol dependence or alcohol consumption. Preclinical models also indicate that these drugs might be effective in cocaine abuse, and there is one placebo-controlled study ongoing. 
 

Parkinson’s Disease

Let’s come to neurology. Preclinical models of Parkinson’s disease have shown neuroprotective activities of GLP-1. Until now, we have three randomized placebo-controlled trials with exenatide, NLY01, and lixisenatide. Two of these studies were positive, showing that the symptoms of Parkinson’s disease were stable over time and deteriorated with placebo. One study was neutral. This means we need more large-scale placebo-controlled studies in the early phases of Parkinson’s disease. 

Another potential use of GIP/GLP-1 receptor agonists is in dementia. These substances, as you know, have positive effects on high blood pressure and vascular risk factors. 

A working group in China analyzed 27 studies on the treatment of diabetes. A small number of randomized studies and a large number of cohort studies showed that modern antidiabetic drugs reduce the risk for dementia. The risk reduction for dementia for the GLP-1 receptor agonists was 75%. At the moment, there are only small prospective studies and they are not conclusive. Again, we need large-scale placebo-controlled studies.

The most important limitation at the moment beyond the cost is the other adverse drug reactions with the GLP-1 receptor agonists; these include nausea, vomiting, diarrhea, and constipation. There might be a slightly increased risk for pancreatitis. The US Food and Drug Administration recently reported there is no increased risk for suicide. Another potential adverse drug reaction is nonatherosclerotic anterior optic neuropathy. 

These drugs, GLP-1 receptor agonists and GIP agonists, are also investigated in a variety of other non-neurologic diseases. The focus here is on metabolic liver disease, such as fatty liver and kidney diseases. Smaller, positive studies have been conducted in this area, and large placebo-controlled trials for both indications are currently underway.

If these diverse therapeutic properties would turn out to be really the case with GLP-1 receptor agonists, this would lead to a significant expansion of the range of indications. If we consider cost, this would be the end of our healthcare systems because we cannot afford this. In addition, the new antidiabetic drugs and the treatment of obesity are available only to a limited extent.

Finally, at least for neurology, it’s unclear whether the impact of these diseases is in the brain or whether it’s indirect, due to the effectiveness on vascular risk factors and concomitant diseases. In the next 5 years, we will learn whether GLP-1 or GIP/GLP-1 receptor agonists are the new wonder drugs in medicine.
 

Dr. Diener is Professor in the Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen, Essen, Germany; he has disclosed conflicts of interest with numerous pharmaceutical companies.
 

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

This transcript has been edited for clarity. 

I usually report five or six studies in the field of neurology that were published in the last months, but July was a vacation month.

I decided to cover another topic, which is the role of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptor agonists beyond diabetes and obesity, and in particular, for the field of neurology and psychiatry. Until a few years ago, the treatment of diabetes with traditional antidiabetic drugs was frustrating for vascular neurologists.

These drugs would lower glucose and had an impact on small-vessel disease, but they had no impact on large-vessel disease, stroke, and vascular mortality. This changed with the sodium-glucose cotransporter 2 antagonists because these drugs were not only effective for diabetes, but they also lowered cardiac mortality, in particular, in patients with cardiac failure.

The next generation of antidiabetic drugs were the GLP-1 receptor agonists and the combined GIP/GLP-1 receptor agonists. These two polypeptides and their receptors play a very important role in diabetes and in obesity. The receptors are found not only in the pancreas but also in the intestinal system, the liver, and the central nervous system.

We have a number of preclinical models, mostly in transgenic mice, which show that these drugs are not effective only in diabetes and obesity, but also in liver disease, kidney failure, and neurodegenerative diseases. GLP-1 receptor agonists also have powerful anti-inflammatory properties. These drugs reduce body weight, and they have positive effects on blood pressure and lipid metabolism. 

In the studies on the use of GLP-1 receptor agonists in diabetes, a meta-analysis with more than 58,000 patients showed a significant risk reduction for stroke compared with placebo, and this risk reduction was in the range of 80%.
 

Stroke, Smoking, and Alcohol

A meta-analysis on the use of GLP-1 receptor agonists in over 30,000 nondiabetic patients with obesity found a significant reduction in blood pressure, mortality, and the risk of myocardial infarction. There was no significant decrease in the risk of stroke, but most probably this is due to the fact that strokes are much less frequent in obesity than in diabetes.

You all know that obesity is also a major risk factor for sleep apnea syndrome. Recently, two large studies with the GIP/GLP-1 receptor agonist tirzepatide found a significant improvement in sleep apnea syndrome compared to placebo, regardless of whether patients needed continuous positive airway pressure therapy or not.

In the therapy studies on diabetes and obesity, there were indications that some smokers in the studies stopped their nicotine consumption. A small pilot study with exenatide in 84 overweight patients who were smokers showed that 46% of patients on exenatide stopped smoking compared with 27% in the placebo group. This could be an indication that GLP-1 receptor agonists have activity on the reward system in the brain. Currently, there are a number of larger placebo-controlled trials ongoing. 

Another aspect is alcohol consumption. An epidemiologic study in Denmark using data from the National Health Registry showed that the incidence of alcohol-related events decreased significantly in almost 40,000 patients with diabetes when they were treated with GLP-1 receptor agonists compared with other antidiabetic drugs.

A retrospective cohort study from the United States with over 80,000 patients with obesity showed that treatment with GLP-1 receptor agonists was associated with a 50%-60% lower risk for occurrence or recurrence of high alcohol consumption. There is only one small study with exenatide, which was not really informative.

There are a number of studies underway for GLP-1 receptor agonists compared with placebo in patients with alcohol dependence or alcohol consumption. Preclinical models also indicate that these drugs might be effective in cocaine abuse, and there is one placebo-controlled study ongoing. 
 

Parkinson’s Disease

Let’s come to neurology. Preclinical models of Parkinson’s disease have shown neuroprotective activities of GLP-1. Until now, we have three randomized placebo-controlled trials with exenatide, NLY01, and lixisenatide. Two of these studies were positive, showing that the symptoms of Parkinson’s disease were stable over time and deteriorated with placebo. One study was neutral. This means we need more large-scale placebo-controlled studies in the early phases of Parkinson’s disease. 

Another potential use of GIP/GLP-1 receptor agonists is in dementia. These substances, as you know, have positive effects on high blood pressure and vascular risk factors. 

A working group in China analyzed 27 studies on the treatment of diabetes. A small number of randomized studies and a large number of cohort studies showed that modern antidiabetic drugs reduce the risk for dementia. The risk reduction for dementia for the GLP-1 receptor agonists was 75%. At the moment, there are only small prospective studies and they are not conclusive. Again, we need large-scale placebo-controlled studies.

The most important limitation at the moment beyond the cost is the other adverse drug reactions with the GLP-1 receptor agonists; these include nausea, vomiting, diarrhea, and constipation. There might be a slightly increased risk for pancreatitis. The US Food and Drug Administration recently reported there is no increased risk for suicide. Another potential adverse drug reaction is nonatherosclerotic anterior optic neuropathy. 

These drugs, GLP-1 receptor agonists and GIP agonists, are also investigated in a variety of other non-neurologic diseases. The focus here is on metabolic liver disease, such as fatty liver and kidney diseases. Smaller, positive studies have been conducted in this area, and large placebo-controlled trials for both indications are currently underway.

If these diverse therapeutic properties would turn out to be really the case with GLP-1 receptor agonists, this would lead to a significant expansion of the range of indications. If we consider cost, this would be the end of our healthcare systems because we cannot afford this. In addition, the new antidiabetic drugs and the treatment of obesity are available only to a limited extent.

Finally, at least for neurology, it’s unclear whether the impact of these diseases is in the brain or whether it’s indirect, due to the effectiveness on vascular risk factors and concomitant diseases. In the next 5 years, we will learn whether GLP-1 or GIP/GLP-1 receptor agonists are the new wonder drugs in medicine.
 

Dr. Diener is Professor in the Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen, Essen, Germany; he has disclosed conflicts of interest with numerous pharmaceutical companies.
 

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