MDedge Neurology

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

“It was my wife’s walker, and I’ve never used one before. Sorry that I keep bumping into things.”

He was in his early 70s, recently widowed. He hadn’t needed a walker until yesterday, and his son had gotten it out of the garage where they’d just stowed it away. I showed him how to change the height setting on it so he didn’t have to lean so far over.

His daughter was a longstanding patient of mine, and now she and her brother were worried about their dad. He’d been so healthy for years, taking care of their mother as she declined with cancer. Now, 2 months since her death, he’d started going downhill. He’d been, understandably, depressed and had lost some weight. A few weeks ago he’d had some nonspecific upper respiratory crud, and now they were worried he wasn’t eating. He’d gotten progressively weaker in the last few days, leading to their getting out the walker.

I knew my patient for several years. She wasn’t given to panicking, and was worried about her dad. By this time, I was too. Twenty-eight years of neurology training and practice puts you on the edge for some things. The “Spidey Sense,” as I’ve always called it, was tingling.

It took a very quick neurologic exam to find what I needed. He was indeed weak, had decreased distal sensation, and was completely areflexic. It was time to take the most-dreaded outpatient neurology gamble: The direct office-to-ER admission.

I told his daughter to take him to the nearby ER and scribbled a note that said “Probable Guillain-Barré. Needs urgent workup.” They were somewhat taken aback, as they had dinner plans that night, but his daughter knew me well enough to know that I don’t pull fire alarms for fun.

As soon as they’d left I called the ER doctor and told her what was coming. My hospital days ended 2 years ago, but I wanted to do everything I could to make sure the right ball was rolling.

Then my part was over. I had other patients waiting, tests to review, phone calls to make.

This is where the anxiety began. Nobody wants to be the person who cries wolf, or admits “dumps.” I’ve been on both sides of admissions, and bashing outpatient docs for unnecessary hospital referrals is a perennial pastime of inpatient care.

I was sure of my actions, but as the hours crept by some doubt came in. What if he got to the hospital and suddenly wasn’t weak? Or it was all from a medication error he’d made at home?

No one wants to claim they saw a flare when there wasn’t one, or get the reputation of being past their game. I was worried about the patient, but also began to worry I’d screwed up and missed something else.

I finished the day and went home. After closing out my usual end-of-the-day stuff I logged into the hospital system to see what was going on.

Normal cervical spine MRI. Spinal fluid had zero cells and elevated protein.

I breathed a sigh of relief and relaxed back into my chair. I’d made the right call. The hospital neurologist had ordered IVIG. The patient would hopefully recover. No one would think I’d screwed up a potentially serious case. And, somewhere in the back of my mind, the Sherlock Holmes inside every neurologist tipped his deerstalker cap at me and gave a slight nod.

There’s the relief of having done the right thing for the patient, having made the correct diagnosis, and, at the end of the day, being reassured that (some days at least) I still know what I’m doing.

It’s those feelings that brought me here and still keep me going.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

“It was my wife’s walker, and I’ve never used one before. Sorry that I keep bumping into things.”

He was in his early 70s, recently widowed. He hadn’t needed a walker until yesterday, and his son had gotten it out of the garage where they’d just stowed it away. I showed him how to change the height setting on it so he didn’t have to lean so far over.

His daughter was a longstanding patient of mine, and now she and her brother were worried about their dad. He’d been so healthy for years, taking care of their mother as she declined with cancer. Now, 2 months since her death, he’d started going downhill. He’d been, understandably, depressed and had lost some weight. A few weeks ago he’d had some nonspecific upper respiratory crud, and now they were worried he wasn’t eating. He’d gotten progressively weaker in the last few days, leading to their getting out the walker.

I knew my patient for several years. She wasn’t given to panicking, and was worried about her dad. By this time, I was too. Twenty-eight years of neurology training and practice puts you on the edge for some things. The “Spidey Sense,” as I’ve always called it, was tingling.

It took a very quick neurologic exam to find what I needed. He was indeed weak, had decreased distal sensation, and was completely areflexic. It was time to take the most-dreaded outpatient neurology gamble: The direct office-to-ER admission.

I told his daughter to take him to the nearby ER and scribbled a note that said “Probable Guillain-Barré. Needs urgent workup.” They were somewhat taken aback, as they had dinner plans that night, but his daughter knew me well enough to know that I don’t pull fire alarms for fun.

As soon as they’d left I called the ER doctor and told her what was coming. My hospital days ended 2 years ago, but I wanted to do everything I could to make sure the right ball was rolling.

Then my part was over. I had other patients waiting, tests to review, phone calls to make.

This is where the anxiety began. Nobody wants to be the person who cries wolf, or admits “dumps.” I’ve been on both sides of admissions, and bashing outpatient docs for unnecessary hospital referrals is a perennial pastime of inpatient care.

I was sure of my actions, but as the hours crept by some doubt came in. What if he got to the hospital and suddenly wasn’t weak? Or it was all from a medication error he’d made at home?

No one wants to claim they saw a flare when there wasn’t one, or get the reputation of being past their game. I was worried about the patient, but also began to worry I’d screwed up and missed something else.

I finished the day and went home. After closing out my usual end-of-the-day stuff I logged into the hospital system to see what was going on.

Normal cervical spine MRI. Spinal fluid had zero cells and elevated protein.

I breathed a sigh of relief and relaxed back into my chair. I’d made the right call. The hospital neurologist had ordered IVIG. The patient would hopefully recover. No one would think I’d screwed up a potentially serious case. And, somewhere in the back of my mind, the Sherlock Holmes inside every neurologist tipped his deerstalker cap at me and gave a slight nod.

There’s the relief of having done the right thing for the patient, having made the correct diagnosis, and, at the end of the day, being reassured that (some days at least) I still know what I’m doing.

It’s those feelings that brought me here and still keep me going.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

“It was my wife’s walker, and I’ve never used one before. Sorry that I keep bumping into things.”

He was in his early 70s, recently widowed. He hadn’t needed a walker until yesterday, and his son had gotten it out of the garage where they’d just stowed it away. I showed him how to change the height setting on it so he didn’t have to lean so far over.

His daughter was a longstanding patient of mine, and now she and her brother were worried about their dad. He’d been so healthy for years, taking care of their mother as she declined with cancer. Now, 2 months since her death, he’d started going downhill. He’d been, understandably, depressed and had lost some weight. A few weeks ago he’d had some nonspecific upper respiratory crud, and now they were worried he wasn’t eating. He’d gotten progressively weaker in the last few days, leading to their getting out the walker.

I knew my patient for several years. She wasn’t given to panicking, and was worried about her dad. By this time, I was too. Twenty-eight years of neurology training and practice puts you on the edge for some things. The “Spidey Sense,” as I’ve always called it, was tingling.

It took a very quick neurologic exam to find what I needed. He was indeed weak, had decreased distal sensation, and was completely areflexic. It was time to take the most-dreaded outpatient neurology gamble: The direct office-to-ER admission.

I told his daughter to take him to the nearby ER and scribbled a note that said “Probable Guillain-Barré. Needs urgent workup.” They were somewhat taken aback, as they had dinner plans that night, but his daughter knew me well enough to know that I don’t pull fire alarms for fun.

As soon as they’d left I called the ER doctor and told her what was coming. My hospital days ended 2 years ago, but I wanted to do everything I could to make sure the right ball was rolling.

Then my part was over. I had other patients waiting, tests to review, phone calls to make.

This is where the anxiety began. Nobody wants to be the person who cries wolf, or admits “dumps.” I’ve been on both sides of admissions, and bashing outpatient docs for unnecessary hospital referrals is a perennial pastime of inpatient care.

I was sure of my actions, but as the hours crept by some doubt came in. What if he got to the hospital and suddenly wasn’t weak? Or it was all from a medication error he’d made at home?

No one wants to claim they saw a flare when there wasn’t one, or get the reputation of being past their game. I was worried about the patient, but also began to worry I’d screwed up and missed something else.

I finished the day and went home. After closing out my usual end-of-the-day stuff I logged into the hospital system to see what was going on.

Normal cervical spine MRI. Spinal fluid had zero cells and elevated protein.

I breathed a sigh of relief and relaxed back into my chair. I’d made the right call. The hospital neurologist had ordered IVIG. The patient would hopefully recover. No one would think I’d screwed up a potentially serious case. And, somewhere in the back of my mind, the Sherlock Holmes inside every neurologist tipped his deerstalker cap at me and gave a slight nod.

There’s the relief of having done the right thing for the patient, having made the correct diagnosis, and, at the end of the day, being reassured that (some days at least) I still know what I’m doing.

It’s those feelings that brought me here and still keep me going.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

A unique ratio of metabolites measured in blood may help supplement a clinical diagnosis of early Alzheimer’s disease (AD), allowing for earlier intervention, early research suggests.

Investigators found that plasma concentrations of 2-aminoethyl dihydrogen phosphate and taurine could distinguish adults with early-stage Alzheimer’s disease from cognitively normal adults.

“Our biomarker for early-stage Alzheimer’s disease represents new thinking and is unique from the amyloid-beta and p-tau molecules that are currently being investigated to diagnose AD,” Sandra Banack, PhD, senior scientist, Brain Chemistry Labs, Jackson, Wyoming, told this news organization.

If further studies pan out, Dr. Banack said this biomarker could “easily be transformed into a test to aid clinical evaluations for Alzheimer’s disease.”

The study was published online in PLOS ONE.
 

New drug target?

The researchers measured concentrations of 2-aminoethyl dihydrogen phosphate and taurine in blood plasma samples in 25 patients (21 men; mean age, 71) with a clinical diagnosis of early-stage Alzheimer’s based on a Clinical Dementia Rating (CDR) score of 0.5, suggesting very mild cognitive impairment, and 25 healthy controls (20 men; mean age, 39).

The concentration of 2-aminoethyl dihydrogen phosphate, normalized by the concentration of taurine, reliably distinguished blood samples of early-stage Alzheimer’s patients from controls in a blinded analysis.

This biomarker “could lead to new understanding of [AD] and lead to new drug candidates,” Dr. Banack told this news organization.

The researchers note that 2-aminoethyl dihydrogen phosphate plays an important role in the structure and function of cellular membranes.

Physiologic effects of increased 2-aminoethyl dihydrogen phosphate concentrations in the blood are not known. However, in one study, concentrations of this molecule were found to be significantly lower in the temporal cortex, frontal cortex, and hippocampus (40%) in patients with Alzheimer’s disease, compared with controls.

“New biomarkers take time before they can be implemented in the clinic. The next step will be to repeat the experiments using a large sample size of AD patient blood samples,” Dr. Banack told this news organization.

The study team is looking to source a larger sample size of AD blood samples to replicate these findings. They are also examining this biomarker relative to other neurodegenerative diseases.

“If verified with larger sample sizes, the quantification of 2-aminoethyl dihydrogen phosphate could potentially assist in the diagnosis of early-stage Alzheimer’s disease when used in conjunction with the patient’s CDR score and other potential AD biomarkers,” Dr. Banack and colleagues say.
 

Caveats, cautionary notes

Commenting on the findings, Rebecca M. Edelmayer, PhD, Alzheimer’s Association senior director of scientific engagement, said the study is “interesting, though very small-scale and very preliminary.”

Dr. Edelmayer said one “major limitation” is that participants did not have their Alzheimer’s diagnosis confirmed with “gold standard biomarkers. They have been diagnosed based only on their cognitive and behavioral symptoms.”

She also cautioned that the study population is not representative – either of the general public or people living with Alzheimer’s disease.

For example, 41 out of all 50 samples are from men, “though we know women are disproportionately impacted by Alzheimer’s.”

“There is a mismatch in the age of the study groups,” Dr. Edelmayer noted. The mean age of controls in the study was 39 and the mean age of people with dementia was 71. Race or ethnicity and other demographic information is also unclear from the article.

“There is an urgent need for simple, inexpensive, noninvasive and easily available diagnostic tools for Alzheimer’s, such as a blood test. A simple blood test for Alzheimer’s would be a great advance for individuals with – and at risk for – the disease, families, doctors, and researchers,” Dr. Edelmayer said.

“Bottom line,” Dr. Edelmayer continued, “these results need to be further tested and verified in long-term, large-scale studies with diverse populations that are representative of those living with Alzheimer’s disease.”

This research was supported by the William Stamps Farish Fund and the Josephine P. & John J. Louis Foundation. Brain Chemistry Labs has applied for a patent related to this research. Dr. Edelmayer has no relevant disclosures.

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

A unique ratio of metabolites measured in blood may help supplement a clinical diagnosis of early Alzheimer’s disease (AD), allowing for earlier intervention, early research suggests.

Investigators found that plasma concentrations of 2-aminoethyl dihydrogen phosphate and taurine could distinguish adults with early-stage Alzheimer’s disease from cognitively normal adults.

“Our biomarker for early-stage Alzheimer’s disease represents new thinking and is unique from the amyloid-beta and p-tau molecules that are currently being investigated to diagnose AD,” Sandra Banack, PhD, senior scientist, Brain Chemistry Labs, Jackson, Wyoming, told this news organization.

If further studies pan out, Dr. Banack said this biomarker could “easily be transformed into a test to aid clinical evaluations for Alzheimer’s disease.”

The study was published online in PLOS ONE.
 

New drug target?

The researchers measured concentrations of 2-aminoethyl dihydrogen phosphate and taurine in blood plasma samples in 25 patients (21 men; mean age, 71) with a clinical diagnosis of early-stage Alzheimer’s based on a Clinical Dementia Rating (CDR) score of 0.5, suggesting very mild cognitive impairment, and 25 healthy controls (20 men; mean age, 39).

The concentration of 2-aminoethyl dihydrogen phosphate, normalized by the concentration of taurine, reliably distinguished blood samples of early-stage Alzheimer’s patients from controls in a blinded analysis.

This biomarker “could lead to new understanding of [AD] and lead to new drug candidates,” Dr. Banack told this news organization.

The researchers note that 2-aminoethyl dihydrogen phosphate plays an important role in the structure and function of cellular membranes.

Physiologic effects of increased 2-aminoethyl dihydrogen phosphate concentrations in the blood are not known. However, in one study, concentrations of this molecule were found to be significantly lower in the temporal cortex, frontal cortex, and hippocampus (40%) in patients with Alzheimer’s disease, compared with controls.

“New biomarkers take time before they can be implemented in the clinic. The next step will be to repeat the experiments using a large sample size of AD patient blood samples,” Dr. Banack told this news organization.

The study team is looking to source a larger sample size of AD blood samples to replicate these findings. They are also examining this biomarker relative to other neurodegenerative diseases.

“If verified with larger sample sizes, the quantification of 2-aminoethyl dihydrogen phosphate could potentially assist in the diagnosis of early-stage Alzheimer’s disease when used in conjunction with the patient’s CDR score and other potential AD biomarkers,” Dr. Banack and colleagues say.
 

Caveats, cautionary notes

Commenting on the findings, Rebecca M. Edelmayer, PhD, Alzheimer’s Association senior director of scientific engagement, said the study is “interesting, though very small-scale and very preliminary.”

Dr. Edelmayer said one “major limitation” is that participants did not have their Alzheimer’s diagnosis confirmed with “gold standard biomarkers. They have been diagnosed based only on their cognitive and behavioral symptoms.”

She also cautioned that the study population is not representative – either of the general public or people living with Alzheimer’s disease.

For example, 41 out of all 50 samples are from men, “though we know women are disproportionately impacted by Alzheimer’s.”

“There is a mismatch in the age of the study groups,” Dr. Edelmayer noted. The mean age of controls in the study was 39 and the mean age of people with dementia was 71. Race or ethnicity and other demographic information is also unclear from the article.

“There is an urgent need for simple, inexpensive, noninvasive and easily available diagnostic tools for Alzheimer’s, such as a blood test. A simple blood test for Alzheimer’s would be a great advance for individuals with – and at risk for – the disease, families, doctors, and researchers,” Dr. Edelmayer said.

“Bottom line,” Dr. Edelmayer continued, “these results need to be further tested and verified in long-term, large-scale studies with diverse populations that are representative of those living with Alzheimer’s disease.”

This research was supported by the William Stamps Farish Fund and the Josephine P. & John J. Louis Foundation. Brain Chemistry Labs has applied for a patent related to this research. Dr. Edelmayer has no relevant disclosures.

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

A unique ratio of metabolites measured in blood may help supplement a clinical diagnosis of early Alzheimer’s disease (AD), allowing for earlier intervention, early research suggests.

Investigators found that plasma concentrations of 2-aminoethyl dihydrogen phosphate and taurine could distinguish adults with early-stage Alzheimer’s disease from cognitively normal adults.

“Our biomarker for early-stage Alzheimer’s disease represents new thinking and is unique from the amyloid-beta and p-tau molecules that are currently being investigated to diagnose AD,” Sandra Banack, PhD, senior scientist, Brain Chemistry Labs, Jackson, Wyoming, told this news organization.

If further studies pan out, Dr. Banack said this biomarker could “easily be transformed into a test to aid clinical evaluations for Alzheimer’s disease.”

The study was published online in PLOS ONE.
 

New drug target?

The researchers measured concentrations of 2-aminoethyl dihydrogen phosphate and taurine in blood plasma samples in 25 patients (21 men; mean age, 71) with a clinical diagnosis of early-stage Alzheimer’s based on a Clinical Dementia Rating (CDR) score of 0.5, suggesting very mild cognitive impairment, and 25 healthy controls (20 men; mean age, 39).

The concentration of 2-aminoethyl dihydrogen phosphate, normalized by the concentration of taurine, reliably distinguished blood samples of early-stage Alzheimer’s patients from controls in a blinded analysis.

This biomarker “could lead to new understanding of [AD] and lead to new drug candidates,” Dr. Banack told this news organization.

The researchers note that 2-aminoethyl dihydrogen phosphate plays an important role in the structure and function of cellular membranes.

Physiologic effects of increased 2-aminoethyl dihydrogen phosphate concentrations in the blood are not known. However, in one study, concentrations of this molecule were found to be significantly lower in the temporal cortex, frontal cortex, and hippocampus (40%) in patients with Alzheimer’s disease, compared with controls.

“New biomarkers take time before they can be implemented in the clinic. The next step will be to repeat the experiments using a large sample size of AD patient blood samples,” Dr. Banack told this news organization.

The study team is looking to source a larger sample size of AD blood samples to replicate these findings. They are also examining this biomarker relative to other neurodegenerative diseases.

“If verified with larger sample sizes, the quantification of 2-aminoethyl dihydrogen phosphate could potentially assist in the diagnosis of early-stage Alzheimer’s disease when used in conjunction with the patient’s CDR score and other potential AD biomarkers,” Dr. Banack and colleagues say.
 

Caveats, cautionary notes

Commenting on the findings, Rebecca M. Edelmayer, PhD, Alzheimer’s Association senior director of scientific engagement, said the study is “interesting, though very small-scale and very preliminary.”

Dr. Edelmayer said one “major limitation” is that participants did not have their Alzheimer’s diagnosis confirmed with “gold standard biomarkers. They have been diagnosed based only on their cognitive and behavioral symptoms.”

She also cautioned that the study population is not representative – either of the general public or people living with Alzheimer’s disease.

For example, 41 out of all 50 samples are from men, “though we know women are disproportionately impacted by Alzheimer’s.”

“There is a mismatch in the age of the study groups,” Dr. Edelmayer noted. The mean age of controls in the study was 39 and the mean age of people with dementia was 71. Race or ethnicity and other demographic information is also unclear from the article.

“There is an urgent need for simple, inexpensive, noninvasive and easily available diagnostic tools for Alzheimer’s, such as a blood test. A simple blood test for Alzheimer’s would be a great advance for individuals with – and at risk for – the disease, families, doctors, and researchers,” Dr. Edelmayer said.

“Bottom line,” Dr. Edelmayer continued, “these results need to be further tested and verified in long-term, large-scale studies with diverse populations that are representative of those living with Alzheimer’s disease.”

This research was supported by the William Stamps Farish Fund and the Josephine P. & John J. Louis Foundation. Brain Chemistry Labs has applied for a patent related to this research. Dr. Edelmayer has no relevant disclosures.

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

Impaired vision in older adults is an underrecognized and modifiable dementia risk factor, new research suggests.

Investigators analyzed estimated population attributable fractions (PAFs) associated with dementia in more than 16,000 older adults. A PAF represents the number of dementia cases that could be prevented if a given risk factor were eliminated.

Results showed the PAF of vision impairment was 1.8%, suggesting that healthy vision had the potential to prevent more than 100,000 cases of dementia in the United States.

“Vision impairment and blindness disproportionately impact older adults, yet vision impairment is often preventable or even correctable,” study investigator Joshua Ehrlich MD, assistant professor of ophthalmology and visual sciences, University of Michigan, Ann Arbor, said in an interview.

Poor vision affects not only how individuals see the world, but also their systemic health and well-being, Dr. Ehrlich said.

“Accordingly, ensuring that older adults receive appropriate eye care is vital to promoting health, independence, and optimal aging,” he added.

The findings were published online in JAMA Neurology.
 

A surprising omission

There is an “urgent need to identify modifiable risk factors for dementia that can be targeted with interventions to slow cognitive decline and prevent dementia,” the investigators wrote.

In 2020, the Lancet Commission report on dementia prevention, intervention, and care proposed a life-course model of 12 potentially modifiable dementia risk factors. This included lower educational level, hearing loss, traumatic brain injury, hypertension, excessive alcohol consumption, obesity, smoking, depression, social isolation, physical inactivity, diabetes, and air pollution.

Together, these factors are associated with about 40% of dementia cases worldwide, the report notes.

Vision impairment was not included in this model, “despite considerable evidence that it is associated with an elevated risk of incident dementia and that it may operate through the same pathways as hearing loss,” the current researchers wrote.

“We have known for some time that vision impairment is a risk factor for dementia [and] we also know that a very large fraction of vision impairment, possibly in excess of 80%, is avoidable or has simply yet to be addressed,” Dr. Ehrlich said.

He and his colleagues found it “surprising that vision impairment had been ignored in key models of modifiable dementia risk factors that are used to shape health policy and resource allocation.” They set out to demonstrate that, “in fact, vision impairment is just as influential as a number of other long accepted modifiable dementia risk factors.”

The investigators assessed data from the Health and Retirement Study (HRS), a panel study that surveys more than 20,000 U.S. adults aged 50 years or older every 2 years.

The investigators applied the same methods used by the Lancet Commission to the HRS dataset and added vision impairment to the Lancet life-course model. Air pollution was excluded in their model “because those data were not readily available in the HRS,” the researchers wrote.

They noted the PAF is “based on the population prevalence and relative risk of dementia for each risk factor” and is “weighted, based on a principal components analysis, to account for communality (clustering of risk factors).”
 

A missed prevention opportunity

The sample included 16,690 participants (54% were women, 51.5% were at least age 65, 80.2% were White, 10.6% were Black, 9.2% were other).

In total, the 12 potentially modifiable risk factors used in the researchers’ model were associated with an estimated 62.4% of dementia cases in the United States, with hypertension as the most prevalent risk factor with the highest weighted PAF.
 

A new focus for prevention

Commenting for this article, Suzann Pershing, MD, associate professor of ophthalmology, Stanford (Calif.) University, called the study “particularly important because, despite growing recognition of its importance in relation to cognition, visual impairment is often an underrecognized risk factor.”

The current research “builds on increasingly robust medical literature linking visual impairment and dementia, applying analogous methods to those used for the life course model recently presented by the Lancet Commission to evaluate potentially modifiable dementia risk factors,” said Dr. Pershing, who was not involved with the study.

The investigators “make a compelling argument for inclusion of visual impairment as one of the potentially modifiable risk factors; practicing clinicians and health care systems may consider screening and targeted therapies to address visual impairment, with a goal of population health and contributing to a reduction in future dementia disease burden,” she added.

In an accompanying editorial), Jennifer Deal, PhD, department of epidemiology and Cochlear Center for Hearing and Public Health, Baltimore, and Julio Rojas, MD, PhD, Memory and Aging Center, department of neurology, Weill Institute for Neurosciences, University of California, San Francisco, call the findings “an important reminder that dementia is a social problem in which potentially treatable risk factors, including visual impairment, are highly prevalent in disadvantaged populations.”

The editorialists noted that 90% of cases of vision impairment are “preventable or have yet to be treated. The two “highly cost-effective interventions” of eyeglasses and/or cataract surgery “remain underused both in the U.S. and globally, especially in disadvantaged communities,” they wrote.

They added that more research is needed to “test the effectiveness of interventions to preserve cognitive health by promoting healthy vision.”

The study was supported by grants from the National Institute on Aging, the National Institutes of Health, and Research to Prevent Blindness. The investigators reported no relevant financial relationships. Dr. Deal reported having received grants from the National Institute on Aging. Dr. Rojas reported serving as site principal investigator on clinical trials for Eli Lilly and Eisai and receiving grants from the National Institute on Aging. Dr. Pershing is a consultant for Acumen, and Verana Health (as DigiSight Technologies).

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

Impaired vision in older adults is an underrecognized and modifiable dementia risk factor, new research suggests.

Investigators analyzed estimated population attributable fractions (PAFs) associated with dementia in more than 16,000 older adults. A PAF represents the number of dementia cases that could be prevented if a given risk factor were eliminated.

Results showed the PAF of vision impairment was 1.8%, suggesting that healthy vision had the potential to prevent more than 100,000 cases of dementia in the United States.

“Vision impairment and blindness disproportionately impact older adults, yet vision impairment is often preventable or even correctable,” study investigator Joshua Ehrlich MD, assistant professor of ophthalmology and visual sciences, University of Michigan, Ann Arbor, said in an interview.

Poor vision affects not only how individuals see the world, but also their systemic health and well-being, Dr. Ehrlich said.

“Accordingly, ensuring that older adults receive appropriate eye care is vital to promoting health, independence, and optimal aging,” he added.

The findings were published online in JAMA Neurology.
 

A surprising omission

There is an “urgent need to identify modifiable risk factors for dementia that can be targeted with interventions to slow cognitive decline and prevent dementia,” the investigators wrote.

In 2020, the Lancet Commission report on dementia prevention, intervention, and care proposed a life-course model of 12 potentially modifiable dementia risk factors. This included lower educational level, hearing loss, traumatic brain injury, hypertension, excessive alcohol consumption, obesity, smoking, depression, social isolation, physical inactivity, diabetes, and air pollution.

Together, these factors are associated with about 40% of dementia cases worldwide, the report notes.

Vision impairment was not included in this model, “despite considerable evidence that it is associated with an elevated risk of incident dementia and that it may operate through the same pathways as hearing loss,” the current researchers wrote.

“We have known for some time that vision impairment is a risk factor for dementia [and] we also know that a very large fraction of vision impairment, possibly in excess of 80%, is avoidable or has simply yet to be addressed,” Dr. Ehrlich said.

He and his colleagues found it “surprising that vision impairment had been ignored in key models of modifiable dementia risk factors that are used to shape health policy and resource allocation.” They set out to demonstrate that, “in fact, vision impairment is just as influential as a number of other long accepted modifiable dementia risk factors.”

The investigators assessed data from the Health and Retirement Study (HRS), a panel study that surveys more than 20,000 U.S. adults aged 50 years or older every 2 years.

The investigators applied the same methods used by the Lancet Commission to the HRS dataset and added vision impairment to the Lancet life-course model. Air pollution was excluded in their model “because those data were not readily available in the HRS,” the researchers wrote.

They noted the PAF is “based on the population prevalence and relative risk of dementia for each risk factor” and is “weighted, based on a principal components analysis, to account for communality (clustering of risk factors).”
 

A missed prevention opportunity

The sample included 16,690 participants (54% were women, 51.5% were at least age 65, 80.2% were White, 10.6% were Black, 9.2% were other).

In total, the 12 potentially modifiable risk factors used in the researchers’ model were associated with an estimated 62.4% of dementia cases in the United States, with hypertension as the most prevalent risk factor with the highest weighted PAF.
 

A new focus for prevention

Commenting for this article, Suzann Pershing, MD, associate professor of ophthalmology, Stanford (Calif.) University, called the study “particularly important because, despite growing recognition of its importance in relation to cognition, visual impairment is often an underrecognized risk factor.”

The current research “builds on increasingly robust medical literature linking visual impairment and dementia, applying analogous methods to those used for the life course model recently presented by the Lancet Commission to evaluate potentially modifiable dementia risk factors,” said Dr. Pershing, who was not involved with the study.

The investigators “make a compelling argument for inclusion of visual impairment as one of the potentially modifiable risk factors; practicing clinicians and health care systems may consider screening and targeted therapies to address visual impairment, with a goal of population health and contributing to a reduction in future dementia disease burden,” she added.

In an accompanying editorial), Jennifer Deal, PhD, department of epidemiology and Cochlear Center for Hearing and Public Health, Baltimore, and Julio Rojas, MD, PhD, Memory and Aging Center, department of neurology, Weill Institute for Neurosciences, University of California, San Francisco, call the findings “an important reminder that dementia is a social problem in which potentially treatable risk factors, including visual impairment, are highly prevalent in disadvantaged populations.”

The editorialists noted that 90% of cases of vision impairment are “preventable or have yet to be treated. The two “highly cost-effective interventions” of eyeglasses and/or cataract surgery “remain underused both in the U.S. and globally, especially in disadvantaged communities,” they wrote.

They added that more research is needed to “test the effectiveness of interventions to preserve cognitive health by promoting healthy vision.”

The study was supported by grants from the National Institute on Aging, the National Institutes of Health, and Research to Prevent Blindness. The investigators reported no relevant financial relationships. Dr. Deal reported having received grants from the National Institute on Aging. Dr. Rojas reported serving as site principal investigator on clinical trials for Eli Lilly and Eisai and receiving grants from the National Institute on Aging. Dr. Pershing is a consultant for Acumen, and Verana Health (as DigiSight Technologies).

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

Impaired vision in older adults is an underrecognized and modifiable dementia risk factor, new research suggests.

Investigators analyzed estimated population attributable fractions (PAFs) associated with dementia in more than 16,000 older adults. A PAF represents the number of dementia cases that could be prevented if a given risk factor were eliminated.

Results showed the PAF of vision impairment was 1.8%, suggesting that healthy vision had the potential to prevent more than 100,000 cases of dementia in the United States.

“Vision impairment and blindness disproportionately impact older adults, yet vision impairment is often preventable or even correctable,” study investigator Joshua Ehrlich MD, assistant professor of ophthalmology and visual sciences, University of Michigan, Ann Arbor, said in an interview.

Poor vision affects not only how individuals see the world, but also their systemic health and well-being, Dr. Ehrlich said.

“Accordingly, ensuring that older adults receive appropriate eye care is vital to promoting health, independence, and optimal aging,” he added.

The findings were published online in JAMA Neurology.
 

A surprising omission

There is an “urgent need to identify modifiable risk factors for dementia that can be targeted with interventions to slow cognitive decline and prevent dementia,” the investigators wrote.

In 2020, the Lancet Commission report on dementia prevention, intervention, and care proposed a life-course model of 12 potentially modifiable dementia risk factors. This included lower educational level, hearing loss, traumatic brain injury, hypertension, excessive alcohol consumption, obesity, smoking, depression, social isolation, physical inactivity, diabetes, and air pollution.

Together, these factors are associated with about 40% of dementia cases worldwide, the report notes.

Vision impairment was not included in this model, “despite considerable evidence that it is associated with an elevated risk of incident dementia and that it may operate through the same pathways as hearing loss,” the current researchers wrote.

“We have known for some time that vision impairment is a risk factor for dementia [and] we also know that a very large fraction of vision impairment, possibly in excess of 80%, is avoidable or has simply yet to be addressed,” Dr. Ehrlich said.

He and his colleagues found it “surprising that vision impairment had been ignored in key models of modifiable dementia risk factors that are used to shape health policy and resource allocation.” They set out to demonstrate that, “in fact, vision impairment is just as influential as a number of other long accepted modifiable dementia risk factors.”

The investigators assessed data from the Health and Retirement Study (HRS), a panel study that surveys more than 20,000 U.S. adults aged 50 years or older every 2 years.

The investigators applied the same methods used by the Lancet Commission to the HRS dataset and added vision impairment to the Lancet life-course model. Air pollution was excluded in their model “because those data were not readily available in the HRS,” the researchers wrote.

They noted the PAF is “based on the population prevalence and relative risk of dementia for each risk factor” and is “weighted, based on a principal components analysis, to account for communality (clustering of risk factors).”
 

A missed prevention opportunity

The sample included 16,690 participants (54% were women, 51.5% were at least age 65, 80.2% were White, 10.6% were Black, 9.2% were other).

In total, the 12 potentially modifiable risk factors used in the researchers’ model were associated with an estimated 62.4% of dementia cases in the United States, with hypertension as the most prevalent risk factor with the highest weighted PAF.
 

A new focus for prevention

Commenting for this article, Suzann Pershing, MD, associate professor of ophthalmology, Stanford (Calif.) University, called the study “particularly important because, despite growing recognition of its importance in relation to cognition, visual impairment is often an underrecognized risk factor.”

The current research “builds on increasingly robust medical literature linking visual impairment and dementia, applying analogous methods to those used for the life course model recently presented by the Lancet Commission to evaluate potentially modifiable dementia risk factors,” said Dr. Pershing, who was not involved with the study.

The investigators “make a compelling argument for inclusion of visual impairment as one of the potentially modifiable risk factors; practicing clinicians and health care systems may consider screening and targeted therapies to address visual impairment, with a goal of population health and contributing to a reduction in future dementia disease burden,” she added.

In an accompanying editorial), Jennifer Deal, PhD, department of epidemiology and Cochlear Center for Hearing and Public Health, Baltimore, and Julio Rojas, MD, PhD, Memory and Aging Center, department of neurology, Weill Institute for Neurosciences, University of California, San Francisco, call the findings “an important reminder that dementia is a social problem in which potentially treatable risk factors, including visual impairment, are highly prevalent in disadvantaged populations.”

The editorialists noted that 90% of cases of vision impairment are “preventable or have yet to be treated. The two “highly cost-effective interventions” of eyeglasses and/or cataract surgery “remain underused both in the U.S. and globally, especially in disadvantaged communities,” they wrote.

They added that more research is needed to “test the effectiveness of interventions to preserve cognitive health by promoting healthy vision.”

The study was supported by grants from the National Institute on Aging, the National Institutes of Health, and Research to Prevent Blindness. The investigators reported no relevant financial relationships. Dr. Deal reported having received grants from the National Institute on Aging. Dr. Rojas reported serving as site principal investigator on clinical trials for Eli Lilly and Eisai and receiving grants from the National Institute on Aging. Dr. Pershing is a consultant for Acumen, and Verana Health (as DigiSight Technologies).

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

Fat shaming doesn’t work. If it did, obesity as we know it wouldn’t exist because if the one thing society ensures isn’t lacking for people with obesity, it’s shame. We know that fat shaming doesn’t lead to weight loss and that it’s actually correlated with weight gain: More shame leads to more gain (Puhl and Suh; Sutin and Terracciano; Tomiyama et al).

Shaming and weight stigma have far more concerning associations than weight gain. People who report experiencing more weight stigma have an increased risk for depression, anxiety, low self-esteem, poor body image, substance abuse, suicidality, unhealthy eating behaviors, disordered eating, increased caloric intake, exercise avoidance, decreased exercise motivation potentially due to heightened cortisol reactivity, elevated C-reactive protein, and elevated blood pressure.

Meanwhile, people with obesity – likely in part owing to negative weight-biased experiences in health care – are reluctant to discuss weight with their health care providers and are less likely to seek care at all for any conditions. When care is sought, people with obesity are more likely to receive substandard treatment, including receiving fewer preventive health screenings, decreased health education, and decreased time spent in appointments.
 

Remember that obesity is not a conscious choice

A fact that is conveniently forgotten by those who are most prone to fat shaming is that obesity, like every chronic noncommunicable disease, isn’t a choice that is consciously made by patients.

And yes, though there are lifestyle means that might affect weight, there are lifestyle means that might affect all chronic diseases – yet obesity is the only one we seem to moralize about. It’s also worth noting that other chronic diseases’ lifestyle levers tend not to be governed by thousands of genes and dozens of hormones; those trying to “lifestyle” their way out of obesity are swimming against strong physiologic currents that influence our most seminally important survival drive: eating.

But forgetting about physiologic currents, there is also staggering privilege associated with intentional perpetual behavior change around food and fitness in the name of health.

Whereas medicine and the world are right and quick to embrace the fights against racism, sexism, and homophobia, the push to confront weight bias is far rarer, despite the fact that it’s been shown to be rampant among health care professionals.
 

Protecting the rights of people with obesity

Perhaps though, times are changing. Movements are popping up to protect the rights of people with obesity while combating hate.

Of note, Brazil seems to have embraced a campaign to fight gordofobia — the Portuguese term used to describe weight-based discrimination. For instance, laws are being passed to ensure appropriate seating is supplied in schools for children with obesity, an annual day was formalized to promote the rights of people with obesity, preferential seating is provided on subways for people with obesity, and fines have been levied against at least one comedian for making fat jokes on the grounds of the state’s duty to protect minorities.

We need to take this fight to medicine. Given the incredibly depressing prevalence of weight bias among trainees, medical schools and residency programs should ensure countering weight bias is not only part of the curriculum but that it’s explicitly examined. National medical licensing examinations should include weight bias as well.

Though we’re closer than ever before to widely effective treatment options for obesity, it’s likely to still be decades before pharmaceutical options to treat obesity are as effective, accepted, and encouraged as medications to treat hypertension, dyslipidemia, diabetes, and more are today.

If you’re curious about your own implicit weight biases, consider taking Harvard’s Implicit Association Test for Weight. You might also want to take a few moments and review the Strategies to Overcome and Prevent Obesity Alliances’ Weight Can’t Wait guide for advice on the management of obesity in primary care.

Treat patients with obesity the same as you would those with any chronic condition.

Also, consider your physical office space. Do you have chairs suitable for patients with obesity (wide base and with arms to help patients rise)? A scale that measures up to high weights that’s in a private location? Appropriately sized blood pressure cuffs?

If not, do you know who is deserving of shame?

Doctors who fat shame or who treat patients with obesity differently than they would any other patient with a chronic medical condition.

Examples include the family doctor who hadn’t checked my patient’s blood pressure in over a decade because he couldn’t be bothered buying an appropriately sized blood pressure cuff. Or the fertility doctor who told one of my patients that perhaps her weight reflected God’s will that she does not have children.

Finally, if reading this article about treating people with obesity the same as you would patients with other chronic, noncommunicable, lifestyle responsive diseases made you angry, there’s a great chance that you’re part of the problem.
 

Dr. Freedhoff, is associate professor of family medicine at the University of Ottawa and medical director of the Bariatric Medical Institute, a nonsurgical weight management center. He is one of Canada’s most outspoken obesity experts and the author of The Diet Fix: Why Diets Fail and How to Make Yours Work. He has disclosed the following: He served as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; has received research grant from Novo Nordisk, and has publicly shared opinions via Weighty Matters and social media. A version of this article first appeared on Medscape.com.

Fat shaming doesn’t work. If it did, obesity as we know it wouldn’t exist because if the one thing society ensures isn’t lacking for people with obesity, it’s shame. We know that fat shaming doesn’t lead to weight loss and that it’s actually correlated with weight gain: More shame leads to more gain (Puhl and Suh; Sutin and Terracciano; Tomiyama et al).

Shaming and weight stigma have far more concerning associations than weight gain. People who report experiencing more weight stigma have an increased risk for depression, anxiety, low self-esteem, poor body image, substance abuse, suicidality, unhealthy eating behaviors, disordered eating, increased caloric intake, exercise avoidance, decreased exercise motivation potentially due to heightened cortisol reactivity, elevated C-reactive protein, and elevated blood pressure.

Meanwhile, people with obesity – likely in part owing to negative weight-biased experiences in health care – are reluctant to discuss weight with their health care providers and are less likely to seek care at all for any conditions. When care is sought, people with obesity are more likely to receive substandard treatment, including receiving fewer preventive health screenings, decreased health education, and decreased time spent in appointments.
 

Remember that obesity is not a conscious choice

A fact that is conveniently forgotten by those who are most prone to fat shaming is that obesity, like every chronic noncommunicable disease, isn’t a choice that is consciously made by patients.

And yes, though there are lifestyle means that might affect weight, there are lifestyle means that might affect all chronic diseases – yet obesity is the only one we seem to moralize about. It’s also worth noting that other chronic diseases’ lifestyle levers tend not to be governed by thousands of genes and dozens of hormones; those trying to “lifestyle” their way out of obesity are swimming against strong physiologic currents that influence our most seminally important survival drive: eating.

But forgetting about physiologic currents, there is also staggering privilege associated with intentional perpetual behavior change around food and fitness in the name of health.

Whereas medicine and the world are right and quick to embrace the fights against racism, sexism, and homophobia, the push to confront weight bias is far rarer, despite the fact that it’s been shown to be rampant among health care professionals.
 

Protecting the rights of people with obesity

Perhaps though, times are changing. Movements are popping up to protect the rights of people with obesity while combating hate.

Of note, Brazil seems to have embraced a campaign to fight gordofobia — the Portuguese term used to describe weight-based discrimination. For instance, laws are being passed to ensure appropriate seating is supplied in schools for children with obesity, an annual day was formalized to promote the rights of people with obesity, preferential seating is provided on subways for people with obesity, and fines have been levied against at least one comedian for making fat jokes on the grounds of the state’s duty to protect minorities.

We need to take this fight to medicine. Given the incredibly depressing prevalence of weight bias among trainees, medical schools and residency programs should ensure countering weight bias is not only part of the curriculum but that it’s explicitly examined. National medical licensing examinations should include weight bias as well.

Though we’re closer than ever before to widely effective treatment options for obesity, it’s likely to still be decades before pharmaceutical options to treat obesity are as effective, accepted, and encouraged as medications to treat hypertension, dyslipidemia, diabetes, and more are today.

If you’re curious about your own implicit weight biases, consider taking Harvard’s Implicit Association Test for Weight. You might also want to take a few moments and review the Strategies to Overcome and Prevent Obesity Alliances’ Weight Can’t Wait guide for advice on the management of obesity in primary care.

Treat patients with obesity the same as you would those with any chronic condition.

Also, consider your physical office space. Do you have chairs suitable for patients with obesity (wide base and with arms to help patients rise)? A scale that measures up to high weights that’s in a private location? Appropriately sized blood pressure cuffs?

If not, do you know who is deserving of shame?

Doctors who fat shame or who treat patients with obesity differently than they would any other patient with a chronic medical condition.

Examples include the family doctor who hadn’t checked my patient’s blood pressure in over a decade because he couldn’t be bothered buying an appropriately sized blood pressure cuff. Or the fertility doctor who told one of my patients that perhaps her weight reflected God’s will that she does not have children.

Finally, if reading this article about treating people with obesity the same as you would patients with other chronic, noncommunicable, lifestyle responsive diseases made you angry, there’s a great chance that you’re part of the problem.
 

Dr. Freedhoff, is associate professor of family medicine at the University of Ottawa and medical director of the Bariatric Medical Institute, a nonsurgical weight management center. He is one of Canada’s most outspoken obesity experts and the author of The Diet Fix: Why Diets Fail and How to Make Yours Work. He has disclosed the following: He served as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; has received research grant from Novo Nordisk, and has publicly shared opinions via Weighty Matters and social media. A version of this article first appeared on Medscape.com.

Fat shaming doesn’t work. If it did, obesity as we know it wouldn’t exist because if the one thing society ensures isn’t lacking for people with obesity, it’s shame. We know that fat shaming doesn’t lead to weight loss and that it’s actually correlated with weight gain: More shame leads to more gain (Puhl and Suh; Sutin and Terracciano; Tomiyama et al).

Shaming and weight stigma have far more concerning associations than weight gain. People who report experiencing more weight stigma have an increased risk for depression, anxiety, low self-esteem, poor body image, substance abuse, suicidality, unhealthy eating behaviors, disordered eating, increased caloric intake, exercise avoidance, decreased exercise motivation potentially due to heightened cortisol reactivity, elevated C-reactive protein, and elevated blood pressure.

Meanwhile, people with obesity – likely in part owing to negative weight-biased experiences in health care – are reluctant to discuss weight with their health care providers and are less likely to seek care at all for any conditions. When care is sought, people with obesity are more likely to receive substandard treatment, including receiving fewer preventive health screenings, decreased health education, and decreased time spent in appointments.
 

Remember that obesity is not a conscious choice

A fact that is conveniently forgotten by those who are most prone to fat shaming is that obesity, like every chronic noncommunicable disease, isn’t a choice that is consciously made by patients.

And yes, though there are lifestyle means that might affect weight, there are lifestyle means that might affect all chronic diseases – yet obesity is the only one we seem to moralize about. It’s also worth noting that other chronic diseases’ lifestyle levers tend not to be governed by thousands of genes and dozens of hormones; those trying to “lifestyle” their way out of obesity are swimming against strong physiologic currents that influence our most seminally important survival drive: eating.

But forgetting about physiologic currents, there is also staggering privilege associated with intentional perpetual behavior change around food and fitness in the name of health.

Whereas medicine and the world are right and quick to embrace the fights against racism, sexism, and homophobia, the push to confront weight bias is far rarer, despite the fact that it’s been shown to be rampant among health care professionals.
 

Protecting the rights of people with obesity

Perhaps though, times are changing. Movements are popping up to protect the rights of people with obesity while combating hate.

Of note, Brazil seems to have embraced a campaign to fight gordofobia — the Portuguese term used to describe weight-based discrimination. For instance, laws are being passed to ensure appropriate seating is supplied in schools for children with obesity, an annual day was formalized to promote the rights of people with obesity, preferential seating is provided on subways for people with obesity, and fines have been levied against at least one comedian for making fat jokes on the grounds of the state’s duty to protect minorities.

We need to take this fight to medicine. Given the incredibly depressing prevalence of weight bias among trainees, medical schools and residency programs should ensure countering weight bias is not only part of the curriculum but that it’s explicitly examined. National medical licensing examinations should include weight bias as well.

Though we’re closer than ever before to widely effective treatment options for obesity, it’s likely to still be decades before pharmaceutical options to treat obesity are as effective, accepted, and encouraged as medications to treat hypertension, dyslipidemia, diabetes, and more are today.

If you’re curious about your own implicit weight biases, consider taking Harvard’s Implicit Association Test for Weight. You might also want to take a few moments and review the Strategies to Overcome and Prevent Obesity Alliances’ Weight Can’t Wait guide for advice on the management of obesity in primary care.

Treat patients with obesity the same as you would those with any chronic condition.

Also, consider your physical office space. Do you have chairs suitable for patients with obesity (wide base and with arms to help patients rise)? A scale that measures up to high weights that’s in a private location? Appropriately sized blood pressure cuffs?

If not, do you know who is deserving of shame?

Doctors who fat shame or who treat patients with obesity differently than they would any other patient with a chronic medical condition.

Examples include the family doctor who hadn’t checked my patient’s blood pressure in over a decade because he couldn’t be bothered buying an appropriately sized blood pressure cuff. Or the fertility doctor who told one of my patients that perhaps her weight reflected God’s will that she does not have children.

Finally, if reading this article about treating people with obesity the same as you would patients with other chronic, noncommunicable, lifestyle responsive diseases made you angry, there’s a great chance that you’re part of the problem.
 

Dr. Freedhoff, is associate professor of family medicine at the University of Ottawa and medical director of the Bariatric Medical Institute, a nonsurgical weight management center. He is one of Canada’s most outspoken obesity experts and the author of The Diet Fix: Why Diets Fail and How to Make Yours Work. He has disclosed the following: He served as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; has received research grant from Novo Nordisk, and has publicly shared opinions via Weighty Matters and social media. A version of this article first appeared on Medscape.com.

Women with systemic lupus erythematosus (SLE) experience worse outcomes after an acute stroke than does the general population, but men with SLE do not, according to an analysis of the U.S. National Inpatient Sample presented at the annual meeting of the British Society for Rheumatology.

In a study of more than 1.5 million cases of acute stroke recorded in the United States between 2015 and 2018, women with SLE were more likely to be hospitalized for longer and less likely to be routinely discharged into their home environment than were those without SLE. No such association was found for men with SLE.

“The findings imply that primary stroke prevention is of utmost importance, especially in females with SLE,” said Sona Jesenakova, a fourth-year medical student at the University of Aberdeen (Scotland).

“There might be a need to explore more effective and targeted treatment strategies to try and minimize these excessive adverse acute stroke outcomes, especially in females with SLE suffering from stroke,” she suggested.

“Even though males form only a minority of the SLE patient population, some studies have shown that they are prone to suffer from worse disease outcomes,” Ms. Jesenakova said.

Importantly, “male sex has been identified as a risk factor for death early in the course of SLE,” she added, highlighting that sex differences do seem to exist in SLE.

Stroke is an important outcome to look at because people with SLE are known to be at higher risk for developing atherosclerosis, which is a widely known risk factor for ischemic stroke, and with antiphospholipid antibody positivity and uncontrolled disease activity, that risk can be increased. A meta-analysis of older studies has suggested that the risk for death after a stroke is 68% higher in people with SLE than in those without.

To examine the risk for death and other in-hospital outcomes in a more contemporary population, Ms. Jesenakova and associates used data from the National Inpatient Sample, a large, publicly available database that contains inpatient health care information from across the United States. Their sample population consisted of 1,581,430 individuals who had been hospitalized for stroke. Of these, there were 6,100 women and 940 men who had SLE; the remainder served as the ‘no-SLE’ control population.

As might be expected, patients with SLE were about 10 years younger than those without SLE; the median age of women and men with SLE and those without SLE were a respective 60, 61, and 71 years.

There was no difference in the type of stroke between the SLE and no-SLE groups; most had an ischemic stroke (around 89%) rather than a hemorrhagic stroke (around 11%).

The researchers analyzed three key outcomes: mortality at discharge, hospitalization prolonged to a stay of more than 4 days, and routine home discharge, meaning that the patient was able to be discharged home versus more specialist facilities such as a nursing home.

They conducted a multivariate analysis with adjustments made for potential confounding factors such as age, ethnicity, type of stroke, and revascularization treatment. Comorbidities, including major cardiovascular disease, were also accounted for.

Although women with SLE were 21% more likely to die than patients without SLE, men with SLE were 24% less likely to die than was the no-SLE population. However, these differences were not statistically significant.

Women with SLE were 20% more likely to have a prolonged hospital stay and 28% less likely to have a routine home discharge, compared with patients who did not have SLE. The 95% confidence intervals were statistically significant, which was not seen when comparing the same outcomes in men with SLE (odds ratios of 1.06 and 1.18, respectively).

“As for males, even though we didn’t find anything of statistical significance, we have to bear in mind that the sample we had was quite small, and thus these results need to be interpreted with caution,” Ms. Jesenakova said. “We also think that we identified a gap in the current knowledge, and as such, further research is needed to help us understand the influence of male sex on acute stroke outcomes in patients with comorbid SLE.”

The researchers performed a secondary analysis looking at the use of revascularization treatments for ischemic stroke and found that there were no differences between individuals with and without SLE. This analysis considered the use of intravenous thrombolysis and endovascular thrombectomy in just over 1.4 million cases but did not look at sex-specific differences.

Ms. Jesenakova had no conflicts of interest to disclose.

Women with systemic lupus erythematosus (SLE) experience worse outcomes after an acute stroke than does the general population, but men with SLE do not, according to an analysis of the U.S. National Inpatient Sample presented at the annual meeting of the British Society for Rheumatology.

In a study of more than 1.5 million cases of acute stroke recorded in the United States between 2015 and 2018, women with SLE were more likely to be hospitalized for longer and less likely to be routinely discharged into their home environment than were those without SLE. No such association was found for men with SLE.

“The findings imply that primary stroke prevention is of utmost importance, especially in females with SLE,” said Sona Jesenakova, a fourth-year medical student at the University of Aberdeen (Scotland).

“There might be a need to explore more effective and targeted treatment strategies to try and minimize these excessive adverse acute stroke outcomes, especially in females with SLE suffering from stroke,” she suggested.

“Even though males form only a minority of the SLE patient population, some studies have shown that they are prone to suffer from worse disease outcomes,” Ms. Jesenakova said.

Importantly, “male sex has been identified as a risk factor for death early in the course of SLE,” she added, highlighting that sex differences do seem to exist in SLE.

Stroke is an important outcome to look at because people with SLE are known to be at higher risk for developing atherosclerosis, which is a widely known risk factor for ischemic stroke, and with antiphospholipid antibody positivity and uncontrolled disease activity, that risk can be increased. A meta-analysis of older studies has suggested that the risk for death after a stroke is 68% higher in people with SLE than in those without.

To examine the risk for death and other in-hospital outcomes in a more contemporary population, Ms. Jesenakova and associates used data from the National Inpatient Sample, a large, publicly available database that contains inpatient health care information from across the United States. Their sample population consisted of 1,581,430 individuals who had been hospitalized for stroke. Of these, there were 6,100 women and 940 men who had SLE; the remainder served as the ‘no-SLE’ control population.

As might be expected, patients with SLE were about 10 years younger than those without SLE; the median age of women and men with SLE and those without SLE were a respective 60, 61, and 71 years.

There was no difference in the type of stroke between the SLE and no-SLE groups; most had an ischemic stroke (around 89%) rather than a hemorrhagic stroke (around 11%).

The researchers analyzed three key outcomes: mortality at discharge, hospitalization prolonged to a stay of more than 4 days, and routine home discharge, meaning that the patient was able to be discharged home versus more specialist facilities such as a nursing home.

They conducted a multivariate analysis with adjustments made for potential confounding factors such as age, ethnicity, type of stroke, and revascularization treatment. Comorbidities, including major cardiovascular disease, were also accounted for.

Although women with SLE were 21% more likely to die than patients without SLE, men with SLE were 24% less likely to die than was the no-SLE population. However, these differences were not statistically significant.

Women with SLE were 20% more likely to have a prolonged hospital stay and 28% less likely to have a routine home discharge, compared with patients who did not have SLE. The 95% confidence intervals were statistically significant, which was not seen when comparing the same outcomes in men with SLE (odds ratios of 1.06 and 1.18, respectively).

“As for males, even though we didn’t find anything of statistical significance, we have to bear in mind that the sample we had was quite small, and thus these results need to be interpreted with caution,” Ms. Jesenakova said. “We also think that we identified a gap in the current knowledge, and as such, further research is needed to help us understand the influence of male sex on acute stroke outcomes in patients with comorbid SLE.”

The researchers performed a secondary analysis looking at the use of revascularization treatments for ischemic stroke and found that there were no differences between individuals with and without SLE. This analysis considered the use of intravenous thrombolysis and endovascular thrombectomy in just over 1.4 million cases but did not look at sex-specific differences.

Ms. Jesenakova had no conflicts of interest to disclose.

Women with systemic lupus erythematosus (SLE) experience worse outcomes after an acute stroke than does the general population, but men with SLE do not, according to an analysis of the U.S. National Inpatient Sample presented at the annual meeting of the British Society for Rheumatology.

In a study of more than 1.5 million cases of acute stroke recorded in the United States between 2015 and 2018, women with SLE were more likely to be hospitalized for longer and less likely to be routinely discharged into their home environment than were those without SLE. No such association was found for men with SLE.

“The findings imply that primary stroke prevention is of utmost importance, especially in females with SLE,” said Sona Jesenakova, a fourth-year medical student at the University of Aberdeen (Scotland).

“There might be a need to explore more effective and targeted treatment strategies to try and minimize these excessive adverse acute stroke outcomes, especially in females with SLE suffering from stroke,” she suggested.

“Even though males form only a minority of the SLE patient population, some studies have shown that they are prone to suffer from worse disease outcomes,” Ms. Jesenakova said.

Importantly, “male sex has been identified as a risk factor for death early in the course of SLE,” she added, highlighting that sex differences do seem to exist in SLE.

Stroke is an important outcome to look at because people with SLE are known to be at higher risk for developing atherosclerosis, which is a widely known risk factor for ischemic stroke, and with antiphospholipid antibody positivity and uncontrolled disease activity, that risk can be increased. A meta-analysis of older studies has suggested that the risk for death after a stroke is 68% higher in people with SLE than in those without.

To examine the risk for death and other in-hospital outcomes in a more contemporary population, Ms. Jesenakova and associates used data from the National Inpatient Sample, a large, publicly available database that contains inpatient health care information from across the United States. Their sample population consisted of 1,581,430 individuals who had been hospitalized for stroke. Of these, there were 6,100 women and 940 men who had SLE; the remainder served as the ‘no-SLE’ control population.

As might be expected, patients with SLE were about 10 years younger than those without SLE; the median age of women and men with SLE and those without SLE were a respective 60, 61, and 71 years.

There was no difference in the type of stroke between the SLE and no-SLE groups; most had an ischemic stroke (around 89%) rather than a hemorrhagic stroke (around 11%).

The researchers analyzed three key outcomes: mortality at discharge, hospitalization prolonged to a stay of more than 4 days, and routine home discharge, meaning that the patient was able to be discharged home versus more specialist facilities such as a nursing home.

They conducted a multivariate analysis with adjustments made for potential confounding factors such as age, ethnicity, type of stroke, and revascularization treatment. Comorbidities, including major cardiovascular disease, were also accounted for.

Although women with SLE were 21% more likely to die than patients without SLE, men with SLE were 24% less likely to die than was the no-SLE population. However, these differences were not statistically significant.

Women with SLE were 20% more likely to have a prolonged hospital stay and 28% less likely to have a routine home discharge, compared with patients who did not have SLE. The 95% confidence intervals were statistically significant, which was not seen when comparing the same outcomes in men with SLE (odds ratios of 1.06 and 1.18, respectively).

“As for males, even though we didn’t find anything of statistical significance, we have to bear in mind that the sample we had was quite small, and thus these results need to be interpreted with caution,” Ms. Jesenakova said. “We also think that we identified a gap in the current knowledge, and as such, further research is needed to help us understand the influence of male sex on acute stroke outcomes in patients with comorbid SLE.”

The researchers performed a secondary analysis looking at the use of revascularization treatments for ischemic stroke and found that there were no differences between individuals with and without SLE. This analysis considered the use of intravenous thrombolysis and endovascular thrombectomy in just over 1.4 million cases but did not look at sex-specific differences.

Ms. Jesenakova had no conflicts of interest to disclose.

This video transcript has been edited for clarity.

Andrew N. Wilner, MD: Welcome to Medscape. I’m Dr Andrew Wilner, reporting from the American Epilepsy Society meeting.

Today, I have the pleasure of speaking with Dr. Chethan Rao, a child and adolescent neurology resident from the Mayo Clinic in Jacksonville, Fla. Dr. Rao has a particular interest in pediatric epilepsy. Welcome, Dr. Rao.

Chethan Rao, DO: Thank you, Dr. Wilner. It’s a pleasure to be here, and thanks for taking the time to highlight our work.

Dr. Wilner: You had a very interesting paper at the meeting that I wanted to talk about, focused on infantile spasms and smartphone video. Before we dive into the paper, tell us: What are infantile spasms, and why is it important to diagnose them early?

Dr. Rao: Infantile spasms, also known as epileptic spasms, are 1- to 2-second seizures, and they typically consist of sudden stiffening of the body with brief bending forward or backward of the arms, legs, and head. They usually happen around age 3-8 months, and they typically occur in clusters, most often after awakening from sleep.

The incidence is about 1 in 2,000-3,000 children. Many kids with spasms go on to develop seizures that are very difficult to treat, like Lennox-Gastaut epilepsy, and many go on to have developmental delays as well.

Dr. Wilner: Are these subtle? In other words, could a parent have a child like that and not really recognize that this is something abnormal? Or are they so dramatic that parents say: “We’re going to the emergency room?”

Dr. Rao: One of the problems that we encounter often is that in this age group of infants, they have benign sleep myoclonus; they have Sandifer syndrome related to reflux. Those can be very difficult mimics of spasms. They’re not the most clear-cut, but they look usually different enough from normal baby movements that they get parents to seek medical attention.

Dr. Wilner: You mentioned that the infantile spasms really are a type of epilepsy and symptomatic, usually, of some underlying neurologic condition. Why is it so important to diagnose them early?

Dr. Rao: Great question. Many studies have looked at developmental outcomes based on when spasms were diagnosed and treated, and all of them have replicated time over time that the earlier you get to treatment for the spasms, the better the outcomes are for seizure control and for development.

For this reason, infantile spasm is considered a neurologic urgency in our world. Like I said, accurate diagnosis is often complicated by these potential mimics. Prompt EEG is one of the most important things for confirmation of diagnosis.

Dr. Wilner: But to get that EEG, it has to get all the way to the neurologist, right? It’s not something they’re going to do in the ER. I saw a statistic: There are millions, if not billions, of smartphones out there. Where does the smartphone come in?

Dr. Rao: Absolutely. One of the things that we have on our side these days is that almost everyone has a smartphone at their disposal. One of the recent polls in 2021 showed that more than 95% of adults of childbearing age have smartphones with video access. As some other studies have shown in the adult world, we all really have an epilepsy monitoring unit minus the EEG in our own pockets.

It’s definitely a useful tool, as that first screening video can be used in adjunct to history and physical. There have been many of studies on the adult epilepsy side showing the predictive value of smartphone video for differentiating things like epileptic seizures and nonepileptic spells. What we wanted to do is use smartphone video to pin the diagnosis early of infantile spasms and get it treated as quickly as possible.

Dr. Wilner: I’m a fan. Every now and then, I do have a patient who brings in a video of some spell. I’m an adult neurologist. The patient had a spell, and you ask them – of course they don’t remember – and you ask the witness, who usually is not a trained observer. There have been one or two occasions where I thought: “Well, I don’t know if that was really a seizure.” Then they show me the video and it’s like, “Wow, that is definitely a convulsion.” A picture definitely can be worth a thousand words.

You studied this systematically for your poster. Tell me about what you did.

Dr. Rao: Since the poster, we’ve actually expanded the study, so I’ll give you the updated version. We looked at 101 infants retrospectively at two large children’s health care centers: Nemours Children’s, associated with Mayo Clinic in Jacksonville, Fla., and Texas Children’s Hospital in Houston. We narrowed it down to 80 patients whom we included. Of these, 43 had smartphone video capture when they first presented and 37 had no video when they first presented.

We found a 17-day difference by median in the time to diagnosis and treatment. In other words, the video group was diagnosed and treated 17 days by median, compared with the no-video group. Although 17 days may not sound like a big number, in this context it can make a huge difference. That’s been shown by one of these key studies in our field called the UK Infantile Spasms Study. The 2-week difference made about a 10-point difference on the developmental scale that they use – so pretty significant.

Dr. Wilner: Let me think about this for a minute. Was that because the parents brought the child in with their video and the doctor said, “Hey, that’s infantile spasms. Here’s your shot of ACTH [or whatever they’re using these days].” Or was it because the parents who were attentive enough to use video brought their kids in sooner?

Or was this the time from when they brought the child in to treatment? Is that the time you looked at? So it wasn’t just that these were more attentive parents and more likely to use the video – you’re looking at the time from presentation with or without video until treatment, is that right?

Dr. Rao: We looked to the time from the start of the spasms, as reported by the parents, to the time of diagnosis and then the start of spasms to the time of treatment. What you asked was a fantastic question. We wanted to know who these parents are who are taking videos versus the ones that are not.

We looked at the race/ethnicity data and socioeconomic status data. There were no significant differences between the video and nonvideo group. That would not explain the difference in our results here.

Dr. Wilner: Do you have plans to follow these approximately 40 children 5 years from now and see who’s riding a bicycle and who’s still stuck in the stroller? Is there going to be a difference?

Dr. Rao: Because time to diagnosis and time to treatment were our primary outcomes, long-term follow-up may not really help as much in this study. We did have a couple of other ideas for future studies. One that we wanted to look at was kids who have risk factors for developing spasms, such as trisomy 21, tuberous sclerosis, and congenital cortical malformations; those kids are at a much higher risk for developing spasms around 3-8 months of life.

In giving targeted counseling to those families about how they can use smartphone video to minimize the time to diagnosis and treatment, we think we may be able to learn more and maybe do that prospectively.

The other interesting idea is using artificial intelligence technology for spasm detection in some of these smartphone videos. They’re already using it for different seizure types. It could be an efficient first pass when we get a whole bunch of smartphone videos to determine which ones we need to pursue further steps – to see whether we need to get long-term EEG monitoring or not.

Dr. Wilner: As an epileptologist, I was going to say that we have smartphone EKG. All we need now is smartphone EEG, and then you’ll have all the information you need on day one. It may be a ways away.

As a bottom line, would it be fair to say that parents should not hesitate to take a video of any suspiciously abnormal behavior and bring it to their family doctor or pediatric neurologist?

Dr. Rao: Yes. I was happy to see the Tuberous Sclerosis Alliance put out a promotional video that had some steps for when parents see things that are suspicious for spasms, and they do recommend using smartphone video and promptly showing it to their doctors. I think the difference that we hope to provide in this study is that we can now quantify the effect of having that smartphone video when they first present.

My takeaway from this study that I would like to show is encouraging the use of smartphone video as an adjunct tool and for providers to ask for the videos, but also for these pediatric centers to develop an infrastructure – either a secure, monitored email address like we have at our center or a patient portal – where parents can submit video concerning for spasms.

Dr. Wilner: Save the trip to the doctor. Get that video out there first.

Dr. Rao: Especially in the pandemic world, right?

Dr. Wilner: Yes. I understand that you are a neurology resident. To wrap up, what’s the next step for you?

Dr. Rao: I’m finishing up my child neurology residency this year, and I’m moving out to Stanford for pediatric epilepsy fellowship. We’re preparing this project we’re talking about for submission soon, and we’re working on another project, which is a systematic review of genetic testing and the presurgical workup for pediatric drug-resistant focal epilepsy.

Dr. Wilner: Excellent. That’s pretty exciting. Good luck to you. I want to thank you very much for telling us about your research.

Dr. Rao: It was a pleasure speaking with you, and I look forward to the next time.

Dr. Wilner: I’m Dr Andrew Wilner, reporting for Medscape. Thanks for watching.

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

This video transcript has been edited for clarity.

Andrew N. Wilner, MD: Welcome to Medscape. I’m Dr Andrew Wilner, reporting from the American Epilepsy Society meeting.

Today, I have the pleasure of speaking with Dr. Chethan Rao, a child and adolescent neurology resident from the Mayo Clinic in Jacksonville, Fla. Dr. Rao has a particular interest in pediatric epilepsy. Welcome, Dr. Rao.

Chethan Rao, DO: Thank you, Dr. Wilner. It’s a pleasure to be here, and thanks for taking the time to highlight our work.

Dr. Wilner: You had a very interesting paper at the meeting that I wanted to talk about, focused on infantile spasms and smartphone video. Before we dive into the paper, tell us: What are infantile spasms, and why is it important to diagnose them early?

Dr. Rao: Infantile spasms, also known as epileptic spasms, are 1- to 2-second seizures, and they typically consist of sudden stiffening of the body with brief bending forward or backward of the arms, legs, and head. They usually happen around age 3-8 months, and they typically occur in clusters, most often after awakening from sleep.

The incidence is about 1 in 2,000-3,000 children. Many kids with spasms go on to develop seizures that are very difficult to treat, like Lennox-Gastaut epilepsy, and many go on to have developmental delays as well.

Dr. Wilner: Are these subtle? In other words, could a parent have a child like that and not really recognize that this is something abnormal? Or are they so dramatic that parents say: “We’re going to the emergency room?”

Dr. Rao: One of the problems that we encounter often is that in this age group of infants, they have benign sleep myoclonus; they have Sandifer syndrome related to reflux. Those can be very difficult mimics of spasms. They’re not the most clear-cut, but they look usually different enough from normal baby movements that they get parents to seek medical attention.

Dr. Wilner: You mentioned that the infantile spasms really are a type of epilepsy and symptomatic, usually, of some underlying neurologic condition. Why is it so important to diagnose them early?

Dr. Rao: Great question. Many studies have looked at developmental outcomes based on when spasms were diagnosed and treated, and all of them have replicated time over time that the earlier you get to treatment for the spasms, the better the outcomes are for seizure control and for development.

For this reason, infantile spasm is considered a neurologic urgency in our world. Like I said, accurate diagnosis is often complicated by these potential mimics. Prompt EEG is one of the most important things for confirmation of diagnosis.

Dr. Wilner: But to get that EEG, it has to get all the way to the neurologist, right? It’s not something they’re going to do in the ER. I saw a statistic: There are millions, if not billions, of smartphones out there. Where does the smartphone come in?

Dr. Rao: Absolutely. One of the things that we have on our side these days is that almost everyone has a smartphone at their disposal. One of the recent polls in 2021 showed that more than 95% of adults of childbearing age have smartphones with video access. As some other studies have shown in the adult world, we all really have an epilepsy monitoring unit minus the EEG in our own pockets.

It’s definitely a useful tool, as that first screening video can be used in adjunct to history and physical. There have been many of studies on the adult epilepsy side showing the predictive value of smartphone video for differentiating things like epileptic seizures and nonepileptic spells. What we wanted to do is use smartphone video to pin the diagnosis early of infantile spasms and get it treated as quickly as possible.

Dr. Wilner: I’m a fan. Every now and then, I do have a patient who brings in a video of some spell. I’m an adult neurologist. The patient had a spell, and you ask them – of course they don’t remember – and you ask the witness, who usually is not a trained observer. There have been one or two occasions where I thought: “Well, I don’t know if that was really a seizure.” Then they show me the video and it’s like, “Wow, that is definitely a convulsion.” A picture definitely can be worth a thousand words.

You studied this systematically for your poster. Tell me about what you did.

Dr. Rao: Since the poster, we’ve actually expanded the study, so I’ll give you the updated version. We looked at 101 infants retrospectively at two large children’s health care centers: Nemours Children’s, associated with Mayo Clinic in Jacksonville, Fla., and Texas Children’s Hospital in Houston. We narrowed it down to 80 patients whom we included. Of these, 43 had smartphone video capture when they first presented and 37 had no video when they first presented.

We found a 17-day difference by median in the time to diagnosis and treatment. In other words, the video group was diagnosed and treated 17 days by median, compared with the no-video group. Although 17 days may not sound like a big number, in this context it can make a huge difference. That’s been shown by one of these key studies in our field called the UK Infantile Spasms Study. The 2-week difference made about a 10-point difference on the developmental scale that they use – so pretty significant.

Dr. Wilner: Let me think about this for a minute. Was that because the parents brought the child in with their video and the doctor said, “Hey, that’s infantile spasms. Here’s your shot of ACTH [or whatever they’re using these days].” Or was it because the parents who were attentive enough to use video brought their kids in sooner?

Or was this the time from when they brought the child in to treatment? Is that the time you looked at? So it wasn’t just that these were more attentive parents and more likely to use the video – you’re looking at the time from presentation with or without video until treatment, is that right?

Dr. Rao: We looked to the time from the start of the spasms, as reported by the parents, to the time of diagnosis and then the start of spasms to the time of treatment. What you asked was a fantastic question. We wanted to know who these parents are who are taking videos versus the ones that are not.

We looked at the race/ethnicity data and socioeconomic status data. There were no significant differences between the video and nonvideo group. That would not explain the difference in our results here.

Dr. Wilner: Do you have plans to follow these approximately 40 children 5 years from now and see who’s riding a bicycle and who’s still stuck in the stroller? Is there going to be a difference?

Dr. Rao: Because time to diagnosis and time to treatment were our primary outcomes, long-term follow-up may not really help as much in this study. We did have a couple of other ideas for future studies. One that we wanted to look at was kids who have risk factors for developing spasms, such as trisomy 21, tuberous sclerosis, and congenital cortical malformations; those kids are at a much higher risk for developing spasms around 3-8 months of life.

In giving targeted counseling to those families about how they can use smartphone video to minimize the time to diagnosis and treatment, we think we may be able to learn more and maybe do that prospectively.

The other interesting idea is using artificial intelligence technology for spasm detection in some of these smartphone videos. They’re already using it for different seizure types. It could be an efficient first pass when we get a whole bunch of smartphone videos to determine which ones we need to pursue further steps – to see whether we need to get long-term EEG monitoring or not.

Dr. Wilner: As an epileptologist, I was going to say that we have smartphone EKG. All we need now is smartphone EEG, and then you’ll have all the information you need on day one. It may be a ways away.

As a bottom line, would it be fair to say that parents should not hesitate to take a video of any suspiciously abnormal behavior and bring it to their family doctor or pediatric neurologist?

Dr. Rao: Yes. I was happy to see the Tuberous Sclerosis Alliance put out a promotional video that had some steps for when parents see things that are suspicious for spasms, and they do recommend using smartphone video and promptly showing it to their doctors. I think the difference that we hope to provide in this study is that we can now quantify the effect of having that smartphone video when they first present.

My takeaway from this study that I would like to show is encouraging the use of smartphone video as an adjunct tool and for providers to ask for the videos, but also for these pediatric centers to develop an infrastructure – either a secure, monitored email address like we have at our center or a patient portal – where parents can submit video concerning for spasms.

Dr. Wilner: Save the trip to the doctor. Get that video out there first.

Dr. Rao: Especially in the pandemic world, right?

Dr. Wilner: Yes. I understand that you are a neurology resident. To wrap up, what’s the next step for you?

Dr. Rao: I’m finishing up my child neurology residency this year, and I’m moving out to Stanford for pediatric epilepsy fellowship. We’re preparing this project we’re talking about for submission soon, and we’re working on another project, which is a systematic review of genetic testing and the presurgical workup for pediatric drug-resistant focal epilepsy.

Dr. Wilner: Excellent. That’s pretty exciting. Good luck to you. I want to thank you very much for telling us about your research.

Dr. Rao: It was a pleasure speaking with you, and I look forward to the next time.

Dr. Wilner: I’m Dr Andrew Wilner, reporting for Medscape. Thanks for watching.

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

This video transcript has been edited for clarity.

Andrew N. Wilner, MD: Welcome to Medscape. I’m Dr Andrew Wilner, reporting from the American Epilepsy Society meeting.

Today, I have the pleasure of speaking with Dr. Chethan Rao, a child and adolescent neurology resident from the Mayo Clinic in Jacksonville, Fla. Dr. Rao has a particular interest in pediatric epilepsy. Welcome, Dr. Rao.

Chethan Rao, DO: Thank you, Dr. Wilner. It’s a pleasure to be here, and thanks for taking the time to highlight our work.

Dr. Wilner: You had a very interesting paper at the meeting that I wanted to talk about, focused on infantile spasms and smartphone video. Before we dive into the paper, tell us: What are infantile spasms, and why is it important to diagnose them early?

Dr. Rao: Infantile spasms, also known as epileptic spasms, are 1- to 2-second seizures, and they typically consist of sudden stiffening of the body with brief bending forward or backward of the arms, legs, and head. They usually happen around age 3-8 months, and they typically occur in clusters, most often after awakening from sleep.

The incidence is about 1 in 2,000-3,000 children. Many kids with spasms go on to develop seizures that are very difficult to treat, like Lennox-Gastaut epilepsy, and many go on to have developmental delays as well.

Dr. Wilner: Are these subtle? In other words, could a parent have a child like that and not really recognize that this is something abnormal? Or are they so dramatic that parents say: “We’re going to the emergency room?”

Dr. Rao: One of the problems that we encounter often is that in this age group of infants, they have benign sleep myoclonus; they have Sandifer syndrome related to reflux. Those can be very difficult mimics of spasms. They’re not the most clear-cut, but they look usually different enough from normal baby movements that they get parents to seek medical attention.

Dr. Wilner: You mentioned that the infantile spasms really are a type of epilepsy and symptomatic, usually, of some underlying neurologic condition. Why is it so important to diagnose them early?

Dr. Rao: Great question. Many studies have looked at developmental outcomes based on when spasms were diagnosed and treated, and all of them have replicated time over time that the earlier you get to treatment for the spasms, the better the outcomes are for seizure control and for development.

For this reason, infantile spasm is considered a neurologic urgency in our world. Like I said, accurate diagnosis is often complicated by these potential mimics. Prompt EEG is one of the most important things for confirmation of diagnosis.

Dr. Wilner: But to get that EEG, it has to get all the way to the neurologist, right? It’s not something they’re going to do in the ER. I saw a statistic: There are millions, if not billions, of smartphones out there. Where does the smartphone come in?

Dr. Rao: Absolutely. One of the things that we have on our side these days is that almost everyone has a smartphone at their disposal. One of the recent polls in 2021 showed that more than 95% of adults of childbearing age have smartphones with video access. As some other studies have shown in the adult world, we all really have an epilepsy monitoring unit minus the EEG in our own pockets.

It’s definitely a useful tool, as that first screening video can be used in adjunct to history and physical. There have been many of studies on the adult epilepsy side showing the predictive value of smartphone video for differentiating things like epileptic seizures and nonepileptic spells. What we wanted to do is use smartphone video to pin the diagnosis early of infantile spasms and get it treated as quickly as possible.

Dr. Wilner: I’m a fan. Every now and then, I do have a patient who brings in a video of some spell. I’m an adult neurologist. The patient had a spell, and you ask them – of course they don’t remember – and you ask the witness, who usually is not a trained observer. There have been one or two occasions where I thought: “Well, I don’t know if that was really a seizure.” Then they show me the video and it’s like, “Wow, that is definitely a convulsion.” A picture definitely can be worth a thousand words.

You studied this systematically for your poster. Tell me about what you did.

Dr. Rao: Since the poster, we’ve actually expanded the study, so I’ll give you the updated version. We looked at 101 infants retrospectively at two large children’s health care centers: Nemours Children’s, associated with Mayo Clinic in Jacksonville, Fla., and Texas Children’s Hospital in Houston. We narrowed it down to 80 patients whom we included. Of these, 43 had smartphone video capture when they first presented and 37 had no video when they first presented.

We found a 17-day difference by median in the time to diagnosis and treatment. In other words, the video group was diagnosed and treated 17 days by median, compared with the no-video group. Although 17 days may not sound like a big number, in this context it can make a huge difference. That’s been shown by one of these key studies in our field called the UK Infantile Spasms Study. The 2-week difference made about a 10-point difference on the developmental scale that they use – so pretty significant.

Dr. Wilner: Let me think about this for a minute. Was that because the parents brought the child in with their video and the doctor said, “Hey, that’s infantile spasms. Here’s your shot of ACTH [or whatever they’re using these days].” Or was it because the parents who were attentive enough to use video brought their kids in sooner?

Or was this the time from when they brought the child in to treatment? Is that the time you looked at? So it wasn’t just that these were more attentive parents and more likely to use the video – you’re looking at the time from presentation with or without video until treatment, is that right?

Dr. Rao: We looked to the time from the start of the spasms, as reported by the parents, to the time of diagnosis and then the start of spasms to the time of treatment. What you asked was a fantastic question. We wanted to know who these parents are who are taking videos versus the ones that are not.

We looked at the race/ethnicity data and socioeconomic status data. There were no significant differences between the video and nonvideo group. That would not explain the difference in our results here.

Dr. Wilner: Do you have plans to follow these approximately 40 children 5 years from now and see who’s riding a bicycle and who’s still stuck in the stroller? Is there going to be a difference?

Dr. Rao: Because time to diagnosis and time to treatment were our primary outcomes, long-term follow-up may not really help as much in this study. We did have a couple of other ideas for future studies. One that we wanted to look at was kids who have risk factors for developing spasms, such as trisomy 21, tuberous sclerosis, and congenital cortical malformations; those kids are at a much higher risk for developing spasms around 3-8 months of life.

In giving targeted counseling to those families about how they can use smartphone video to minimize the time to diagnosis and treatment, we think we may be able to learn more and maybe do that prospectively.

The other interesting idea is using artificial intelligence technology for spasm detection in some of these smartphone videos. They’re already using it for different seizure types. It could be an efficient first pass when we get a whole bunch of smartphone videos to determine which ones we need to pursue further steps – to see whether we need to get long-term EEG monitoring or not.

Dr. Wilner: As an epileptologist, I was going to say that we have smartphone EKG. All we need now is smartphone EEG, and then you’ll have all the information you need on day one. It may be a ways away.

As a bottom line, would it be fair to say that parents should not hesitate to take a video of any suspiciously abnormal behavior and bring it to their family doctor or pediatric neurologist?

Dr. Rao: Yes. I was happy to see the Tuberous Sclerosis Alliance put out a promotional video that had some steps for when parents see things that are suspicious for spasms, and they do recommend using smartphone video and promptly showing it to their doctors. I think the difference that we hope to provide in this study is that we can now quantify the effect of having that smartphone video when they first present.

My takeaway from this study that I would like to show is encouraging the use of smartphone video as an adjunct tool and for providers to ask for the videos, but also for these pediatric centers to develop an infrastructure – either a secure, monitored email address like we have at our center or a patient portal – where parents can submit video concerning for spasms.

Dr. Wilner: Save the trip to the doctor. Get that video out there first.

Dr. Rao: Especially in the pandemic world, right?

Dr. Wilner: Yes. I understand that you are a neurology resident. To wrap up, what’s the next step for you?

Dr. Rao: I’m finishing up my child neurology residency this year, and I’m moving out to Stanford for pediatric epilepsy fellowship. We’re preparing this project we’re talking about for submission soon, and we’re working on another project, which is a systematic review of genetic testing and the presurgical workup for pediatric drug-resistant focal epilepsy.

Dr. Wilner: Excellent. That’s pretty exciting. Good luck to you. I want to thank you very much for telling us about your research.

Dr. Rao: It was a pleasure speaking with you, and I look forward to the next time.

Dr. Wilner: I’m Dr Andrew Wilner, reporting for Medscape. Thanks for watching.

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

Air traffic controllers face mandatory retirement at age 56, with exceptions up to 61. Commercial airline pilots must bow out at 65; same for foreign service employees. Physicians, however, have no age limit, regardless of specialty.

That doesn’t mean the topic of “how old is too old” hasn’t been one of the profession’s most heated debates for many years now.

As the profession rapidly ages – some 30% of the physician workforce is currently a senior, according to the American Medical Association – the topic of whether or not there should be a standard measure or age for retirement is front and center. The AMA’s Council on Medical Education formed a workgroup to look into the issue in 2015 and 2018, and in 2021, delegates adopted a set of guidelines for screening and assessing physicians, but stopped short of a mandate.

Mark Katlic, MD, chair of surgery at Lifebridge Health System, Baltimore, has devoted a decade to studying this topic. “I’m a bit of an outlier looking into this,” he says. “The public is unaware and seemingly unconcerned about the issue. Even among the medical profession, there’s been a series of fits and starts to develop a cohesive approach.”

One of the reasons guidelines – mandatory or otherwise – have been tough to come by is that aging brings with it a huge degree of variability. “If you look at a group of 80-year-olds, there will be much more variability than within a group of 40-year-olds,” Dr. Katlic pointed out.

Indeed, some 80-year-olds can easily continue to teach college courses, keep up in 10K running races, or perform delicate surgeries. Yet others in their peer group might struggle to properly button a shirt, walk a flight of stairs, or remember yesterday’s meals. Functional age is not the same as chronological age.

Frank Stockdale, MD, PhD, an 86-year-old practicing oncologist at Stanford (Calif.) University Health, counts himself in the camp opposed to age-based assessments. “It’s age discrimination,” he says. “Physicians receive assessments throughout their careers as part of the accreditation process – there’s no need to change that as doctors reach a certain age.”

Dr. Stockdale suggests that in many cases, malpractice suits are filed against mid-career doctors, not those of advanced age. “If you’re using the argument that there is an accumulation of deficits with age, the fact is that those deficits begin well before your 70s,” he said. “It’s better to have a uniform screening policy and begin at a much younger age.”

At Stanford, in fact, there was a former assessment policy that included cognitive testing, but physicians were successful in seeing that portion of testing eliminated. “It is a physical examination, by a physician of choice, certifying that for the privileges requested there is no physical or mental reason the candidate cannot safely perform them,” Dr. Stockdale explained.

In some cases, medical staffs have filed lawsuits to fight age-related testing. In New Haven, Conn., for instance, the U.S. Equal Employment Opportunity Commission (EEOC) filed a suit in 2020 on behalf of the Yale New Haven Hospital staff, alleging a discriminatory “late career practitioner policy.”

A similar case in Minnesota reached a settlement in 2021, providing monetary relief to staff impacted by out-of-pocket costs for the assessment, in addition to requiring that the hospital in question report to the EEOC any complaints related to age discrimination.

James Ellison, MD, MPH, chair in Memory Care and Geriatrics with ChristianaCare in Wilmington, Del., points out that aging can bring benefits for practicing physicians. “Age is very individualized and there are good and bad consequences,” he said. “Experience can build knowledge and confidence and expertise, and it does improve diagnostic accuracy.”

On the flip side, however, age-related brain changes include loss of volume and lower levels of some neurotransmitters, resulting in cognitive changes. “Functional changes occur too,” Dr. Ellison said.

“Just as some aging athletes may lose a degree of speed, strength, and flexibility, and some aging scientists may lose a part of their former cognitive speed, flexibility, and mental strength, aging health care providers can lose some of the physical coordination, strength, and visual acuity necessary to perform demanding surgical operations. They can also lose some of the processing speed, working memory, and executive function that allows them to excel in cognitive professional tasks.”

An estimated 5.8 million Americans age 65 and older have Alzheimer’s dementia, according to the Alzheimer’s Association.

Picking an arbitrary age for mandatory retirement isn’t the right approach for physicians, said Dr. Katlic. Rather, he said, the answer is to establish late-practitioner screening programs. “Very few hospitals have them, however,” he pointed out. “We do [at Lifebridge Health], and so do a few dozen others, but that’s out of hundreds.”

Instead, what typically plays out is that hospital staff might begin to notice a decline in a colleague. Things like a disheveled appearance or lack of hygiene, or trouble with memory, such as getting lost en route back to his or her office. Even dangerous behaviors such as nodding off during a procedure are not unheard of.

There are many examples of physician decline that fly under the radar. “Unfortunately, it’s unusual for cognitively impaired health care providers to recognize and report their own difficulties,” said Dr. Ellison. “Although peers are expected to report cognitively impaired colleagues, they often fail to do so. In some other countries, age-based assessment is an accepted policy. In the U.S., this is not a uniform policy.”

Sometimes physicians can remain on the job in spite of decline thanks to certain “props,” according to Dr. Ellison. “Good procedures, efficient supports, and various workarounds compensate,” he said, “but often are not sufficient to maintain high-quality practice.”

Most often, these situations play out slowly, until the problem becomes glaringly obvious and potentially dangerous, and someone in a position of power must step in.

“Often, it’s hearsay from a nurse or another staff member, and then a hospital president or chief of staff must make a career-affecting decision for the doctor in question,” said Dr. Katlic.

Because there is little self- or colleague policing – and barring official or binding guidelines on the aging physician issue – both Dr. Katlic and Dr. Ellison are proponents of late-career screening.
 

How screening can help  

As it stands, Dr. Katlic maintains that the profession isn’t doing enough to ensure public safety. “We have peer review and recertification processes, but when you get down to it, we don’t police ourselves well,” he said. “All physicians are assessed throughout their careers as part of the hospital accreditation process, which is fair and adequate.”

Dr. Katlic said that there are three main benchmarks that physicians should be able to meet at an agreed upon age: a physical exam, a neurocognitive screening, and an eye exam. “At some reasonable age, I personally believe these exams should take place,” he said. “We can allow doctors to pick their own practitioners for the eye and physical exams, but the neurocognitive exam should be completed by a PhD neuropsychologist.”

At Lifebridge, for instance, these screenings begin at age 75 and take place every 2 years, during the recredentialing process. It applies to all specialties, not just surgeons. “Surgery is a little different in that it requires fine motor skills in addition to the others we test, but you want any physician to be cognitively intact,” Dr. Katlic pointed out. “All doctors need the ability to make decisions quickly, often under noisy, distracting conditions.”

Dr. Ellison supports applying the screenings to all specialties. “Let’s not forget that all physicians must be alert to the many ways in which their patients reveal what needs attention, evaluation, and treatment,” he said. “Some health care tasks could be performed without visual input; for example, perhaps psychotherapy could be provided competently by a clinician who lacks visual acuity. Auditory input might not be necessary for reading x-rays – but the information a health care provider gets from their eyes and ears is important, not just for surgeons.”

University of California San Diego has established what it calls its Physician Assessment and Clinical Education (PACE) program. One of the nation’s oldest and largest such programs, the hospital founded PACE in 1996. Most physicians taking part arrive as a requirement of disciplinary action from the state medical board, but a small percentage self-refers.

PACE involves two phases. The first is a 2-day set of tests and measures core competency knowledge. Phase 2 is more comprehensive and lasts 5 days. Here, within their specialty, physicians participate in the activities of the corresponding residency program. Faculty evaluates the physician, and a multidisciplinary team meets to review all the findings of the combined phases.

Depending on the results, doctors may face remediation steps that range from programs to address performance deficiencies to residency-level clinical experiences. According to a paper on the program published by the institution, “most physicians referred to the PACE program are found to have mild to moderate performance dyscompetence.”

In the case of the 2021 guidelines adopted by AMA delegates, there are nine principles for assessment. They should be evidence-based, ethical, relevant, accountable, fair and equitable, transparent, supportive, and nonburdensome, and should afford physicians due process protections.
 

Looking ahead

Even Dr. Katlic worries about the possibility of Congress intervening to establish federal-level, mandatory retirement age. “This just doesn’t make sense for our profession given the great variability we see,” he said. “My biggest hope is that more individual hospitals will institute these screenings.”

As the physician population ages – and the influx of new doctors shrinks – the slope becomes even more slippery. The AMA is predicting a physician shortage of nearly 40,000 by the year 2034. This strengthens arguments to keep existing physicians practicing for as long as possible and might make institutions less likely to screen.

It’s all a delicate balancing act and a continuing work in progress, said Dr. Ellison. “Ultimately, I believe we need to find a way to understand and address the possible implications for public safety, while at the same time protecting the privacy and dignity of our valued older physicians and other health care providers.”

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

Air traffic controllers face mandatory retirement at age 56, with exceptions up to 61. Commercial airline pilots must bow out at 65; same for foreign service employees. Physicians, however, have no age limit, regardless of specialty.

That doesn’t mean the topic of “how old is too old” hasn’t been one of the profession’s most heated debates for many years now.

As the profession rapidly ages – some 30% of the physician workforce is currently a senior, according to the American Medical Association – the topic of whether or not there should be a standard measure or age for retirement is front and center. The AMA’s Council on Medical Education formed a workgroup to look into the issue in 2015 and 2018, and in 2021, delegates adopted a set of guidelines for screening and assessing physicians, but stopped short of a mandate.

Mark Katlic, MD, chair of surgery at Lifebridge Health System, Baltimore, has devoted a decade to studying this topic. “I’m a bit of an outlier looking into this,” he says. “The public is unaware and seemingly unconcerned about the issue. Even among the medical profession, there’s been a series of fits and starts to develop a cohesive approach.”

One of the reasons guidelines – mandatory or otherwise – have been tough to come by is that aging brings with it a huge degree of variability. “If you look at a group of 80-year-olds, there will be much more variability than within a group of 40-year-olds,” Dr. Katlic pointed out.

Indeed, some 80-year-olds can easily continue to teach college courses, keep up in 10K running races, or perform delicate surgeries. Yet others in their peer group might struggle to properly button a shirt, walk a flight of stairs, or remember yesterday’s meals. Functional age is not the same as chronological age.

Frank Stockdale, MD, PhD, an 86-year-old practicing oncologist at Stanford (Calif.) University Health, counts himself in the camp opposed to age-based assessments. “It’s age discrimination,” he says. “Physicians receive assessments throughout their careers as part of the accreditation process – there’s no need to change that as doctors reach a certain age.”

Dr. Stockdale suggests that in many cases, malpractice suits are filed against mid-career doctors, not those of advanced age. “If you’re using the argument that there is an accumulation of deficits with age, the fact is that those deficits begin well before your 70s,” he said. “It’s better to have a uniform screening policy and begin at a much younger age.”

At Stanford, in fact, there was a former assessment policy that included cognitive testing, but physicians were successful in seeing that portion of testing eliminated. “It is a physical examination, by a physician of choice, certifying that for the privileges requested there is no physical or mental reason the candidate cannot safely perform them,” Dr. Stockdale explained.

In some cases, medical staffs have filed lawsuits to fight age-related testing. In New Haven, Conn., for instance, the U.S. Equal Employment Opportunity Commission (EEOC) filed a suit in 2020 on behalf of the Yale New Haven Hospital staff, alleging a discriminatory “late career practitioner policy.”

A similar case in Minnesota reached a settlement in 2021, providing monetary relief to staff impacted by out-of-pocket costs for the assessment, in addition to requiring that the hospital in question report to the EEOC any complaints related to age discrimination.

James Ellison, MD, MPH, chair in Memory Care and Geriatrics with ChristianaCare in Wilmington, Del., points out that aging can bring benefits for practicing physicians. “Age is very individualized and there are good and bad consequences,” he said. “Experience can build knowledge and confidence and expertise, and it does improve diagnostic accuracy.”

On the flip side, however, age-related brain changes include loss of volume and lower levels of some neurotransmitters, resulting in cognitive changes. “Functional changes occur too,” Dr. Ellison said.

“Just as some aging athletes may lose a degree of speed, strength, and flexibility, and some aging scientists may lose a part of their former cognitive speed, flexibility, and mental strength, aging health care providers can lose some of the physical coordination, strength, and visual acuity necessary to perform demanding surgical operations. They can also lose some of the processing speed, working memory, and executive function that allows them to excel in cognitive professional tasks.”

An estimated 5.8 million Americans age 65 and older have Alzheimer’s dementia, according to the Alzheimer’s Association.

Picking an arbitrary age for mandatory retirement isn’t the right approach for physicians, said Dr. Katlic. Rather, he said, the answer is to establish late-practitioner screening programs. “Very few hospitals have them, however,” he pointed out. “We do [at Lifebridge Health], and so do a few dozen others, but that’s out of hundreds.”

Instead, what typically plays out is that hospital staff might begin to notice a decline in a colleague. Things like a disheveled appearance or lack of hygiene, or trouble with memory, such as getting lost en route back to his or her office. Even dangerous behaviors such as nodding off during a procedure are not unheard of.

There are many examples of physician decline that fly under the radar. “Unfortunately, it’s unusual for cognitively impaired health care providers to recognize and report their own difficulties,” said Dr. Ellison. “Although peers are expected to report cognitively impaired colleagues, they often fail to do so. In some other countries, age-based assessment is an accepted policy. In the U.S., this is not a uniform policy.”

Sometimes physicians can remain on the job in spite of decline thanks to certain “props,” according to Dr. Ellison. “Good procedures, efficient supports, and various workarounds compensate,” he said, “but often are not sufficient to maintain high-quality practice.”

Most often, these situations play out slowly, until the problem becomes glaringly obvious and potentially dangerous, and someone in a position of power must step in.

“Often, it’s hearsay from a nurse or another staff member, and then a hospital president or chief of staff must make a career-affecting decision for the doctor in question,” said Dr. Katlic.

Because there is little self- or colleague policing – and barring official or binding guidelines on the aging physician issue – both Dr. Katlic and Dr. Ellison are proponents of late-career screening.
 

How screening can help  

As it stands, Dr. Katlic maintains that the profession isn’t doing enough to ensure public safety. “We have peer review and recertification processes, but when you get down to it, we don’t police ourselves well,” he said. “All physicians are assessed throughout their careers as part of the hospital accreditation process, which is fair and adequate.”

Dr. Katlic said that there are three main benchmarks that physicians should be able to meet at an agreed upon age: a physical exam, a neurocognitive screening, and an eye exam. “At some reasonable age, I personally believe these exams should take place,” he said. “We can allow doctors to pick their own practitioners for the eye and physical exams, but the neurocognitive exam should be completed by a PhD neuropsychologist.”

At Lifebridge, for instance, these screenings begin at age 75 and take place every 2 years, during the recredentialing process. It applies to all specialties, not just surgeons. “Surgery is a little different in that it requires fine motor skills in addition to the others we test, but you want any physician to be cognitively intact,” Dr. Katlic pointed out. “All doctors need the ability to make decisions quickly, often under noisy, distracting conditions.”

Dr. Ellison supports applying the screenings to all specialties. “Let’s not forget that all physicians must be alert to the many ways in which their patients reveal what needs attention, evaluation, and treatment,” he said. “Some health care tasks could be performed without visual input; for example, perhaps psychotherapy could be provided competently by a clinician who lacks visual acuity. Auditory input might not be necessary for reading x-rays – but the information a health care provider gets from their eyes and ears is important, not just for surgeons.”

University of California San Diego has established what it calls its Physician Assessment and Clinical Education (PACE) program. One of the nation’s oldest and largest such programs, the hospital founded PACE in 1996. Most physicians taking part arrive as a requirement of disciplinary action from the state medical board, but a small percentage self-refers.

PACE involves two phases. The first is a 2-day set of tests and measures core competency knowledge. Phase 2 is more comprehensive and lasts 5 days. Here, within their specialty, physicians participate in the activities of the corresponding residency program. Faculty evaluates the physician, and a multidisciplinary team meets to review all the findings of the combined phases.

Depending on the results, doctors may face remediation steps that range from programs to address performance deficiencies to residency-level clinical experiences. According to a paper on the program published by the institution, “most physicians referred to the PACE program are found to have mild to moderate performance dyscompetence.”

In the case of the 2021 guidelines adopted by AMA delegates, there are nine principles for assessment. They should be evidence-based, ethical, relevant, accountable, fair and equitable, transparent, supportive, and nonburdensome, and should afford physicians due process protections.
 

Looking ahead

Even Dr. Katlic worries about the possibility of Congress intervening to establish federal-level, mandatory retirement age. “This just doesn’t make sense for our profession given the great variability we see,” he said. “My biggest hope is that more individual hospitals will institute these screenings.”

As the physician population ages – and the influx of new doctors shrinks – the slope becomes even more slippery. The AMA is predicting a physician shortage of nearly 40,000 by the year 2034. This strengthens arguments to keep existing physicians practicing for as long as possible and might make institutions less likely to screen.

It’s all a delicate balancing act and a continuing work in progress, said Dr. Ellison. “Ultimately, I believe we need to find a way to understand and address the possible implications for public safety, while at the same time protecting the privacy and dignity of our valued older physicians and other health care providers.”

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

Air traffic controllers face mandatory retirement at age 56, with exceptions up to 61. Commercial airline pilots must bow out at 65; same for foreign service employees. Physicians, however, have no age limit, regardless of specialty.

That doesn’t mean the topic of “how old is too old” hasn’t been one of the profession’s most heated debates for many years now.

As the profession rapidly ages – some 30% of the physician workforce is currently a senior, according to the American Medical Association – the topic of whether or not there should be a standard measure or age for retirement is front and center. The AMA’s Council on Medical Education formed a workgroup to look into the issue in 2015 and 2018, and in 2021, delegates adopted a set of guidelines for screening and assessing physicians, but stopped short of a mandate.

Mark Katlic, MD, chair of surgery at Lifebridge Health System, Baltimore, has devoted a decade to studying this topic. “I’m a bit of an outlier looking into this,” he says. “The public is unaware and seemingly unconcerned about the issue. Even among the medical profession, there’s been a series of fits and starts to develop a cohesive approach.”

One of the reasons guidelines – mandatory or otherwise – have been tough to come by is that aging brings with it a huge degree of variability. “If you look at a group of 80-year-olds, there will be much more variability than within a group of 40-year-olds,” Dr. Katlic pointed out.

Indeed, some 80-year-olds can easily continue to teach college courses, keep up in 10K running races, or perform delicate surgeries. Yet others in their peer group might struggle to properly button a shirt, walk a flight of stairs, or remember yesterday’s meals. Functional age is not the same as chronological age.

Frank Stockdale, MD, PhD, an 86-year-old practicing oncologist at Stanford (Calif.) University Health, counts himself in the camp opposed to age-based assessments. “It’s age discrimination,” he says. “Physicians receive assessments throughout their careers as part of the accreditation process – there’s no need to change that as doctors reach a certain age.”

Dr. Stockdale suggests that in many cases, malpractice suits are filed against mid-career doctors, not those of advanced age. “If you’re using the argument that there is an accumulation of deficits with age, the fact is that those deficits begin well before your 70s,” he said. “It’s better to have a uniform screening policy and begin at a much younger age.”

At Stanford, in fact, there was a former assessment policy that included cognitive testing, but physicians were successful in seeing that portion of testing eliminated. “It is a physical examination, by a physician of choice, certifying that for the privileges requested there is no physical or mental reason the candidate cannot safely perform them,” Dr. Stockdale explained.

In some cases, medical staffs have filed lawsuits to fight age-related testing. In New Haven, Conn., for instance, the U.S. Equal Employment Opportunity Commission (EEOC) filed a suit in 2020 on behalf of the Yale New Haven Hospital staff, alleging a discriminatory “late career practitioner policy.”

A similar case in Minnesota reached a settlement in 2021, providing monetary relief to staff impacted by out-of-pocket costs for the assessment, in addition to requiring that the hospital in question report to the EEOC any complaints related to age discrimination.

James Ellison, MD, MPH, chair in Memory Care and Geriatrics with ChristianaCare in Wilmington, Del., points out that aging can bring benefits for practicing physicians. “Age is very individualized and there are good and bad consequences,” he said. “Experience can build knowledge and confidence and expertise, and it does improve diagnostic accuracy.”

On the flip side, however, age-related brain changes include loss of volume and lower levels of some neurotransmitters, resulting in cognitive changes. “Functional changes occur too,” Dr. Ellison said.

“Just as some aging athletes may lose a degree of speed, strength, and flexibility, and some aging scientists may lose a part of their former cognitive speed, flexibility, and mental strength, aging health care providers can lose some of the physical coordination, strength, and visual acuity necessary to perform demanding surgical operations. They can also lose some of the processing speed, working memory, and executive function that allows them to excel in cognitive professional tasks.”

An estimated 5.8 million Americans age 65 and older have Alzheimer’s dementia, according to the Alzheimer’s Association.

Picking an arbitrary age for mandatory retirement isn’t the right approach for physicians, said Dr. Katlic. Rather, he said, the answer is to establish late-practitioner screening programs. “Very few hospitals have them, however,” he pointed out. “We do [at Lifebridge Health], and so do a few dozen others, but that’s out of hundreds.”

Instead, what typically plays out is that hospital staff might begin to notice a decline in a colleague. Things like a disheveled appearance or lack of hygiene, or trouble with memory, such as getting lost en route back to his or her office. Even dangerous behaviors such as nodding off during a procedure are not unheard of.

There are many examples of physician decline that fly under the radar. “Unfortunately, it’s unusual for cognitively impaired health care providers to recognize and report their own difficulties,” said Dr. Ellison. “Although peers are expected to report cognitively impaired colleagues, they often fail to do so. In some other countries, age-based assessment is an accepted policy. In the U.S., this is not a uniform policy.”

Sometimes physicians can remain on the job in spite of decline thanks to certain “props,” according to Dr. Ellison. “Good procedures, efficient supports, and various workarounds compensate,” he said, “but often are not sufficient to maintain high-quality practice.”

Most often, these situations play out slowly, until the problem becomes glaringly obvious and potentially dangerous, and someone in a position of power must step in.

“Often, it’s hearsay from a nurse or another staff member, and then a hospital president or chief of staff must make a career-affecting decision for the doctor in question,” said Dr. Katlic.

Because there is little self- or colleague policing – and barring official or binding guidelines on the aging physician issue – both Dr. Katlic and Dr. Ellison are proponents of late-career screening.
 

How screening can help  

As it stands, Dr. Katlic maintains that the profession isn’t doing enough to ensure public safety. “We have peer review and recertification processes, but when you get down to it, we don’t police ourselves well,” he said. “All physicians are assessed throughout their careers as part of the hospital accreditation process, which is fair and adequate.”

Dr. Katlic said that there are three main benchmarks that physicians should be able to meet at an agreed upon age: a physical exam, a neurocognitive screening, and an eye exam. “At some reasonable age, I personally believe these exams should take place,” he said. “We can allow doctors to pick their own practitioners for the eye and physical exams, but the neurocognitive exam should be completed by a PhD neuropsychologist.”

At Lifebridge, for instance, these screenings begin at age 75 and take place every 2 years, during the recredentialing process. It applies to all specialties, not just surgeons. “Surgery is a little different in that it requires fine motor skills in addition to the others we test, but you want any physician to be cognitively intact,” Dr. Katlic pointed out. “All doctors need the ability to make decisions quickly, often under noisy, distracting conditions.”

Dr. Ellison supports applying the screenings to all specialties. “Let’s not forget that all physicians must be alert to the many ways in which their patients reveal what needs attention, evaluation, and treatment,” he said. “Some health care tasks could be performed without visual input; for example, perhaps psychotherapy could be provided competently by a clinician who lacks visual acuity. Auditory input might not be necessary for reading x-rays – but the information a health care provider gets from their eyes and ears is important, not just for surgeons.”

University of California San Diego has established what it calls its Physician Assessment and Clinical Education (PACE) program. One of the nation’s oldest and largest such programs, the hospital founded PACE in 1996. Most physicians taking part arrive as a requirement of disciplinary action from the state medical board, but a small percentage self-refers.

PACE involves two phases. The first is a 2-day set of tests and measures core competency knowledge. Phase 2 is more comprehensive and lasts 5 days. Here, within their specialty, physicians participate in the activities of the corresponding residency program. Faculty evaluates the physician, and a multidisciplinary team meets to review all the findings of the combined phases.

Depending on the results, doctors may face remediation steps that range from programs to address performance deficiencies to residency-level clinical experiences. According to a paper on the program published by the institution, “most physicians referred to the PACE program are found to have mild to moderate performance dyscompetence.”

In the case of the 2021 guidelines adopted by AMA delegates, there are nine principles for assessment. They should be evidence-based, ethical, relevant, accountable, fair and equitable, transparent, supportive, and nonburdensome, and should afford physicians due process protections.
 

Looking ahead

Even Dr. Katlic worries about the possibility of Congress intervening to establish federal-level, mandatory retirement age. “This just doesn’t make sense for our profession given the great variability we see,” he said. “My biggest hope is that more individual hospitals will institute these screenings.”

As the physician population ages – and the influx of new doctors shrinks – the slope becomes even more slippery. The AMA is predicting a physician shortage of nearly 40,000 by the year 2034. This strengthens arguments to keep existing physicians practicing for as long as possible and might make institutions less likely to screen.

It’s all a delicate balancing act and a continuing work in progress, said Dr. Ellison. “Ultimately, I believe we need to find a way to understand and address the possible implications for public safety, while at the same time protecting the privacy and dignity of our valued older physicians and other health care providers.”

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