MDedge Neurology

Loss of smell, not disease severity, predicts persistent cognitive impairment 1 year after SARS-CoV-2 infection, preliminary results of new research suggest.

The findings provide important insight into the long-term cognitive impact of COVID-19, said study investigator Gabriela Gonzalez-Alemán, PhD, professor at Pontifical Catholic University of Argentina, Buenos Aires.

The more information that can be gathered on factors increasing risks for this cognitive impact, “the better we can track it and begin to develop methods to prevent it,” she said.

The findings were presented at the Alzheimer’s Association International Conference.
 

Memory, attention problems

COVID-19 has infected more than 570 million people worldwide. Related infections may result in long-term sequelae, including neuropsychiatric symptoms, said Dr. Gonzalez-Alemán.

In older adults, COVID-19 sequelae may resemble early Alzheimer’s disease, and the two conditions may share risk factors and blood biomarkers.

The new study highlighted 1-year results from a large, prospective cohort study from Argentina. Researchers used measures to evaluate long-term consequences of COVID-19 in older adults recommended by the Alzheimer’s Association Consortium on Chronic Neuropsychiatric Sequelae of SARS-CoV-2 infection (CNS SC2).

Harmonizing definitions and methodologies for studying COVID-19’s impact on the brain allows consortium members to compare study results, said Dr. Gonzalez-Alemán.

The investigators used the health registry in the province of Jujuy, situated in the extreme northwestern part of Argentina. The registry includes all SARS-CoV-2 testing data for the entire region.

The investigators randomly invited adults aged 60 years and older from the registry to participate in the study. The current analysis included 766 adults aged 55-95 years (mean age 66.9 years; 57% female) with an average of 10.4 years of education. The education system in Argentina includes 12 years of school before university.

Investigators stratified subjects by polymerase chain reaction testing status. Of the total, 88.4% were infected with COVID and 11.6% were controls (subjects without COVID).

The neurocognitive assessment of participants included four cognitive domains: memory, attention, language, and executive function, and an olfactory test that determined degree of olfactory dysfunction. Cognitive impairment was defined as z scores below –2.

Researchers divided participants into groups according to cognitive performance. These included normal cognition, memory-only impairment (single domain; 11.7%), impairment in attention and executive function without memory impairment (two domains; 8.3%), and multiple domain impairment (11.6%).

“Our participants showed a predominance of memory impairment as would be seen in Alzheimer’s disease,” noted Dr. Gonzalez-Alemán. “And a large group showed a combination of memory and attention problems.”

About 40% of the study sample – but no controls – had olfactory dysfunction.

“All the subjects that had a severe cognitive impairment also had anosmia [loss of smell],” said Dr. Gonzalez-Alemán. “We established an association between olfactory dysfunction and cognitive performance and impairment.”

The analysis showed that severity of anosmia, but not clinical status, significantly predicted cognitive impairment. “So, anosmia could be a good predictor of cognitive impairment after COVID-19 infection,” said Dr. Gonzalez-Alemán.

For individuals older than 60 years, cognitive impairment can be persistent, as can be olfactory dysfunction, she added.

Results of a 1-year phone survey showed about 71.8% of subjects had received three vaccine doses and 24.9% two doses. About 12.5% of those with three doses were reinfected and 23.3% of those with two doses were reinfected.
 

Longest follow-up to date

Commenting on the research, Heather Snyder, PhD, vice president, medical and scientific relations at the Alzheimer’s Association, noted the study is “the longest follow-up we’ve seen” looking at the connection between persistent loss of smell and cognitive changes after a COVID-19 infection.

The study included a “fairly large” sample size and was “unique” in that it was set up in a part of the country with centralized testing, said Dr. Snyder.

The Argentinian group is among the most advanced of those connected to the CNS SC2, said Dr. Snyder.

Members of this Alzheimer’s Association consortium, said Dr. Snyder, regularly share updates of ongoing studies, which are at different stages and looking at various neuropsychiatric impacts of COVID-19. It is important to bring these groups together to determine what those impacts are “because no one group will be able to do this on their own,” she said. “We saw pretty early on that some individuals had changes in the brain, or changes in cognition, and loss of sense of smell or taste, which indicates there’s a connection to the brain.”

However, she added, “there’s still a lot we don’t know” about this connection.

The study was funded by Alzheimer’s Association and FULTRA.

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

Loss of smell, not disease severity, predicts persistent cognitive impairment 1 year after SARS-CoV-2 infection, preliminary results of new research suggest.

The findings provide important insight into the long-term cognitive impact of COVID-19, said study investigator Gabriela Gonzalez-Alemán, PhD, professor at Pontifical Catholic University of Argentina, Buenos Aires.

The more information that can be gathered on factors increasing risks for this cognitive impact, “the better we can track it and begin to develop methods to prevent it,” she said.

The findings were presented at the Alzheimer’s Association International Conference.
 

Memory, attention problems

COVID-19 has infected more than 570 million people worldwide. Related infections may result in long-term sequelae, including neuropsychiatric symptoms, said Dr. Gonzalez-Alemán.

In older adults, COVID-19 sequelae may resemble early Alzheimer’s disease, and the two conditions may share risk factors and blood biomarkers.

The new study highlighted 1-year results from a large, prospective cohort study from Argentina. Researchers used measures to evaluate long-term consequences of COVID-19 in older adults recommended by the Alzheimer’s Association Consortium on Chronic Neuropsychiatric Sequelae of SARS-CoV-2 infection (CNS SC2).

Harmonizing definitions and methodologies for studying COVID-19’s impact on the brain allows consortium members to compare study results, said Dr. Gonzalez-Alemán.

The investigators used the health registry in the province of Jujuy, situated in the extreme northwestern part of Argentina. The registry includes all SARS-CoV-2 testing data for the entire region.

The investigators randomly invited adults aged 60 years and older from the registry to participate in the study. The current analysis included 766 adults aged 55-95 years (mean age 66.9 years; 57% female) with an average of 10.4 years of education. The education system in Argentina includes 12 years of school before university.

Investigators stratified subjects by polymerase chain reaction testing status. Of the total, 88.4% were infected with COVID and 11.6% were controls (subjects without COVID).

The neurocognitive assessment of participants included four cognitive domains: memory, attention, language, and executive function, and an olfactory test that determined degree of olfactory dysfunction. Cognitive impairment was defined as z scores below –2.

Researchers divided participants into groups according to cognitive performance. These included normal cognition, memory-only impairment (single domain; 11.7%), impairment in attention and executive function without memory impairment (two domains; 8.3%), and multiple domain impairment (11.6%).

“Our participants showed a predominance of memory impairment as would be seen in Alzheimer’s disease,” noted Dr. Gonzalez-Alemán. “And a large group showed a combination of memory and attention problems.”

About 40% of the study sample – but no controls – had olfactory dysfunction.

“All the subjects that had a severe cognitive impairment also had anosmia [loss of smell],” said Dr. Gonzalez-Alemán. “We established an association between olfactory dysfunction and cognitive performance and impairment.”

The analysis showed that severity of anosmia, but not clinical status, significantly predicted cognitive impairment. “So, anosmia could be a good predictor of cognitive impairment after COVID-19 infection,” said Dr. Gonzalez-Alemán.

For individuals older than 60 years, cognitive impairment can be persistent, as can be olfactory dysfunction, she added.

Results of a 1-year phone survey showed about 71.8% of subjects had received three vaccine doses and 24.9% two doses. About 12.5% of those with three doses were reinfected and 23.3% of those with two doses were reinfected.
 

Longest follow-up to date

Commenting on the research, Heather Snyder, PhD, vice president, medical and scientific relations at the Alzheimer’s Association, noted the study is “the longest follow-up we’ve seen” looking at the connection between persistent loss of smell and cognitive changes after a COVID-19 infection.

The study included a “fairly large” sample size and was “unique” in that it was set up in a part of the country with centralized testing, said Dr. Snyder.

The Argentinian group is among the most advanced of those connected to the CNS SC2, said Dr. Snyder.

Members of this Alzheimer’s Association consortium, said Dr. Snyder, regularly share updates of ongoing studies, which are at different stages and looking at various neuropsychiatric impacts of COVID-19. It is important to bring these groups together to determine what those impacts are “because no one group will be able to do this on their own,” she said. “We saw pretty early on that some individuals had changes in the brain, or changes in cognition, and loss of sense of smell or taste, which indicates there’s a connection to the brain.”

However, she added, “there’s still a lot we don’t know” about this connection.

The study was funded by Alzheimer’s Association and FULTRA.

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

Loss of smell, not disease severity, predicts persistent cognitive impairment 1 year after SARS-CoV-2 infection, preliminary results of new research suggest.

The findings provide important insight into the long-term cognitive impact of COVID-19, said study investigator Gabriela Gonzalez-Alemán, PhD, professor at Pontifical Catholic University of Argentina, Buenos Aires.

The more information that can be gathered on factors increasing risks for this cognitive impact, “the better we can track it and begin to develop methods to prevent it,” she said.

The findings were presented at the Alzheimer’s Association International Conference.
 

Memory, attention problems

COVID-19 has infected more than 570 million people worldwide. Related infections may result in long-term sequelae, including neuropsychiatric symptoms, said Dr. Gonzalez-Alemán.

In older adults, COVID-19 sequelae may resemble early Alzheimer’s disease, and the two conditions may share risk factors and blood biomarkers.

The new study highlighted 1-year results from a large, prospective cohort study from Argentina. Researchers used measures to evaluate long-term consequences of COVID-19 in older adults recommended by the Alzheimer’s Association Consortium on Chronic Neuropsychiatric Sequelae of SARS-CoV-2 infection (CNS SC2).

Harmonizing definitions and methodologies for studying COVID-19’s impact on the brain allows consortium members to compare study results, said Dr. Gonzalez-Alemán.

The investigators used the health registry in the province of Jujuy, situated in the extreme northwestern part of Argentina. The registry includes all SARS-CoV-2 testing data for the entire region.

The investigators randomly invited adults aged 60 years and older from the registry to participate in the study. The current analysis included 766 adults aged 55-95 years (mean age 66.9 years; 57% female) with an average of 10.4 years of education. The education system in Argentina includes 12 years of school before university.

Investigators stratified subjects by polymerase chain reaction testing status. Of the total, 88.4% were infected with COVID and 11.6% were controls (subjects without COVID).

The neurocognitive assessment of participants included four cognitive domains: memory, attention, language, and executive function, and an olfactory test that determined degree of olfactory dysfunction. Cognitive impairment was defined as z scores below –2.

Researchers divided participants into groups according to cognitive performance. These included normal cognition, memory-only impairment (single domain; 11.7%), impairment in attention and executive function without memory impairment (two domains; 8.3%), and multiple domain impairment (11.6%).

“Our participants showed a predominance of memory impairment as would be seen in Alzheimer’s disease,” noted Dr. Gonzalez-Alemán. “And a large group showed a combination of memory and attention problems.”

About 40% of the study sample – but no controls – had olfactory dysfunction.

“All the subjects that had a severe cognitive impairment also had anosmia [loss of smell],” said Dr. Gonzalez-Alemán. “We established an association between olfactory dysfunction and cognitive performance and impairment.”

The analysis showed that severity of anosmia, but not clinical status, significantly predicted cognitive impairment. “So, anosmia could be a good predictor of cognitive impairment after COVID-19 infection,” said Dr. Gonzalez-Alemán.

For individuals older than 60 years, cognitive impairment can be persistent, as can be olfactory dysfunction, she added.

Results of a 1-year phone survey showed about 71.8% of subjects had received three vaccine doses and 24.9% two doses. About 12.5% of those with three doses were reinfected and 23.3% of those with two doses were reinfected.
 

Longest follow-up to date

Commenting on the research, Heather Snyder, PhD, vice president, medical and scientific relations at the Alzheimer’s Association, noted the study is “the longest follow-up we’ve seen” looking at the connection between persistent loss of smell and cognitive changes after a COVID-19 infection.

The study included a “fairly large” sample size and was “unique” in that it was set up in a part of the country with centralized testing, said Dr. Snyder.

The Argentinian group is among the most advanced of those connected to the CNS SC2, said Dr. Snyder.

Members of this Alzheimer’s Association consortium, said Dr. Snyder, regularly share updates of ongoing studies, which are at different stages and looking at various neuropsychiatric impacts of COVID-19. It is important to bring these groups together to determine what those impacts are “because no one group will be able to do this on their own,” she said. “We saw pretty early on that some individuals had changes in the brain, or changes in cognition, and loss of sense of smell or taste, which indicates there’s a connection to the brain.”

However, she added, “there’s still a lot we don’t know” about this connection.

The study was funded by Alzheimer’s Association and FULTRA.

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

Rapid deterioration in sense of smell is a strong predictor of both Alzheimer’s-related cognitive impairment and loss of volume in specific brain regions linked to both Alzheimer’s disease and smell, according to new research findings.

Olfactory dysfunction is common in late life and well documented among people with Alzheimer’s disease. However, it was unknown whether faster olfactory decline predicts either onset of Alzheimer’s disease or structural brain changes associated with Alzheimer’s disease.

In a study published online in Alzheimer’s and Dementia, Jayant M. Pinto, MD, and his colleagues at the University of Chicago Medical Center reported that among older adults with normal cognition at baseline, people who experienced rapid loss of sense of smell were more likely to be subsequently diagnosed with mild cognitive impairment (MCI) or dementia, compared with those who did not.

Participants were recruited from Rush University’s Memory and Aging Project, a longitudinal cohort of older adults who undergo yearly cognitive and sensory exams, including a scratch test of 12 common smells to identify. The Rush study “was ahead of the curve in looking at smell,” Dr. Pinto said in an interview. “It gave us a very valuable resource with which to attack these questions.”

Dr. Pinto has long investigated links between smell and accelerated aging; in 2014 his group published the finding that olfactory dysfunction could predict death within 5 years in older adults, and in 2018 they reported that olfactory dysfunction could predict dementia.
 

Smell and cognition over time

For the current study, Dr. Pinto said, “we were able to look at the question not just using a single point in time, but a more granular trajectory of smell loss. Measuring change year by year showed that the faster people’s sense of smell declined, the more likely they were to be diagnosed with MCI or Alzheimer’s disease.”

Dr. Pinto and his colleagues evaluated results from 515 adults (mean age 76.6, 78% female, 94% White) with no cognitive impairment and at least 3 years of normal results on smell tests at baseline. The subjects were followed for a mean 8 years. One hundred subjects (19%) were diagnosed with MCI or dementia by the end of the study period. A subset of the cohort (n = 121) underwent structural magnetic resonance imaging (MRI) between their final smell tests and the study’s end. Of these, most still had normal cognition; 17 individuals had MCI.

Patients’ individual trajectories of smell loss were mapped as slopes. After adjusting for expected differences in age and sex, the investigators found steeper decline associated with greater risk of incident MCI or dementia (odds ratio, 1.89; 95% confidence interval, 1.26-2.90; P < .01). The risk was comparable to that of carrying an apo E ε4 allele, the key risk variant for late-onset Alzheimer’s disease, but was independent of apo E status. The association was strongest among subjects younger than 76 years.
 

Olfactory decline and brain volume

Dr. Pinto and his colleagues, including lead author Rachel R. Pacyna, a 4th-year medical student at the University of Chicago, also sought to identify brain volume changes corresponding with olfactory decline and Alzheimer’s disease. The researchers hypothesized that certain brain regions not seen affected in Alzheimer’s disease would remain unchanged regardless of olfactory status, but that regions associated with smell and Alzheimer’s disease would see smaller volumes linked with olfactory decline.

Faster olfactory decline did predict lower gray matter volume in olfactory regions, even after controlling for apo E status and other known risk factors. Conversely, cognitively unimpaired patients undergoing MRI saw more gray matter volume in primary olfactory and temporal brain regions, compared with those with cognitive symptoms.

Taken together, the findings suggest that “change in sense of smell is better than looking at sense of smell at one time point,” Dr. Pinto commented. “There are other reasons people have impaired sense of smell: car accidents, COVID, other viruses and infections. But if you identify on a time course those who are starting to lose it faster, these are the people on whom we need to focus.”
 

Not yet diagnostic

More work needs to be done to establish thresholds for smell loss that could be useful in clinical or investigative settings as a marker of dementia risk, Dr. Pinto acknowledged. “Everyone gets their hearing tested; everyone gets their vision tested. It’s not as easy to get your sense of smell tested. But this study is telling people that if we were to start measuring it routinely, we could actually use it.”

Smell testing “could become a component of a diagnostic battery that includes things like genotyping and cerebrospinal fluid markers, but adds a little more information. It could be useful in clinical prevention trials to identify people at the highest risk, as smell loss presents quite a few years before MCI or Alzheimer’s disease.”

The investigators acknowledged that their findings need to be replicated in more diverse cohorts that better represent the Alzheimer’s population in the United States. Another limitation of their study, they said, was that the method used to calculate the rate of olfactory decline “was based on slope of measured time points assuming linearity, which may oversimplify the complexity of olfactory changes in normal aging and during the preclinical Alzheimer’s disease period.” The study was funded by the National Institutes of Health. Dr. Pinto disclosed receiving consulting fees from Sanofi/Regeneron, Optinose, and Genentech not related to this work.

Rapid deterioration in sense of smell is a strong predictor of both Alzheimer’s-related cognitive impairment and loss of volume in specific brain regions linked to both Alzheimer’s disease and smell, according to new research findings.

Olfactory dysfunction is common in late life and well documented among people with Alzheimer’s disease. However, it was unknown whether faster olfactory decline predicts either onset of Alzheimer’s disease or structural brain changes associated with Alzheimer’s disease.

In a study published online in Alzheimer’s and Dementia, Jayant M. Pinto, MD, and his colleagues at the University of Chicago Medical Center reported that among older adults with normal cognition at baseline, people who experienced rapid loss of sense of smell were more likely to be subsequently diagnosed with mild cognitive impairment (MCI) or dementia, compared with those who did not.

Participants were recruited from Rush University’s Memory and Aging Project, a longitudinal cohort of older adults who undergo yearly cognitive and sensory exams, including a scratch test of 12 common smells to identify. The Rush study “was ahead of the curve in looking at smell,” Dr. Pinto said in an interview. “It gave us a very valuable resource with which to attack these questions.”

Dr. Pinto has long investigated links between smell and accelerated aging; in 2014 his group published the finding that olfactory dysfunction could predict death within 5 years in older adults, and in 2018 they reported that olfactory dysfunction could predict dementia.
 

Smell and cognition over time

For the current study, Dr. Pinto said, “we were able to look at the question not just using a single point in time, but a more granular trajectory of smell loss. Measuring change year by year showed that the faster people’s sense of smell declined, the more likely they were to be diagnosed with MCI or Alzheimer’s disease.”

Dr. Pinto and his colleagues evaluated results from 515 adults (mean age 76.6, 78% female, 94% White) with no cognitive impairment and at least 3 years of normal results on smell tests at baseline. The subjects were followed for a mean 8 years. One hundred subjects (19%) were diagnosed with MCI or dementia by the end of the study period. A subset of the cohort (n = 121) underwent structural magnetic resonance imaging (MRI) between their final smell tests and the study’s end. Of these, most still had normal cognition; 17 individuals had MCI.

Patients’ individual trajectories of smell loss were mapped as slopes. After adjusting for expected differences in age and sex, the investigators found steeper decline associated with greater risk of incident MCI or dementia (odds ratio, 1.89; 95% confidence interval, 1.26-2.90; P < .01). The risk was comparable to that of carrying an apo E ε4 allele, the key risk variant for late-onset Alzheimer’s disease, but was independent of apo E status. The association was strongest among subjects younger than 76 years.
 

Olfactory decline and brain volume

Dr. Pinto and his colleagues, including lead author Rachel R. Pacyna, a 4th-year medical student at the University of Chicago, also sought to identify brain volume changes corresponding with olfactory decline and Alzheimer’s disease. The researchers hypothesized that certain brain regions not seen affected in Alzheimer’s disease would remain unchanged regardless of olfactory status, but that regions associated with smell and Alzheimer’s disease would see smaller volumes linked with olfactory decline.

Faster olfactory decline did predict lower gray matter volume in olfactory regions, even after controlling for apo E status and other known risk factors. Conversely, cognitively unimpaired patients undergoing MRI saw more gray matter volume in primary olfactory and temporal brain regions, compared with those with cognitive symptoms.

Taken together, the findings suggest that “change in sense of smell is better than looking at sense of smell at one time point,” Dr. Pinto commented. “There are other reasons people have impaired sense of smell: car accidents, COVID, other viruses and infections. But if you identify on a time course those who are starting to lose it faster, these are the people on whom we need to focus.”
 

Not yet diagnostic

More work needs to be done to establish thresholds for smell loss that could be useful in clinical or investigative settings as a marker of dementia risk, Dr. Pinto acknowledged. “Everyone gets their hearing tested; everyone gets their vision tested. It’s not as easy to get your sense of smell tested. But this study is telling people that if we were to start measuring it routinely, we could actually use it.”

Smell testing “could become a component of a diagnostic battery that includes things like genotyping and cerebrospinal fluid markers, but adds a little more information. It could be useful in clinical prevention trials to identify people at the highest risk, as smell loss presents quite a few years before MCI or Alzheimer’s disease.”

The investigators acknowledged that their findings need to be replicated in more diverse cohorts that better represent the Alzheimer’s population in the United States. Another limitation of their study, they said, was that the method used to calculate the rate of olfactory decline “was based on slope of measured time points assuming linearity, which may oversimplify the complexity of olfactory changes in normal aging and during the preclinical Alzheimer’s disease period.” The study was funded by the National Institutes of Health. Dr. Pinto disclosed receiving consulting fees from Sanofi/Regeneron, Optinose, and Genentech not related to this work.

Rapid deterioration in sense of smell is a strong predictor of both Alzheimer’s-related cognitive impairment and loss of volume in specific brain regions linked to both Alzheimer’s disease and smell, according to new research findings.

Olfactory dysfunction is common in late life and well documented among people with Alzheimer’s disease. However, it was unknown whether faster olfactory decline predicts either onset of Alzheimer’s disease or structural brain changes associated with Alzheimer’s disease.

In a study published online in Alzheimer’s and Dementia, Jayant M. Pinto, MD, and his colleagues at the University of Chicago Medical Center reported that among older adults with normal cognition at baseline, people who experienced rapid loss of sense of smell were more likely to be subsequently diagnosed with mild cognitive impairment (MCI) or dementia, compared with those who did not.

Participants were recruited from Rush University’s Memory and Aging Project, a longitudinal cohort of older adults who undergo yearly cognitive and sensory exams, including a scratch test of 12 common smells to identify. The Rush study “was ahead of the curve in looking at smell,” Dr. Pinto said in an interview. “It gave us a very valuable resource with which to attack these questions.”

Dr. Pinto has long investigated links between smell and accelerated aging; in 2014 his group published the finding that olfactory dysfunction could predict death within 5 years in older adults, and in 2018 they reported that olfactory dysfunction could predict dementia.
 

Smell and cognition over time

For the current study, Dr. Pinto said, “we were able to look at the question not just using a single point in time, but a more granular trajectory of smell loss. Measuring change year by year showed that the faster people’s sense of smell declined, the more likely they were to be diagnosed with MCI or Alzheimer’s disease.”

Dr. Pinto and his colleagues evaluated results from 515 adults (mean age 76.6, 78% female, 94% White) with no cognitive impairment and at least 3 years of normal results on smell tests at baseline. The subjects were followed for a mean 8 years. One hundred subjects (19%) were diagnosed with MCI or dementia by the end of the study period. A subset of the cohort (n = 121) underwent structural magnetic resonance imaging (MRI) between their final smell tests and the study’s end. Of these, most still had normal cognition; 17 individuals had MCI.

Patients’ individual trajectories of smell loss were mapped as slopes. After adjusting for expected differences in age and sex, the investigators found steeper decline associated with greater risk of incident MCI or dementia (odds ratio, 1.89; 95% confidence interval, 1.26-2.90; P < .01). The risk was comparable to that of carrying an apo E ε4 allele, the key risk variant for late-onset Alzheimer’s disease, but was independent of apo E status. The association was strongest among subjects younger than 76 years.
 

Olfactory decline and brain volume

Dr. Pinto and his colleagues, including lead author Rachel R. Pacyna, a 4th-year medical student at the University of Chicago, also sought to identify brain volume changes corresponding with olfactory decline and Alzheimer’s disease. The researchers hypothesized that certain brain regions not seen affected in Alzheimer’s disease would remain unchanged regardless of olfactory status, but that regions associated with smell and Alzheimer’s disease would see smaller volumes linked with olfactory decline.

Faster olfactory decline did predict lower gray matter volume in olfactory regions, even after controlling for apo E status and other known risk factors. Conversely, cognitively unimpaired patients undergoing MRI saw more gray matter volume in primary olfactory and temporal brain regions, compared with those with cognitive symptoms.

Taken together, the findings suggest that “change in sense of smell is better than looking at sense of smell at one time point,” Dr. Pinto commented. “There are other reasons people have impaired sense of smell: car accidents, COVID, other viruses and infections. But if you identify on a time course those who are starting to lose it faster, these are the people on whom we need to focus.”
 

Not yet diagnostic

More work needs to be done to establish thresholds for smell loss that could be useful in clinical or investigative settings as a marker of dementia risk, Dr. Pinto acknowledged. “Everyone gets their hearing tested; everyone gets their vision tested. It’s not as easy to get your sense of smell tested. But this study is telling people that if we were to start measuring it routinely, we could actually use it.”

Smell testing “could become a component of a diagnostic battery that includes things like genotyping and cerebrospinal fluid markers, but adds a little more information. It could be useful in clinical prevention trials to identify people at the highest risk, as smell loss presents quite a few years before MCI or Alzheimer’s disease.”

The investigators acknowledged that their findings need to be replicated in more diverse cohorts that better represent the Alzheimer’s population in the United States. Another limitation of their study, they said, was that the method used to calculate the rate of olfactory decline “was based on slope of measured time points assuming linearity, which may oversimplify the complexity of olfactory changes in normal aging and during the preclinical Alzheimer’s disease period.” The study was funded by the National Institutes of Health. Dr. Pinto disclosed receiving consulting fees from Sanofi/Regeneron, Optinose, and Genentech not related to this work.

SAN DIEGO – For the first time, the Alzheimer’s Association has released recommendations for the use of blood-based biomarkers in clinical trials and certain clinical situations. The organization has previously published recommendations for use of amyloid positron emission tomography (PET) and cerebrospinal fluid (CSF) biomarkers for Alzheimer’s disease.

The recommendations were the subject of a presentation at the 2022 Alzheimer’s Association International Conference and were published online in Alzheimer’s & Dementia.

During his presentation, Oskar Hansson, MD, PhD, stressed that the document describes recommendations, not criteria, for use of blood-based biomarkers. He suggested that the recommendations will need to be updated within 9-12 months, and that criteria for blood-based biomarkers use could come within 2 years.

The new recommendations reflect the recent acceleration of progress in the field, according to Wiesje M. van der Flier, PhD, who moderated the session. “It’s just growing so quickly. I think within 5 years the whole field will have transformed. By starting to use them in specialized memory clinics first, but then also local memory clinics, and then finally, I think that they may also transform primary care,” said Dr. van der Flier, who is a professor of neurology at Amsterdam University Medical Center.
 

Guidance for clinical trials and memory clinics

The guidelines were created in part because blood-based biomarkers for Alzheimer’s disease have become increasingly available, and there has been a call from the community for guidance, according to Dr. Hansson. There is also a hazard that widespread adoption could interfere with the field itself, especially if physicians don’t understand how to interpret the results. That’s a particularly acute problem since Alzheimer’s disease pathology can precede symptoms. “It’s important to have some guidance about regulating their use so we don’t get the problem that they are misused and get a bad reputation,” said Dr. Hansson in an interview.

The current recommendations are for use in clinical trials to identify patients likely to have Alzheimer’s disease, as well as in memory clinics, though “we’re still a bit cautious. We still need to confirm it with other biomarkers. The reason for that is we still don’t know how these will perform in the clinical reality. So it’s a bit trying it out. You can start using these blood biomarkers to some degree,” said Dr. Hansson.

However, he offered the caveat that plasma-based biomarkers should only be used while confirming that the blood-based biomarkers agree with CSF tests, ideally more than 90% of the time. “If suddenly only 60% of the plasma biomarkers agree with CSF, you have a problem and you need to stop,” said Dr. Hansson.

The authors recommend that blood-based biomarkers be used in clinical trials to help select patients and identify healthy controls. Dr. Hansson said that there is not enough evidence that blood-based biomarkers have sufficient positive predictive value to be used as the sole criteria for clinical trial admission. However, they could also be used to inform decision-making in adaptive clinical trials.

Specifically, plasma Abeta42/Abeta40 and P-tau assays using established thresholds can be used in clinical studies first-screening step for clinical trials, though they should be confirmed by PET or CSF in those with abnormal blood biomarker levels. The biomarkers could also be used in non–Alzheimer’s disease clinical trials to exclude patients with probable Alzheimer’s disease copathology.

In memory clinics, the authors recommend that BBMs be used only in patients who are symptomatic and, when possible, should be confirmed by PET or CSF.
 

More work to be done

Dr. Hansson noted that 50%-70% of patients with Alzheimer’s disease are misdiagnosed in primary care, showing a clear need for biomarkers that could improve diagnosis. However, he stressed that blood-based biomarkers are not yet ready for use in that setting.

Still, they could eventually become a boon. “The majority of patients now do not get any biomarker support to diagnosis. They do not have access to amyloid PET or [CSF] biomarkers, but when the blood-based biomarkers are good enough, that means that biomarker support for an Alzheimer’s diagnosis [will be] available to many patients … across the globe,” said Dr. van der Flier.

There are numerous research efforts underway to validate blood-based biomarkers in more diverse groups of patients. That’s because the retrospective studies typically used to identify and validate biomarkers tend to recruit carefully selected patients, with clearly defined cases and good CSF characterization, according to Charlotte Teunissen, PhD, who is also a coauthor of the guidelines and professor of neuropsychiatry at Amsterdam University Medical Center. “Now we want to go one step further to go real-life practice, and there are several initiatives,” she said.

Dr. Hansson, Dr. Tenuissen, and Dr. van der Flier have no relevant financial disclosures.

SAN DIEGO – For the first time, the Alzheimer’s Association has released recommendations for the use of blood-based biomarkers in clinical trials and certain clinical situations. The organization has previously published recommendations for use of amyloid positron emission tomography (PET) and cerebrospinal fluid (CSF) biomarkers for Alzheimer’s disease.

The recommendations were the subject of a presentation at the 2022 Alzheimer’s Association International Conference and were published online in Alzheimer’s & Dementia.

During his presentation, Oskar Hansson, MD, PhD, stressed that the document describes recommendations, not criteria, for use of blood-based biomarkers. He suggested that the recommendations will need to be updated within 9-12 months, and that criteria for blood-based biomarkers use could come within 2 years.

The new recommendations reflect the recent acceleration of progress in the field, according to Wiesje M. van der Flier, PhD, who moderated the session. “It’s just growing so quickly. I think within 5 years the whole field will have transformed. By starting to use them in specialized memory clinics first, but then also local memory clinics, and then finally, I think that they may also transform primary care,” said Dr. van der Flier, who is a professor of neurology at Amsterdam University Medical Center.
 

Guidance for clinical trials and memory clinics

The guidelines were created in part because blood-based biomarkers for Alzheimer’s disease have become increasingly available, and there has been a call from the community for guidance, according to Dr. Hansson. There is also a hazard that widespread adoption could interfere with the field itself, especially if physicians don’t understand how to interpret the results. That’s a particularly acute problem since Alzheimer’s disease pathology can precede symptoms. “It’s important to have some guidance about regulating their use so we don’t get the problem that they are misused and get a bad reputation,” said Dr. Hansson in an interview.

The current recommendations are for use in clinical trials to identify patients likely to have Alzheimer’s disease, as well as in memory clinics, though “we’re still a bit cautious. We still need to confirm it with other biomarkers. The reason for that is we still don’t know how these will perform in the clinical reality. So it’s a bit trying it out. You can start using these blood biomarkers to some degree,” said Dr. Hansson.

However, he offered the caveat that plasma-based biomarkers should only be used while confirming that the blood-based biomarkers agree with CSF tests, ideally more than 90% of the time. “If suddenly only 60% of the plasma biomarkers agree with CSF, you have a problem and you need to stop,” said Dr. Hansson.

The authors recommend that blood-based biomarkers be used in clinical trials to help select patients and identify healthy controls. Dr. Hansson said that there is not enough evidence that blood-based biomarkers have sufficient positive predictive value to be used as the sole criteria for clinical trial admission. However, they could also be used to inform decision-making in adaptive clinical trials.

Specifically, plasma Abeta42/Abeta40 and P-tau assays using established thresholds can be used in clinical studies first-screening step for clinical trials, though they should be confirmed by PET or CSF in those with abnormal blood biomarker levels. The biomarkers could also be used in non–Alzheimer’s disease clinical trials to exclude patients with probable Alzheimer’s disease copathology.

In memory clinics, the authors recommend that BBMs be used only in patients who are symptomatic and, when possible, should be confirmed by PET or CSF.
 

More work to be done

Dr. Hansson noted that 50%-70% of patients with Alzheimer’s disease are misdiagnosed in primary care, showing a clear need for biomarkers that could improve diagnosis. However, he stressed that blood-based biomarkers are not yet ready for use in that setting.

Still, they could eventually become a boon. “The majority of patients now do not get any biomarker support to diagnosis. They do not have access to amyloid PET or [CSF] biomarkers, but when the blood-based biomarkers are good enough, that means that biomarker support for an Alzheimer’s diagnosis [will be] available to many patients … across the globe,” said Dr. van der Flier.

There are numerous research efforts underway to validate blood-based biomarkers in more diverse groups of patients. That’s because the retrospective studies typically used to identify and validate biomarkers tend to recruit carefully selected patients, with clearly defined cases and good CSF characterization, according to Charlotte Teunissen, PhD, who is also a coauthor of the guidelines and professor of neuropsychiatry at Amsterdam University Medical Center. “Now we want to go one step further to go real-life practice, and there are several initiatives,” she said.

Dr. Hansson, Dr. Tenuissen, and Dr. van der Flier have no relevant financial disclosures.

SAN DIEGO – For the first time, the Alzheimer’s Association has released recommendations for the use of blood-based biomarkers in clinical trials and certain clinical situations. The organization has previously published recommendations for use of amyloid positron emission tomography (PET) and cerebrospinal fluid (CSF) biomarkers for Alzheimer’s disease.

The recommendations were the subject of a presentation at the 2022 Alzheimer’s Association International Conference and were published online in Alzheimer’s & Dementia.

During his presentation, Oskar Hansson, MD, PhD, stressed that the document describes recommendations, not criteria, for use of blood-based biomarkers. He suggested that the recommendations will need to be updated within 9-12 months, and that criteria for blood-based biomarkers use could come within 2 years.

The new recommendations reflect the recent acceleration of progress in the field, according to Wiesje M. van der Flier, PhD, who moderated the session. “It’s just growing so quickly. I think within 5 years the whole field will have transformed. By starting to use them in specialized memory clinics first, but then also local memory clinics, and then finally, I think that they may also transform primary care,” said Dr. van der Flier, who is a professor of neurology at Amsterdam University Medical Center.
 

Guidance for clinical trials and memory clinics

The guidelines were created in part because blood-based biomarkers for Alzheimer’s disease have become increasingly available, and there has been a call from the community for guidance, according to Dr. Hansson. There is also a hazard that widespread adoption could interfere with the field itself, especially if physicians don’t understand how to interpret the results. That’s a particularly acute problem since Alzheimer’s disease pathology can precede symptoms. “It’s important to have some guidance about regulating their use so we don’t get the problem that they are misused and get a bad reputation,” said Dr. Hansson in an interview.

The current recommendations are for use in clinical trials to identify patients likely to have Alzheimer’s disease, as well as in memory clinics, though “we’re still a bit cautious. We still need to confirm it with other biomarkers. The reason for that is we still don’t know how these will perform in the clinical reality. So it’s a bit trying it out. You can start using these blood biomarkers to some degree,” said Dr. Hansson.

However, he offered the caveat that plasma-based biomarkers should only be used while confirming that the blood-based biomarkers agree with CSF tests, ideally more than 90% of the time. “If suddenly only 60% of the plasma biomarkers agree with CSF, you have a problem and you need to stop,” said Dr. Hansson.

The authors recommend that blood-based biomarkers be used in clinical trials to help select patients and identify healthy controls. Dr. Hansson said that there is not enough evidence that blood-based biomarkers have sufficient positive predictive value to be used as the sole criteria for clinical trial admission. However, they could also be used to inform decision-making in adaptive clinical trials.

Specifically, plasma Abeta42/Abeta40 and P-tau assays using established thresholds can be used in clinical studies first-screening step for clinical trials, though they should be confirmed by PET or CSF in those with abnormal blood biomarker levels. The biomarkers could also be used in non–Alzheimer’s disease clinical trials to exclude patients with probable Alzheimer’s disease copathology.

In memory clinics, the authors recommend that BBMs be used only in patients who are symptomatic and, when possible, should be confirmed by PET or CSF.
 

More work to be done

Dr. Hansson noted that 50%-70% of patients with Alzheimer’s disease are misdiagnosed in primary care, showing a clear need for biomarkers that could improve diagnosis. However, he stressed that blood-based biomarkers are not yet ready for use in that setting.

Still, they could eventually become a boon. “The majority of patients now do not get any biomarker support to diagnosis. They do not have access to amyloid PET or [CSF] biomarkers, but when the blood-based biomarkers are good enough, that means that biomarker support for an Alzheimer’s diagnosis [will be] available to many patients … across the globe,” said Dr. van der Flier.

There are numerous research efforts underway to validate blood-based biomarkers in more diverse groups of patients. That’s because the retrospective studies typically used to identify and validate biomarkers tend to recruit carefully selected patients, with clearly defined cases and good CSF characterization, according to Charlotte Teunissen, PhD, who is also a coauthor of the guidelines and professor of neuropsychiatry at Amsterdam University Medical Center. “Now we want to go one step further to go real-life practice, and there are several initiatives,” she said.

Dr. Hansson, Dr. Tenuissen, and Dr. van der Flier have no relevant financial disclosures.

Older adults who have spent time in the intensive care unit have double the risk of developing dementia in later years, compared with older adults who have never stayed in the ICU, new research suggests.

“ICU hospitalization may be an underrecognized risk factor for dementia in older adults,” Bryan D. James, PhD, epidemiologist with Rush Alzheimer’s Disease Center, Chicago, said in an interview.

“Health care providers caring for older patients who have experienced a hospitalization for critical illness should be prepared to assess and monitor their patients’ cognitive status as part of their long-term care plan,” Dr. James added.

The findings were presented at the Alzheimer’s Association International Conference.
 

Hidden risk factor?

ICU hospitalization as a result of critical illness has been linked to subsequent cognitive impairment in older patients. However, how ICU hospitalization relates to the long-term risk of developing Alzheimer’s and other age-related dementias is unknown.

“Given the high rate of ICU hospitalization in older persons, especially during the COVID-19 pandemic, it is critical to explore this relationship, Dr. James said.

The Rush team assessed the impact of an ICU stay on dementia risk in 3,822 older adults (mean age, 77 years) without known dementia at baseline participating in five diverse epidemiologic cohorts.

Participants were checked annually for development of Alzheimer’s and all-type dementia using standardized cognitive assessments.

Over an average of 7.8 years, 1,991 (52%) adults had at least one ICU stay; 1,031 (27%) had an ICU stay before study enrollment; and 961 (25%) had an ICU stay during the study period.

In models adjusted for age, sex, education, and race, ICU hospitalization was associated with 63% higher risk of Alzheimer’s dementia (hazard ratio, 1.63; 95% confidence interval, 1.41-1.88) and 71% higher risk of all-type dementia (HR, 1.71; 95% CI, 1.48-1.97).

In models further adjusted for other health factors such as vascular risk factors and disease, other chronic medical conditions and functional disabilities, the association was even stronger: ICU hospitalization was associated with roughly double the risk of Alzheimer’s dementia (HR 2.10; 95% CI, 1.66-2.65) and all-type dementia (HR, 2.20; 95% CI, 1.75-2.77).

Dr. James said in an interview that it remains unclear why an ICU stay may raise the dementia risk.

“This study was not designed to assess the causes of the higher risk of dementia in persons who had ICU hospitalizations. However, researchers have looked into a number of factors that could account for this increased risk,” he explained.

One is critical illness itself that leads to hospitalization, which could result in damage to the brain; for example, severe COVID-19 has been shown to directly harm the brain, Dr. James said.

He also noted that specific events experienced during ICU stay have been shown to increase risk for cognitive impairment, including infection and severe sepsis, acute dialysis, neurologic dysfunction and delirium, and sedation.
 

Important work

Commenting on the study, Heather Snyder, PhD, vice president of medical & scientific relations at the Alzheimer’s Association, said what’s interesting about the study is that it looks at individuals in the ICU, regardless of the cause.

“The study shows that having some type of health issue that results in some type of ICU stay is associated with an increased risk of declining cognition,” Dr. Snyder said.

“That’s really important,” she said, “especially given the increase in individuals, particularly those 60 and older, who did experience an ICU stay over the last couple of years and understanding how that might impact their long-term risk related to Alzheimer’s and other changes in memory.”

“If an individual has been in the ICU, that should be part of the conversation with their physician or health care provider,” Dr. Snyder advised.

The study was funded by the National Institute on Aging. Dr. James and Dr. Snyder disclosed no relevant financial relationships.

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

Older adults who have spent time in the intensive care unit have double the risk of developing dementia in later years, compared with older adults who have never stayed in the ICU, new research suggests.

“ICU hospitalization may be an underrecognized risk factor for dementia in older adults,” Bryan D. James, PhD, epidemiologist with Rush Alzheimer’s Disease Center, Chicago, said in an interview.

“Health care providers caring for older patients who have experienced a hospitalization for critical illness should be prepared to assess and monitor their patients’ cognitive status as part of their long-term care plan,” Dr. James added.

The findings were presented at the Alzheimer’s Association International Conference.
 

Hidden risk factor?

ICU hospitalization as a result of critical illness has been linked to subsequent cognitive impairment in older patients. However, how ICU hospitalization relates to the long-term risk of developing Alzheimer’s and other age-related dementias is unknown.

“Given the high rate of ICU hospitalization in older persons, especially during the COVID-19 pandemic, it is critical to explore this relationship, Dr. James said.

The Rush team assessed the impact of an ICU stay on dementia risk in 3,822 older adults (mean age, 77 years) without known dementia at baseline participating in five diverse epidemiologic cohorts.

Participants were checked annually for development of Alzheimer’s and all-type dementia using standardized cognitive assessments.

Over an average of 7.8 years, 1,991 (52%) adults had at least one ICU stay; 1,031 (27%) had an ICU stay before study enrollment; and 961 (25%) had an ICU stay during the study period.

In models adjusted for age, sex, education, and race, ICU hospitalization was associated with 63% higher risk of Alzheimer’s dementia (hazard ratio, 1.63; 95% confidence interval, 1.41-1.88) and 71% higher risk of all-type dementia (HR, 1.71; 95% CI, 1.48-1.97).

In models further adjusted for other health factors such as vascular risk factors and disease, other chronic medical conditions and functional disabilities, the association was even stronger: ICU hospitalization was associated with roughly double the risk of Alzheimer’s dementia (HR 2.10; 95% CI, 1.66-2.65) and all-type dementia (HR, 2.20; 95% CI, 1.75-2.77).

Dr. James said in an interview that it remains unclear why an ICU stay may raise the dementia risk.

“This study was not designed to assess the causes of the higher risk of dementia in persons who had ICU hospitalizations. However, researchers have looked into a number of factors that could account for this increased risk,” he explained.

One is critical illness itself that leads to hospitalization, which could result in damage to the brain; for example, severe COVID-19 has been shown to directly harm the brain, Dr. James said.

He also noted that specific events experienced during ICU stay have been shown to increase risk for cognitive impairment, including infection and severe sepsis, acute dialysis, neurologic dysfunction and delirium, and sedation.
 

Important work

Commenting on the study, Heather Snyder, PhD, vice president of medical & scientific relations at the Alzheimer’s Association, said what’s interesting about the study is that it looks at individuals in the ICU, regardless of the cause.

“The study shows that having some type of health issue that results in some type of ICU stay is associated with an increased risk of declining cognition,” Dr. Snyder said.

“That’s really important,” she said, “especially given the increase in individuals, particularly those 60 and older, who did experience an ICU stay over the last couple of years and understanding how that might impact their long-term risk related to Alzheimer’s and other changes in memory.”

“If an individual has been in the ICU, that should be part of the conversation with their physician or health care provider,” Dr. Snyder advised.

The study was funded by the National Institute on Aging. Dr. James and Dr. Snyder disclosed no relevant financial relationships.

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

Older adults who have spent time in the intensive care unit have double the risk of developing dementia in later years, compared with older adults who have never stayed in the ICU, new research suggests.

“ICU hospitalization may be an underrecognized risk factor for dementia in older adults,” Bryan D. James, PhD, epidemiologist with Rush Alzheimer’s Disease Center, Chicago, said in an interview.

“Health care providers caring for older patients who have experienced a hospitalization for critical illness should be prepared to assess and monitor their patients’ cognitive status as part of their long-term care plan,” Dr. James added.

The findings were presented at the Alzheimer’s Association International Conference.
 

Hidden risk factor?

ICU hospitalization as a result of critical illness has been linked to subsequent cognitive impairment in older patients. However, how ICU hospitalization relates to the long-term risk of developing Alzheimer’s and other age-related dementias is unknown.

“Given the high rate of ICU hospitalization in older persons, especially during the COVID-19 pandemic, it is critical to explore this relationship, Dr. James said.

The Rush team assessed the impact of an ICU stay on dementia risk in 3,822 older adults (mean age, 77 years) without known dementia at baseline participating in five diverse epidemiologic cohorts.

Participants were checked annually for development of Alzheimer’s and all-type dementia using standardized cognitive assessments.

Over an average of 7.8 years, 1,991 (52%) adults had at least one ICU stay; 1,031 (27%) had an ICU stay before study enrollment; and 961 (25%) had an ICU stay during the study period.

In models adjusted for age, sex, education, and race, ICU hospitalization was associated with 63% higher risk of Alzheimer’s dementia (hazard ratio, 1.63; 95% confidence interval, 1.41-1.88) and 71% higher risk of all-type dementia (HR, 1.71; 95% CI, 1.48-1.97).

In models further adjusted for other health factors such as vascular risk factors and disease, other chronic medical conditions and functional disabilities, the association was even stronger: ICU hospitalization was associated with roughly double the risk of Alzheimer’s dementia (HR 2.10; 95% CI, 1.66-2.65) and all-type dementia (HR, 2.20; 95% CI, 1.75-2.77).

Dr. James said in an interview that it remains unclear why an ICU stay may raise the dementia risk.

“This study was not designed to assess the causes of the higher risk of dementia in persons who had ICU hospitalizations. However, researchers have looked into a number of factors that could account for this increased risk,” he explained.

One is critical illness itself that leads to hospitalization, which could result in damage to the brain; for example, severe COVID-19 has been shown to directly harm the brain, Dr. James said.

He also noted that specific events experienced during ICU stay have been shown to increase risk for cognitive impairment, including infection and severe sepsis, acute dialysis, neurologic dysfunction and delirium, and sedation.
 

Important work

Commenting on the study, Heather Snyder, PhD, vice president of medical & scientific relations at the Alzheimer’s Association, said what’s interesting about the study is that it looks at individuals in the ICU, regardless of the cause.

“The study shows that having some type of health issue that results in some type of ICU stay is associated with an increased risk of declining cognition,” Dr. Snyder said.

“That’s really important,” she said, “especially given the increase in individuals, particularly those 60 and older, who did experience an ICU stay over the last couple of years and understanding how that might impact their long-term risk related to Alzheimer’s and other changes in memory.”

“If an individual has been in the ICU, that should be part of the conversation with their physician or health care provider,” Dr. Snyder advised.

The study was funded by the National Institute on Aging. Dr. James and Dr. Snyder disclosed no relevant financial relationships.

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

Cardiovascular disease (CVD) mortality rose significantly during the COVID-19 pandemic and persists more than 2 years on and, once again, Blacks and African Americans have been disproportionately affected, an analysis of death certificates shows.

The findings “suggest that the pandemic may reverse years or decades of work aimed at reducing gaps in cardiovascular outcomes,” Sadeer G. Al-Kindi, MD, Case Western Reserve University, Cleveland, said in an interview.

Although the disparities are in line with previous research, he said, “what was surprising is the persistence of excess cardiovascular mortality approximately 2 years after the pandemic started, even during a period of low COVID-19 mortality.”

“This suggests that the pandemic resulted in a disruption of health care access and, along with disparities in COVID-19 infection and its complications, he said, “may have a long-lasting effect on health care disparities, especially among vulnerable populations.”

The study was published online in Mayo Clinic Proceedings with lead author Scott E. Janus, MD, also of Case Western Reserve University.
 

Impact consistently greater for Blacks

Dr. Al-Kindi and colleagues used 3,598,352 U.S. death files to investigate trends in deaths caused specifically by CVD as well as its subtypes myocardial infarction, stroke, and heart failure (HF) in 2018 and 2019 (prepandemic) and the pandemic years 2020 and 2021. Baseline demographics showed a higher percentage of older, female, and Black individuals among the CVD subtypes of interest.

Overall, there was an excess CVD mortality of 6.7% during the pandemic, compared with prepandemic years, including a 2.5% rise in MI deaths and an 8.5% rise in stroke deaths. HF mortality remained relatively steady, rising only 0.1%.

Subgroup analyses revealed “striking differences” in excess mortality between Blacks and Whites, the authors noted. Blacks had an overall excess mortality of 13.8% versus 5.1% for Whites, compared with the prepandemic years. The differences were consistent across subtypes: MI (9.6% vs. 1.0%); stroke (14.5% vs. 6.9%); and HF (5.1% vs. –1.2%; P value for all < .001).

When the investigators looked at deaths on a yearly basis with 2018 as the baseline, they found CVD deaths increased by 1.5% in 2019, 15.8% in 2020, and 13.5% in 2021 among Black Americans, compared with 0.5%, 5.1%, and 5.7%, respectively, among White Americans.

Excess deaths from MI rose by 9.5% in 2020 and by 6.7% in 2021 among Blacks but fell by 1.2% in 2020 and by 1.0% in 2021 among Whites.

Disparities in excess HF mortality were similar, rising 9.1% and 4.1% in 2020 and 2021 among Blacks, while dipping 0.1% and 0.8% in 2020 and 2021 among Whites.

The “most striking difference” was in excess stroke mortality, which doubled among Blacks compared with whites in 2020 (14.9% vs. 6.7%) and in 2021 (17.5% vs. 8.1%), according to the authors.
 

Awareness urged

Although the disparities were expected, “there is clear value in documenting and quantifying the magnitude of these disparities,” Amil M. Shah, MD, MPH, of Harvard Medical School and Brigham and Women’s Hospital, both in Boston, said in an interview.

In addition to being observational, the main limitation of the study, he noted, is the quality and resolution of the death certificate data, which may limit the accuracy of the cause of death ascertainment and classification of race or ethnicity. “However, I think these potential inaccuracies are unlikely to materially impact the overall study findings.”

Dr. Shah, who was not involved in the study, said he would like to see additional research into the diversity and heterogeneity in risk among Black communities. “Understanding the environmental, social, and health care factors – both harmful and protective – that influence risk for CVD morbidity and mortality among Black individuals and communities offers the promise to provide actionable insights to mitigate these disparities.”

“Intervention studies testing approaches to mitigate disparities based on race/ethnicity” are also needed, he added. These may be at the policy, community, health system, or individual level, and community involvement in phases will be essential.”

Meanwhile, both Dr. Al-Kindi and Dr. Shah urged clinicians to be aware of the disparities and the need to improve access to care and address social determinants of health in vulnerable populations.

These disparities “are driven by structural factors, and are reinforced by individual behaviors. In this context, implicit bias training is important to help clinicians recognize and mitigate bias in their own practice,” Dr. Shah said. “Supporting diversity, equity, and inclusion efforts, and advocating for anti-racist policies and practices in their health systems” can also help.

Dr. Al-Kindi and Dr. Shah disclosed no relevant financial relationships.

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

Cardiovascular disease (CVD) mortality rose significantly during the COVID-19 pandemic and persists more than 2 years on and, once again, Blacks and African Americans have been disproportionately affected, an analysis of death certificates shows.

The findings “suggest that the pandemic may reverse years or decades of work aimed at reducing gaps in cardiovascular outcomes,” Sadeer G. Al-Kindi, MD, Case Western Reserve University, Cleveland, said in an interview.

Although the disparities are in line with previous research, he said, “what was surprising is the persistence of excess cardiovascular mortality approximately 2 years after the pandemic started, even during a period of low COVID-19 mortality.”

“This suggests that the pandemic resulted in a disruption of health care access and, along with disparities in COVID-19 infection and its complications, he said, “may have a long-lasting effect on health care disparities, especially among vulnerable populations.”

The study was published online in Mayo Clinic Proceedings with lead author Scott E. Janus, MD, also of Case Western Reserve University.
 

Impact consistently greater for Blacks

Dr. Al-Kindi and colleagues used 3,598,352 U.S. death files to investigate trends in deaths caused specifically by CVD as well as its subtypes myocardial infarction, stroke, and heart failure (HF) in 2018 and 2019 (prepandemic) and the pandemic years 2020 and 2021. Baseline demographics showed a higher percentage of older, female, and Black individuals among the CVD subtypes of interest.

Overall, there was an excess CVD mortality of 6.7% during the pandemic, compared with prepandemic years, including a 2.5% rise in MI deaths and an 8.5% rise in stroke deaths. HF mortality remained relatively steady, rising only 0.1%.

Subgroup analyses revealed “striking differences” in excess mortality between Blacks and Whites, the authors noted. Blacks had an overall excess mortality of 13.8% versus 5.1% for Whites, compared with the prepandemic years. The differences were consistent across subtypes: MI (9.6% vs. 1.0%); stroke (14.5% vs. 6.9%); and HF (5.1% vs. –1.2%; P value for all < .001).

When the investigators looked at deaths on a yearly basis with 2018 as the baseline, they found CVD deaths increased by 1.5% in 2019, 15.8% in 2020, and 13.5% in 2021 among Black Americans, compared with 0.5%, 5.1%, and 5.7%, respectively, among White Americans.

Excess deaths from MI rose by 9.5% in 2020 and by 6.7% in 2021 among Blacks but fell by 1.2% in 2020 and by 1.0% in 2021 among Whites.

Disparities in excess HF mortality were similar, rising 9.1% and 4.1% in 2020 and 2021 among Blacks, while dipping 0.1% and 0.8% in 2020 and 2021 among Whites.

The “most striking difference” was in excess stroke mortality, which doubled among Blacks compared with whites in 2020 (14.9% vs. 6.7%) and in 2021 (17.5% vs. 8.1%), according to the authors.
 

Awareness urged

Although the disparities were expected, “there is clear value in documenting and quantifying the magnitude of these disparities,” Amil M. Shah, MD, MPH, of Harvard Medical School and Brigham and Women’s Hospital, both in Boston, said in an interview.

In addition to being observational, the main limitation of the study, he noted, is the quality and resolution of the death certificate data, which may limit the accuracy of the cause of death ascertainment and classification of race or ethnicity. “However, I think these potential inaccuracies are unlikely to materially impact the overall study findings.”

Dr. Shah, who was not involved in the study, said he would like to see additional research into the diversity and heterogeneity in risk among Black communities. “Understanding the environmental, social, and health care factors – both harmful and protective – that influence risk for CVD morbidity and mortality among Black individuals and communities offers the promise to provide actionable insights to mitigate these disparities.”

“Intervention studies testing approaches to mitigate disparities based on race/ethnicity” are also needed, he added. These may be at the policy, community, health system, or individual level, and community involvement in phases will be essential.”

Meanwhile, both Dr. Al-Kindi and Dr. Shah urged clinicians to be aware of the disparities and the need to improve access to care and address social determinants of health in vulnerable populations.

These disparities “are driven by structural factors, and are reinforced by individual behaviors. In this context, implicit bias training is important to help clinicians recognize and mitigate bias in their own practice,” Dr. Shah said. “Supporting diversity, equity, and inclusion efforts, and advocating for anti-racist policies and practices in their health systems” can also help.

Dr. Al-Kindi and Dr. Shah disclosed no relevant financial relationships.

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

Cardiovascular disease (CVD) mortality rose significantly during the COVID-19 pandemic and persists more than 2 years on and, once again, Blacks and African Americans have been disproportionately affected, an analysis of death certificates shows.

The findings “suggest that the pandemic may reverse years or decades of work aimed at reducing gaps in cardiovascular outcomes,” Sadeer G. Al-Kindi, MD, Case Western Reserve University, Cleveland, said in an interview.

Although the disparities are in line with previous research, he said, “what was surprising is the persistence of excess cardiovascular mortality approximately 2 years after the pandemic started, even during a period of low COVID-19 mortality.”

“This suggests that the pandemic resulted in a disruption of health care access and, along with disparities in COVID-19 infection and its complications, he said, “may have a long-lasting effect on health care disparities, especially among vulnerable populations.”

The study was published online in Mayo Clinic Proceedings with lead author Scott E. Janus, MD, also of Case Western Reserve University.
 

Impact consistently greater for Blacks

Dr. Al-Kindi and colleagues used 3,598,352 U.S. death files to investigate trends in deaths caused specifically by CVD as well as its subtypes myocardial infarction, stroke, and heart failure (HF) in 2018 and 2019 (prepandemic) and the pandemic years 2020 and 2021. Baseline demographics showed a higher percentage of older, female, and Black individuals among the CVD subtypes of interest.

Overall, there was an excess CVD mortality of 6.7% during the pandemic, compared with prepandemic years, including a 2.5% rise in MI deaths and an 8.5% rise in stroke deaths. HF mortality remained relatively steady, rising only 0.1%.

Subgroup analyses revealed “striking differences” in excess mortality between Blacks and Whites, the authors noted. Blacks had an overall excess mortality of 13.8% versus 5.1% for Whites, compared with the prepandemic years. The differences were consistent across subtypes: MI (9.6% vs. 1.0%); stroke (14.5% vs. 6.9%); and HF (5.1% vs. –1.2%; P value for all < .001).

When the investigators looked at deaths on a yearly basis with 2018 as the baseline, they found CVD deaths increased by 1.5% in 2019, 15.8% in 2020, and 13.5% in 2021 among Black Americans, compared with 0.5%, 5.1%, and 5.7%, respectively, among White Americans.

Excess deaths from MI rose by 9.5% in 2020 and by 6.7% in 2021 among Blacks but fell by 1.2% in 2020 and by 1.0% in 2021 among Whites.

Disparities in excess HF mortality were similar, rising 9.1% and 4.1% in 2020 and 2021 among Blacks, while dipping 0.1% and 0.8% in 2020 and 2021 among Whites.

The “most striking difference” was in excess stroke mortality, which doubled among Blacks compared with whites in 2020 (14.9% vs. 6.7%) and in 2021 (17.5% vs. 8.1%), according to the authors.
 

Awareness urged

Although the disparities were expected, “there is clear value in documenting and quantifying the magnitude of these disparities,” Amil M. Shah, MD, MPH, of Harvard Medical School and Brigham and Women’s Hospital, both in Boston, said in an interview.

In addition to being observational, the main limitation of the study, he noted, is the quality and resolution of the death certificate data, which may limit the accuracy of the cause of death ascertainment and classification of race or ethnicity. “However, I think these potential inaccuracies are unlikely to materially impact the overall study findings.”

Dr. Shah, who was not involved in the study, said he would like to see additional research into the diversity and heterogeneity in risk among Black communities. “Understanding the environmental, social, and health care factors – both harmful and protective – that influence risk for CVD morbidity and mortality among Black individuals and communities offers the promise to provide actionable insights to mitigate these disparities.”

“Intervention studies testing approaches to mitigate disparities based on race/ethnicity” are also needed, he added. These may be at the policy, community, health system, or individual level, and community involvement in phases will be essential.”

Meanwhile, both Dr. Al-Kindi and Dr. Shah urged clinicians to be aware of the disparities and the need to improve access to care and address social determinants of health in vulnerable populations.

These disparities “are driven by structural factors, and are reinforced by individual behaviors. In this context, implicit bias training is important to help clinicians recognize and mitigate bias in their own practice,” Dr. Shah said. “Supporting diversity, equity, and inclusion efforts, and advocating for anti-racist policies and practices in their health systems” can also help.

Dr. Al-Kindi and Dr. Shah disclosed no relevant financial relationships.

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

The same genes that send people to the bathroom with an irritable bowel syndrome flare-up may be involved in future brain health, according to a new study. Researchers have found a genetic correlation between individuals with gastrointestinal tract (GIT) disorders and Alzheimer’s disease (AD).

Analyzing years of genetic data from AD studies and similar data from six GIT disorders, the scientists at the Center for Precision Health at Edith Cowan University in Australia found that many disease-specific genes shared the same loci, or chromosomal location, in each group.

The researchers say it is the first comprehensive look at the genetic relationship between these disorders. Prior to this, it was widely believed that there was a link between gastrointestinal disorders and AD. A 2020 longitudinal study noted that people with irritable bowel disease were six times more likely to suffer from AD. But the gut-brain axis had not yet been examined on a genetic basis.

“The study provides a novel insight into the genetics behind the observed co-occurrence of AD and gut disorders,” Emmanuel Adewuyi, PhD, MPH, said in an interview with EurekaAlert. Dr. Adewuyi, a postdoctoral research fellow at the Center for Precision Health at Edith Cowan University, led the study.

The authors say that understanding the underlying genetics of AD can provide clues about how the disease works, which is largely a mystery. Treatment of the disease is increasingly urgent in a world with growing life expectancy and incidence of AD. By 2030, over 82 million people will likely suffer from AD, according to the 2015 World Alzheimer’s Report.

The Australian study relied upon previously performed genome-wide association studies. They searched data for patients with AD, gastroesophageal reflux disease, peptic ulcer disease, gastritis-duodenitis, irritable bowel syndrome, diverticulosis, and irritable bowel disorder.

The final cohort represented over 450,000 people. Of those analyzed, they found that all the GIT disorders except irritable bowel disorder were correlated with AD.

One of the biological factors that underscored this relationship was the amount of abnormal cholesterol in both sets studied. From the study, It appears that altered cholesterol was a risk factor for both AD and gut disorders. Therefore, the authors suggest that next steps should investigate the use of statins, such as atorvastatin or lovastatin, which lower cholesterol to see whether they help protect the gut and, in turn, the brain.

Although these results point toward a correlation, the researchers caution that a causal relationship cannot be established between these two sets of disorders. The data advance the idea of the gut-brain axis but don’t show that GI problems cause AD or vice versa. Nor do the findings mean that someone with AD will always have gut problems or that a person with gut problems will develop AD.

The authors suggest the role of diet in health maintenance. They specifically highlight the Mediterranean diet, which is rich in natural fats and vegetables.

The study was independently supported. The authors report no relevant financial relationships.

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

The same genes that send people to the bathroom with an irritable bowel syndrome flare-up may be involved in future brain health, according to a new study. Researchers have found a genetic correlation between individuals with gastrointestinal tract (GIT) disorders and Alzheimer’s disease (AD).

Analyzing years of genetic data from AD studies and similar data from six GIT disorders, the scientists at the Center for Precision Health at Edith Cowan University in Australia found that many disease-specific genes shared the same loci, or chromosomal location, in each group.

The researchers say it is the first comprehensive look at the genetic relationship between these disorders. Prior to this, it was widely believed that there was a link between gastrointestinal disorders and AD. A 2020 longitudinal study noted that people with irritable bowel disease were six times more likely to suffer from AD. But the gut-brain axis had not yet been examined on a genetic basis.

“The study provides a novel insight into the genetics behind the observed co-occurrence of AD and gut disorders,” Emmanuel Adewuyi, PhD, MPH, said in an interview with EurekaAlert. Dr. Adewuyi, a postdoctoral research fellow at the Center for Precision Health at Edith Cowan University, led the study.

The authors say that understanding the underlying genetics of AD can provide clues about how the disease works, which is largely a mystery. Treatment of the disease is increasingly urgent in a world with growing life expectancy and incidence of AD. By 2030, over 82 million people will likely suffer from AD, according to the 2015 World Alzheimer’s Report.

The Australian study relied upon previously performed genome-wide association studies. They searched data for patients with AD, gastroesophageal reflux disease, peptic ulcer disease, gastritis-duodenitis, irritable bowel syndrome, diverticulosis, and irritable bowel disorder.

The final cohort represented over 450,000 people. Of those analyzed, they found that all the GIT disorders except irritable bowel disorder were correlated with AD.

One of the biological factors that underscored this relationship was the amount of abnormal cholesterol in both sets studied. From the study, It appears that altered cholesterol was a risk factor for both AD and gut disorders. Therefore, the authors suggest that next steps should investigate the use of statins, such as atorvastatin or lovastatin, which lower cholesterol to see whether they help protect the gut and, in turn, the brain.

Although these results point toward a correlation, the researchers caution that a causal relationship cannot be established between these two sets of disorders. The data advance the idea of the gut-brain axis but don’t show that GI problems cause AD or vice versa. Nor do the findings mean that someone with AD will always have gut problems or that a person with gut problems will develop AD.

The authors suggest the role of diet in health maintenance. They specifically highlight the Mediterranean diet, which is rich in natural fats and vegetables.

The study was independently supported. The authors report no relevant financial relationships.

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

The same genes that send people to the bathroom with an irritable bowel syndrome flare-up may be involved in future brain health, according to a new study. Researchers have found a genetic correlation between individuals with gastrointestinal tract (GIT) disorders and Alzheimer’s disease (AD).

Analyzing years of genetic data from AD studies and similar data from six GIT disorders, the scientists at the Center for Precision Health at Edith Cowan University in Australia found that many disease-specific genes shared the same loci, or chromosomal location, in each group.

The researchers say it is the first comprehensive look at the genetic relationship between these disorders. Prior to this, it was widely believed that there was a link between gastrointestinal disorders and AD. A 2020 longitudinal study noted that people with irritable bowel disease were six times more likely to suffer from AD. But the gut-brain axis had not yet been examined on a genetic basis.

“The study provides a novel insight into the genetics behind the observed co-occurrence of AD and gut disorders,” Emmanuel Adewuyi, PhD, MPH, said in an interview with EurekaAlert. Dr. Adewuyi, a postdoctoral research fellow at the Center for Precision Health at Edith Cowan University, led the study.

The authors say that understanding the underlying genetics of AD can provide clues about how the disease works, which is largely a mystery. Treatment of the disease is increasingly urgent in a world with growing life expectancy and incidence of AD. By 2030, over 82 million people will likely suffer from AD, according to the 2015 World Alzheimer’s Report.

The Australian study relied upon previously performed genome-wide association studies. They searched data for patients with AD, gastroesophageal reflux disease, peptic ulcer disease, gastritis-duodenitis, irritable bowel syndrome, diverticulosis, and irritable bowel disorder.

The final cohort represented over 450,000 people. Of those analyzed, they found that all the GIT disorders except irritable bowel disorder were correlated with AD.

One of the biological factors that underscored this relationship was the amount of abnormal cholesterol in both sets studied. From the study, It appears that altered cholesterol was a risk factor for both AD and gut disorders. Therefore, the authors suggest that next steps should investigate the use of statins, such as atorvastatin or lovastatin, which lower cholesterol to see whether they help protect the gut and, in turn, the brain.

Although these results point toward a correlation, the researchers caution that a causal relationship cannot be established between these two sets of disorders. The data advance the idea of the gut-brain axis but don’t show that GI problems cause AD or vice versa. Nor do the findings mean that someone with AD will always have gut problems or that a person with gut problems will develop AD.

The authors suggest the role of diet in health maintenance. They specifically highlight the Mediterranean diet, which is rich in natural fats and vegetables.

The study was independently supported. The authors report no relevant financial relationships.

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

Exercise in a pill? Sign us up

You just got home from a long shift and you know you should go to the gym, but the bed is calling and you just answered. We know sometimes we have to make sacrifices in the name of fitness, but there just aren’t enough hours in the day. Unless our prayers have been answered. There could be a pill that has the benefits of working out without having to work out.

In a study published in Nature, investigators reported that they have identified a molecule made during exercise and used it on mice, which took in less food after being given the pill, which may open doors to understanding how exercise affects hunger.

©Rido/Fotolia.com

Gonorrhea and grandparents: A match made in prehistoric heaven

*Editorial note: LOTME takes no responsibility for any unfortunate imagery the reader may have experienced from the above headline.

Old people are the greatest. Back pains, cognitive decline, aches in all the diodes down your left side, there’s nothing quite like your golden years. Notably, however, humans are one of the few animals who experience true old age, as most creatures are adapted to maximize reproductive potential. As such, living past menopause is rare in the animal kingdom.

CDC/John Martin Jr.

This is where the “grandmother hypothesis” comes in: Back in Ye Olde Stone Age, women who lived into old age could provide child care for younger women, because human babies require a lot more time and attention than other animal offspring. But how did humans end up living so long? Enter a group of Californian researchers, who believe they have an answer. It was gonorrhea.

When compared with the chimpanzee genome (as well as with Neanderthals and Denisovans, our closest ancestors), humans have a unique mutated version of the CD33 gene that lacks a sugar-binding site; the standard version uses the sugar-binding site to protect against autoimmune response in the body, but that same site actually suppresses the brain’s ability to clear away damaged brain cells and amyloid, which eventually leads to diseases like dementia. The mutated version allows microglia (brain immune cells) to attack and clear out this unwanted material. People with higher levels of this mutated CD33 variant actually have higher protection against Alzheimer’s.

Interestingly, gonorrhea bacteria are coated in the same sugar that standard CD33 receptors bind to, thus allowing them to bypass the body’s immune system. According to the researchers, the mutated CD33 version likely emerged as a protection against gonorrhea, depriving the bacteria of their “molecular mimicry” abilities. In one of life’s happy accidents, it turned out this mutation also protects against age-related diseases, thus allowing humans with the mutation to live longer. Obviously, this was a good thing, and we ran with it until the modern day. Now we have senior citizens climbing Everest, and all our politicians keep on politicking into their 70s and 80s ... well, everything has its drawbacks.
 

Parents raise a glass to children’s food addiction

There can be something pretty addicting about processed foods. Have you ever eaten just one french fry? Or taken just one cookie? If so, your willpower is incredible. For many of us, it can be a struggle to stop.

© Aleksandr Stennikov/Fotolia.com

A recent study from the University of Michigan, which considered the existence of an eating phenotype, suggests our parents’ habits could be to blame.

By administering a series of questionnaires that inquired about food addiction, alcohol use disorders, cannabis use disorder, nicotine/e-cigarette dependence, and their family tree, investigators found that participants with a “paternal history of problematic alcohol use” had higher risk of food addiction but not obesity.

Apparently about one in five people display a clinically significant addiction to highly processed foods. It was noted that foods like ice cream, pizza, and french fries have high amounts of refined carbs and fats, which could trigger an addictive response.

Lindzey Hoover, a graduate student at the university who was the study’s lead author, noted that living in an environment where these foods are cheap and accessible can be really challenging for those with a family history of addiction. The investigators suggested that public health approaches, like restriction of other substances and marketing to kids, should be put in place for highly processed foods.

Maybe french fries should come with a warning label.
 

A prescription for America’s traffic problems

Nostalgia is a funny thing. Do you ever feel nostalgic about things that really weren’t very pleasant in the first place? Take, for instance, the morning commute. Here in the Washington area, more than 2 years into the COVID era, the traffic is still not what it used to be … and we kind of miss it.

PhotoDisk

Nah, not really. That was just a way to get everyone thinking about driving, because AAA has something of an explanation for the situation out there on the highways and byways of America. It’s drugs. No, not those kinds of drugs. This time it’s prescription drugs that are the problem. Well, part of the problem, anyway.

AAA did a survey last summer and found that nearly 50% of drivers “used one or more potentially impairing medications in the past 30 days. … The proportion of those choosing to drive is higher among those taking multiple medications.” How much higher? More than 63% of those with two or more prescriptions were driving within 2 hours of taking at least one of those meds, as were 71% of those taking three or more.

The 2,657 respondents also were asked about the types of potentially impairing drugs they were taking: 61% of those using antidepressants had been on the road within 2 hours of use at least once in the past 30 days, as had 73% of those taking an amphetamine, AAA said.

So there you have it. That guy in the BMW who’s been tailgating you for the last 3 miles? He may be a jerk, but there’s a good chance he’s a jerk with a prescription … or two … or three.

Exercise in a pill? Sign us up

You just got home from a long shift and you know you should go to the gym, but the bed is calling and you just answered. We know sometimes we have to make sacrifices in the name of fitness, but there just aren’t enough hours in the day. Unless our prayers have been answered. There could be a pill that has the benefits of working out without having to work out.

In a study published in Nature, investigators reported that they have identified a molecule made during exercise and used it on mice, which took in less food after being given the pill, which may open doors to understanding how exercise affects hunger.

©Rido/Fotolia.com

Gonorrhea and grandparents: A match made in prehistoric heaven

*Editorial note: LOTME takes no responsibility for any unfortunate imagery the reader may have experienced from the above headline.

Old people are the greatest. Back pains, cognitive decline, aches in all the diodes down your left side, there’s nothing quite like your golden years. Notably, however, humans are one of the few animals who experience true old age, as most creatures are adapted to maximize reproductive potential. As such, living past menopause is rare in the animal kingdom.

CDC/John Martin Jr.

This is where the “grandmother hypothesis” comes in: Back in Ye Olde Stone Age, women who lived into old age could provide child care for younger women, because human babies require a lot more time and attention than other animal offspring. But how did humans end up living so long? Enter a group of Californian researchers, who believe they have an answer. It was gonorrhea.

When compared with the chimpanzee genome (as well as with Neanderthals and Denisovans, our closest ancestors), humans have a unique mutated version of the CD33 gene that lacks a sugar-binding site; the standard version uses the sugar-binding site to protect against autoimmune response in the body, but that same site actually suppresses the brain’s ability to clear away damaged brain cells and amyloid, which eventually leads to diseases like dementia. The mutated version allows microglia (brain immune cells) to attack and clear out this unwanted material. People with higher levels of this mutated CD33 variant actually have higher protection against Alzheimer’s.

Interestingly, gonorrhea bacteria are coated in the same sugar that standard CD33 receptors bind to, thus allowing them to bypass the body’s immune system. According to the researchers, the mutated CD33 version likely emerged as a protection against gonorrhea, depriving the bacteria of their “molecular mimicry” abilities. In one of life’s happy accidents, it turned out this mutation also protects against age-related diseases, thus allowing humans with the mutation to live longer. Obviously, this was a good thing, and we ran with it until the modern day. Now we have senior citizens climbing Everest, and all our politicians keep on politicking into their 70s and 80s ... well, everything has its drawbacks.
 

Parents raise a glass to children’s food addiction

There can be something pretty addicting about processed foods. Have you ever eaten just one french fry? Or taken just one cookie? If so, your willpower is incredible. For many of us, it can be a struggle to stop.

© Aleksandr Stennikov/Fotolia.com

A recent study from the University of Michigan, which considered the existence of an eating phenotype, suggests our parents’ habits could be to blame.

By administering a series of questionnaires that inquired about food addiction, alcohol use disorders, cannabis use disorder, nicotine/e-cigarette dependence, and their family tree, investigators found that participants with a “paternal history of problematic alcohol use” had higher risk of food addiction but not obesity.

Apparently about one in five people display a clinically significant addiction to highly processed foods. It was noted that foods like ice cream, pizza, and french fries have high amounts of refined carbs and fats, which could trigger an addictive response.

Lindzey Hoover, a graduate student at the university who was the study’s lead author, noted that living in an environment where these foods are cheap and accessible can be really challenging for those with a family history of addiction. The investigators suggested that public health approaches, like restriction of other substances and marketing to kids, should be put in place for highly processed foods.

Maybe french fries should come with a warning label.
 

A prescription for America’s traffic problems

Nostalgia is a funny thing. Do you ever feel nostalgic about things that really weren’t very pleasant in the first place? Take, for instance, the morning commute. Here in the Washington area, more than 2 years into the COVID era, the traffic is still not what it used to be … and we kind of miss it.

PhotoDisk

Nah, not really. That was just a way to get everyone thinking about driving, because AAA has something of an explanation for the situation out there on the highways and byways of America. It’s drugs. No, not those kinds of drugs. This time it’s prescription drugs that are the problem. Well, part of the problem, anyway.

AAA did a survey last summer and found that nearly 50% of drivers “used one or more potentially impairing medications in the past 30 days. … The proportion of those choosing to drive is higher among those taking multiple medications.” How much higher? More than 63% of those with two or more prescriptions were driving within 2 hours of taking at least one of those meds, as were 71% of those taking three or more.

The 2,657 respondents also were asked about the types of potentially impairing drugs they were taking: 61% of those using antidepressants had been on the road within 2 hours of use at least once in the past 30 days, as had 73% of those taking an amphetamine, AAA said.

So there you have it. That guy in the BMW who’s been tailgating you for the last 3 miles? He may be a jerk, but there’s a good chance he’s a jerk with a prescription … or two … or three.

Exercise in a pill? Sign us up

You just got home from a long shift and you know you should go to the gym, but the bed is calling and you just answered. We know sometimes we have to make sacrifices in the name of fitness, but there just aren’t enough hours in the day. Unless our prayers have been answered. There could be a pill that has the benefits of working out without having to work out.

In a study published in Nature, investigators reported that they have identified a molecule made during exercise and used it on mice, which took in less food after being given the pill, which may open doors to understanding how exercise affects hunger.

©Rido/Fotolia.com

Gonorrhea and grandparents: A match made in prehistoric heaven

*Editorial note: LOTME takes no responsibility for any unfortunate imagery the reader may have experienced from the above headline.

Old people are the greatest. Back pains, cognitive decline, aches in all the diodes down your left side, there’s nothing quite like your golden years. Notably, however, humans are one of the few animals who experience true old age, as most creatures are adapted to maximize reproductive potential. As such, living past menopause is rare in the animal kingdom.

CDC/John Martin Jr.

This is where the “grandmother hypothesis” comes in: Back in Ye Olde Stone Age, women who lived into old age could provide child care for younger women, because human babies require a lot more time and attention than other animal offspring. But how did humans end up living so long? Enter a group of Californian researchers, who believe they have an answer. It was gonorrhea.

When compared with the chimpanzee genome (as well as with Neanderthals and Denisovans, our closest ancestors), humans have a unique mutated version of the CD33 gene that lacks a sugar-binding site; the standard version uses the sugar-binding site to protect against autoimmune response in the body, but that same site actually suppresses the brain’s ability to clear away damaged brain cells and amyloid, which eventually leads to diseases like dementia. The mutated version allows microglia (brain immune cells) to attack and clear out this unwanted material. People with higher levels of this mutated CD33 variant actually have higher protection against Alzheimer’s.

Interestingly, gonorrhea bacteria are coated in the same sugar that standard CD33 receptors bind to, thus allowing them to bypass the body’s immune system. According to the researchers, the mutated CD33 version likely emerged as a protection against gonorrhea, depriving the bacteria of their “molecular mimicry” abilities. In one of life’s happy accidents, it turned out this mutation also protects against age-related diseases, thus allowing humans with the mutation to live longer. Obviously, this was a good thing, and we ran with it until the modern day. Now we have senior citizens climbing Everest, and all our politicians keep on politicking into their 70s and 80s ... well, everything has its drawbacks.
 

Parents raise a glass to children’s food addiction

There can be something pretty addicting about processed foods. Have you ever eaten just one french fry? Or taken just one cookie? If so, your willpower is incredible. For many of us, it can be a struggle to stop.

© Aleksandr Stennikov/Fotolia.com

A recent study from the University of Michigan, which considered the existence of an eating phenotype, suggests our parents’ habits could be to blame.

By administering a series of questionnaires that inquired about food addiction, alcohol use disorders, cannabis use disorder, nicotine/e-cigarette dependence, and their family tree, investigators found that participants with a “paternal history of problematic alcohol use” had higher risk of food addiction but not obesity.

Apparently about one in five people display a clinically significant addiction to highly processed foods. It was noted that foods like ice cream, pizza, and french fries have high amounts of refined carbs and fats, which could trigger an addictive response.

Lindzey Hoover, a graduate student at the university who was the study’s lead author, noted that living in an environment where these foods are cheap and accessible can be really challenging for those with a family history of addiction. The investigators suggested that public health approaches, like restriction of other substances and marketing to kids, should be put in place for highly processed foods.

Maybe french fries should come with a warning label.
 

A prescription for America’s traffic problems

Nostalgia is a funny thing. Do you ever feel nostalgic about things that really weren’t very pleasant in the first place? Take, for instance, the morning commute. Here in the Washington area, more than 2 years into the COVID era, the traffic is still not what it used to be … and we kind of miss it.

PhotoDisk

Nah, not really. That was just a way to get everyone thinking about driving, because AAA has something of an explanation for the situation out there on the highways and byways of America. It’s drugs. No, not those kinds of drugs. This time it’s prescription drugs that are the problem. Well, part of the problem, anyway.

AAA did a survey last summer and found that nearly 50% of drivers “used one or more potentially impairing medications in the past 30 days. … The proportion of those choosing to drive is higher among those taking multiple medications.” How much higher? More than 63% of those with two or more prescriptions were driving within 2 hours of taking at least one of those meds, as were 71% of those taking three or more.

The 2,657 respondents also were asked about the types of potentially impairing drugs they were taking: 61% of those using antidepressants had been on the road within 2 hours of use at least once in the past 30 days, as had 73% of those taking an amphetamine, AAA said.

So there you have it. That guy in the BMW who’s been tailgating you for the last 3 miles? He may be a jerk, but there’s a good chance he’s a jerk with a prescription … or two … or three.

There’s little doubt that long COVID is real. Even as doctors and federal agencies struggle to define the syndrome, hospitals and health care systems are opening long COVID specialty treatment programs. As of July 25, there’s at least one long COVID center in almost every state – 48 out of 50, according to the patient advocacy group Survivor Corps.

Among the biggest challenges will be treating the mental health effects of long COVID. Well after people recover from acute COVID infections, they can still have a wide range of lingering symptoms, including depression, anxiety, brain fog, and PTSD.

courtesy Oregon Health &amp; Science University

Specialized centers will be tackling these problems even as the United States struggles to deal with mental health needs.

One study of COVID patients found more than one-third of them had symptoms of depression, anxiety, or PTSD 3-6 months after their initial infection. Another analysis of 30 previous studies of long COVID patients found roughly one in eight of them had severe depression – and that the risk was similar regardless of whether people were hospitalized for COVID-19.

“Many of these symptoms can emerge months into the course of long COVID illness,” said Jordan Anderson, DO, a neuropsychiatrist who sees patients at the Long COVID-19 Program at Oregon Health & Science University, Portland. Psychological symptoms are often made worse by physical setbacks like extreme fatigue and by challenges of working, caring for children, and keeping up with daily routines, he said.

“This impact is not only severe, but also chronic for many,” he said.

Like dozens of hospitals around the country, Oregon Health & Science opened its center for long COVID as it became clear that more patients would need help for ongoing physical and mental health symptoms. Today, there’s at least one long COVID center – sometimes called post-COVID care centers or clinics – in every state but Kansas and South Dakota, Survivor Corps said.

Many long COVID care centers aim to tackle both physical and mental health symptoms, said Tracy Vannorsdall, PhD, a neuropsychologist with the Johns Hopkins Post-Acute COVID-19 Team program. One goal at Hopkins is to identify patients with psychological issues that might otherwise get overlooked.

A sizable minority of patients at the Johns Hopkins center – up to about 35% – report mental health problems that they didn’t have until after they got COVID-19, Dr. Vannorsdall says. The most common mental health issues providers see are depression, anxiety, and trauma-related distress.

“Routine assessment is key,” Dr. Vannorsdall said. “If patients are not asked about their mental health symptoms, they may not spontaneously report them to their provider due to fear of stigma or simply not appreciating that there are effective treatments available for these issues.”

Fear that doctors won’t take symptoms seriously is common, says Heather Murray MD, a senior instructor in psychiatry at the University of Colorado at Denver, Aurora.

“Many patients worry their physicians, loved ones, and society will not believe them or will minimize their symptoms and suffering,” said Dr. Murray, who treats patients at the UCHealth Post-COVID Clinic.

Diagnostic tests in long COVID patients often don’t have conclusive results, which can lead doctors and patients themselves to question whether symptoms are truly “physical versus psychosomatic,” she said. “It is important that providers believe their patients and treat their symptoms, even when diagnostic tests are unrevealing.”
 

Growing mental health crisis

Patients often find their way to academic treatment centers after surviving severe COVID-19 infections. But a growing number of long COVID patients show up at these centers after milder cases. These patients were never hospitalized for COVID-19 but still have persistent symptoms like fatigue, thinking problems, and mood disorders.

Among the major challenges is a shortage of mental health care providers to meet the surging need for care since the start of the pandemic. Around the world, anxiety and depression surged 25% during the first year of the pandemic, according to the World Health Organization.

In the United States, 40% of adults report feelings of anxiety and depression, and one in three high school students have feelings of sadness and hopelessness, according to a March 2022 statement from the White House.

Despite this surging need for care, almost half of Americans live in areas with a severe shortage of mental health care providers, according to the Health Resources and Services Administration. As of 2019, the United States had a shortage of about 6,790 mental health providers. Since then, the shortage has worsened; it’s now about 7,500 providers.

“One of the biggest challenges for hospitals and clinics in treating mental health disorders in long COVID is the limited resources and long wait times to get in for evaluations and treatment,” said Nyaz Didehbani, PhD, a neuropsychologist who treats long COVID patients at the COVID Recover program at the University of Texas Southwestern Medical Center, Dallas.

These delays can lead to worse outcomes, Dr. Didehbani said. “Additionally, patients do not feel that they are being heard, as many providers are not aware of the mental health impact and relationship with physical and cognitive symptoms.” .

Even when doctors recognize that psychological challenges are common with long COVID, they still have to think creatively to come up with treatments that meet the unique needs of these patients, said Thida Thant, MD, an assistant professor of psychiatry at the University of Colorado who treats patients at the UCHealth Post-COVID Clinic.

“There are at least two major factors that make treating psychological issues in long COVID more complex: The fact that the pandemic is still ongoing and still so divisive throughout society, and the fact that we don’t know a single best way to treat all symptoms of long COVID,” she said.

Some common treatments for anxiety and depression, like psychotherapy and medication, can be used for long COVID patients with these conditions. But another intervention that can work wonders for many people with mood disorders – exercise – doesn’t always work for long COVID patients. That’s because many of them struggle with physical challenges like chronic fatigue and what’s known as postexertional malaise, or a worsening of symptoms after even limited physical effort.

“While we normally encourage patients to be active, have a daily routine, and to engage in physical activity as part of their mental health treatment, some long COVID patients find that their symptoms worsen after increased activity,” Dr. Vannorsdall said.

Patients who are able to reach long COVID care centers are much more apt to get mental health problems diagnosed and treated, doctors at many programs around the country agree. But many patients hardest hit by the pandemic – the poor and racial and ethnic minorities – are also less likely to have ready access to hospitals that offer these programs, said Dr. Anderson.

“Affluent, predominantly White populations are showing up in these clinics, while we know that non-White populations have disproportionally high rates of acute infection, hospitalization, and death related to the virus,” he said.

Clinics are also concentrated in academic medical centers and in urban areas, limiting options for people in rural communities who may have to drive for hours to access care, Dr. Anderson said.

“Even before long COVID, we already knew that many people live in areas where there simply aren’t enough mental health services available,” said John Zulueta, MD, an assistant professor of clinical psychiatry at the University of Illinois at Chicago who provides mental health evaluations at the UI Health Post-COVID Clinic.

“As more patients develop mental health issues associated with long COVID, it’s going to put more stress on an already stressed system,” he said.

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

There’s little doubt that long COVID is real. Even as doctors and federal agencies struggle to define the syndrome, hospitals and health care systems are opening long COVID specialty treatment programs. As of July 25, there’s at least one long COVID center in almost every state – 48 out of 50, according to the patient advocacy group Survivor Corps.

Among the biggest challenges will be treating the mental health effects of long COVID. Well after people recover from acute COVID infections, they can still have a wide range of lingering symptoms, including depression, anxiety, brain fog, and PTSD.

courtesy Oregon Health &amp; Science University

Specialized centers will be tackling these problems even as the United States struggles to deal with mental health needs.

One study of COVID patients found more than one-third of them had symptoms of depression, anxiety, or PTSD 3-6 months after their initial infection. Another analysis of 30 previous studies of long COVID patients found roughly one in eight of them had severe depression – and that the risk was similar regardless of whether people were hospitalized for COVID-19.

“Many of these symptoms can emerge months into the course of long COVID illness,” said Jordan Anderson, DO, a neuropsychiatrist who sees patients at the Long COVID-19 Program at Oregon Health & Science University, Portland. Psychological symptoms are often made worse by physical setbacks like extreme fatigue and by challenges of working, caring for children, and keeping up with daily routines, he said.

“This impact is not only severe, but also chronic for many,” he said.

Like dozens of hospitals around the country, Oregon Health & Science opened its center for long COVID as it became clear that more patients would need help for ongoing physical and mental health symptoms. Today, there’s at least one long COVID center – sometimes called post-COVID care centers or clinics – in every state but Kansas and South Dakota, Survivor Corps said.

Many long COVID care centers aim to tackle both physical and mental health symptoms, said Tracy Vannorsdall, PhD, a neuropsychologist with the Johns Hopkins Post-Acute COVID-19 Team program. One goal at Hopkins is to identify patients with psychological issues that might otherwise get overlooked.

A sizable minority of patients at the Johns Hopkins center – up to about 35% – report mental health problems that they didn’t have until after they got COVID-19, Dr. Vannorsdall says. The most common mental health issues providers see are depression, anxiety, and trauma-related distress.

“Routine assessment is key,” Dr. Vannorsdall said. “If patients are not asked about their mental health symptoms, they may not spontaneously report them to their provider due to fear of stigma or simply not appreciating that there are effective treatments available for these issues.”

Fear that doctors won’t take symptoms seriously is common, says Heather Murray MD, a senior instructor in psychiatry at the University of Colorado at Denver, Aurora.

“Many patients worry their physicians, loved ones, and society will not believe them or will minimize their symptoms and suffering,” said Dr. Murray, who treats patients at the UCHealth Post-COVID Clinic.

Diagnostic tests in long COVID patients often don’t have conclusive results, which can lead doctors and patients themselves to question whether symptoms are truly “physical versus psychosomatic,” she said. “It is important that providers believe their patients and treat their symptoms, even when diagnostic tests are unrevealing.”
 

Growing mental health crisis

Patients often find their way to academic treatment centers after surviving severe COVID-19 infections. But a growing number of long COVID patients show up at these centers after milder cases. These patients were never hospitalized for COVID-19 but still have persistent symptoms like fatigue, thinking problems, and mood disorders.

Among the major challenges is a shortage of mental health care providers to meet the surging need for care since the start of the pandemic. Around the world, anxiety and depression surged 25% during the first year of the pandemic, according to the World Health Organization.

In the United States, 40% of adults report feelings of anxiety and depression, and one in three high school students have feelings of sadness and hopelessness, according to a March 2022 statement from the White House.

Despite this surging need for care, almost half of Americans live in areas with a severe shortage of mental health care providers, according to the Health Resources and Services Administration. As of 2019, the United States had a shortage of about 6,790 mental health providers. Since then, the shortage has worsened; it’s now about 7,500 providers.

“One of the biggest challenges for hospitals and clinics in treating mental health disorders in long COVID is the limited resources and long wait times to get in for evaluations and treatment,” said Nyaz Didehbani, PhD, a neuropsychologist who treats long COVID patients at the COVID Recover program at the University of Texas Southwestern Medical Center, Dallas.

These delays can lead to worse outcomes, Dr. Didehbani said. “Additionally, patients do not feel that they are being heard, as many providers are not aware of the mental health impact and relationship with physical and cognitive symptoms.” .

Even when doctors recognize that psychological challenges are common with long COVID, they still have to think creatively to come up with treatments that meet the unique needs of these patients, said Thida Thant, MD, an assistant professor of psychiatry at the University of Colorado who treats patients at the UCHealth Post-COVID Clinic.

“There are at least two major factors that make treating psychological issues in long COVID more complex: The fact that the pandemic is still ongoing and still so divisive throughout society, and the fact that we don’t know a single best way to treat all symptoms of long COVID,” she said.

Some common treatments for anxiety and depression, like psychotherapy and medication, can be used for long COVID patients with these conditions. But another intervention that can work wonders for many people with mood disorders – exercise – doesn’t always work for long COVID patients. That’s because many of them struggle with physical challenges like chronic fatigue and what’s known as postexertional malaise, or a worsening of symptoms after even limited physical effort.

“While we normally encourage patients to be active, have a daily routine, and to engage in physical activity as part of their mental health treatment, some long COVID patients find that their symptoms worsen after increased activity,” Dr. Vannorsdall said.

Patients who are able to reach long COVID care centers are much more apt to get mental health problems diagnosed and treated, doctors at many programs around the country agree. But many patients hardest hit by the pandemic – the poor and racial and ethnic minorities – are also less likely to have ready access to hospitals that offer these programs, said Dr. Anderson.

“Affluent, predominantly White populations are showing up in these clinics, while we know that non-White populations have disproportionally high rates of acute infection, hospitalization, and death related to the virus,” he said.

Clinics are also concentrated in academic medical centers and in urban areas, limiting options for people in rural communities who may have to drive for hours to access care, Dr. Anderson said.

“Even before long COVID, we already knew that many people live in areas where there simply aren’t enough mental health services available,” said John Zulueta, MD, an assistant professor of clinical psychiatry at the University of Illinois at Chicago who provides mental health evaluations at the UI Health Post-COVID Clinic.

“As more patients develop mental health issues associated with long COVID, it’s going to put more stress on an already stressed system,” he said.

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

There’s little doubt that long COVID is real. Even as doctors and federal agencies struggle to define the syndrome, hospitals and health care systems are opening long COVID specialty treatment programs. As of July 25, there’s at least one long COVID center in almost every state – 48 out of 50, according to the patient advocacy group Survivor Corps.

Among the biggest challenges will be treating the mental health effects of long COVID. Well after people recover from acute COVID infections, they can still have a wide range of lingering symptoms, including depression, anxiety, brain fog, and PTSD.

courtesy Oregon Health &amp; Science University

Specialized centers will be tackling these problems even as the United States struggles to deal with mental health needs.

One study of COVID patients found more than one-third of them had symptoms of depression, anxiety, or PTSD 3-6 months after their initial infection. Another analysis of 30 previous studies of long COVID patients found roughly one in eight of them had severe depression – and that the risk was similar regardless of whether people were hospitalized for COVID-19.

“Many of these symptoms can emerge months into the course of long COVID illness,” said Jordan Anderson, DO, a neuropsychiatrist who sees patients at the Long COVID-19 Program at Oregon Health & Science University, Portland. Psychological symptoms are often made worse by physical setbacks like extreme fatigue and by challenges of working, caring for children, and keeping up with daily routines, he said.

“This impact is not only severe, but also chronic for many,” he said.

Like dozens of hospitals around the country, Oregon Health & Science opened its center for long COVID as it became clear that more patients would need help for ongoing physical and mental health symptoms. Today, there’s at least one long COVID center – sometimes called post-COVID care centers or clinics – in every state but Kansas and South Dakota, Survivor Corps said.

Many long COVID care centers aim to tackle both physical and mental health symptoms, said Tracy Vannorsdall, PhD, a neuropsychologist with the Johns Hopkins Post-Acute COVID-19 Team program. One goal at Hopkins is to identify patients with psychological issues that might otherwise get overlooked.

A sizable minority of patients at the Johns Hopkins center – up to about 35% – report mental health problems that they didn’t have until after they got COVID-19, Dr. Vannorsdall says. The most common mental health issues providers see are depression, anxiety, and trauma-related distress.

“Routine assessment is key,” Dr. Vannorsdall said. “If patients are not asked about their mental health symptoms, they may not spontaneously report them to their provider due to fear of stigma or simply not appreciating that there are effective treatments available for these issues.”

Fear that doctors won’t take symptoms seriously is common, says Heather Murray MD, a senior instructor in psychiatry at the University of Colorado at Denver, Aurora.

“Many patients worry their physicians, loved ones, and society will not believe them or will minimize their symptoms and suffering,” said Dr. Murray, who treats patients at the UCHealth Post-COVID Clinic.

Diagnostic tests in long COVID patients often don’t have conclusive results, which can lead doctors and patients themselves to question whether symptoms are truly “physical versus psychosomatic,” she said. “It is important that providers believe their patients and treat their symptoms, even when diagnostic tests are unrevealing.”
 

Growing mental health crisis

Patients often find their way to academic treatment centers after surviving severe COVID-19 infections. But a growing number of long COVID patients show up at these centers after milder cases. These patients were never hospitalized for COVID-19 but still have persistent symptoms like fatigue, thinking problems, and mood disorders.

Among the major challenges is a shortage of mental health care providers to meet the surging need for care since the start of the pandemic. Around the world, anxiety and depression surged 25% during the first year of the pandemic, according to the World Health Organization.

In the United States, 40% of adults report feelings of anxiety and depression, and one in three high school students have feelings of sadness and hopelessness, according to a March 2022 statement from the White House.

Despite this surging need for care, almost half of Americans live in areas with a severe shortage of mental health care providers, according to the Health Resources and Services Administration. As of 2019, the United States had a shortage of about 6,790 mental health providers. Since then, the shortage has worsened; it’s now about 7,500 providers.

“One of the biggest challenges for hospitals and clinics in treating mental health disorders in long COVID is the limited resources and long wait times to get in for evaluations and treatment,” said Nyaz Didehbani, PhD, a neuropsychologist who treats long COVID patients at the COVID Recover program at the University of Texas Southwestern Medical Center, Dallas.

These delays can lead to worse outcomes, Dr. Didehbani said. “Additionally, patients do not feel that they are being heard, as many providers are not aware of the mental health impact and relationship with physical and cognitive symptoms.” .

Even when doctors recognize that psychological challenges are common with long COVID, they still have to think creatively to come up with treatments that meet the unique needs of these patients, said Thida Thant, MD, an assistant professor of psychiatry at the University of Colorado who treats patients at the UCHealth Post-COVID Clinic.

“There are at least two major factors that make treating psychological issues in long COVID more complex: The fact that the pandemic is still ongoing and still so divisive throughout society, and the fact that we don’t know a single best way to treat all symptoms of long COVID,” she said.

Some common treatments for anxiety and depression, like psychotherapy and medication, can be used for long COVID patients with these conditions. But another intervention that can work wonders for many people with mood disorders – exercise – doesn’t always work for long COVID patients. That’s because many of them struggle with physical challenges like chronic fatigue and what’s known as postexertional malaise, or a worsening of symptoms after even limited physical effort.

“While we normally encourage patients to be active, have a daily routine, and to engage in physical activity as part of their mental health treatment, some long COVID patients find that their symptoms worsen after increased activity,” Dr. Vannorsdall said.

Patients who are able to reach long COVID care centers are much more apt to get mental health problems diagnosed and treated, doctors at many programs around the country agree. But many patients hardest hit by the pandemic – the poor and racial and ethnic minorities – are also less likely to have ready access to hospitals that offer these programs, said Dr. Anderson.

“Affluent, predominantly White populations are showing up in these clinics, while we know that non-White populations have disproportionally high rates of acute infection, hospitalization, and death related to the virus,” he said.

Clinics are also concentrated in academic medical centers and in urban areas, limiting options for people in rural communities who may have to drive for hours to access care, Dr. Anderson said.

“Even before long COVID, we already knew that many people live in areas where there simply aren’t enough mental health services available,” said John Zulueta, MD, an assistant professor of clinical psychiatry at the University of Illinois at Chicago who provides mental health evaluations at the UI Health Post-COVID Clinic.

“As more patients develop mental health issues associated with long COVID, it’s going to put more stress on an already stressed system,” he said.

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

The more components of metabolic syndrome a person has in midlife seems to raise their risk of dementia, although that relationship seems to go away after age 70, a post hoc analysis of data from a major European cohort study has found.

A team of European researchers reported online in the journal Diabetes Care that the follow-up of the Whitehall II cohort study, a study of more than 10,000 civil servants in London that was established in the late 1980s, also found that cardiovascular disease (CVD) may only partially contribute to the risk of dementia in study participants.

They found that each additional metabolic syndrome component before age 60 years was linked to a 13% rise in the risk of dementia (hazard ratio, 1.13; 95% confidence interval [CI], 1.05-1.23) and, from age 60 to 70, the risk rose 8% (HR, 1.08; 95% CI, 1.00-1.16). However, in people aged 70 years and older, the relationship wasn’t statistically significant (HR, 1.04; 95% CI, 0.96-1.13]).

The study used “the latest harmonized definition” of metabolic syndrome; that is, participants were classified as having metabolic syndrome if they had three or more of the five components. As lead author Marcos D. Machado-Fragua, PhD, noted in an email interview, those components are abdominal obesity, high triglycerides, low HDL cholesterol levels, high blood pressure, and high fasting glucose.

“Our research question was on the association between metabolic syndrome and late-life dementia. We found that the presence of one metabolic syndrome component and the presence of metabolic risk before age 60, but not after, is associated with higher risk of dementia,” said Dr. Machado-Fragua, a post-doctoral researcher at the French Institute for Health and Medical Research in Paris.

The study cohort consisted of 10,308 London-based civil servants aged 35-55 years. Every 4-5 years after enrollment, from 1991 through 2016, they completed a questionnaire and had a clinical examination. The U.K. National Health Service electronic health record system tracked outcomes for all but 10 participants through March 2019.

The study identified the individual metabolic syndrome components that posed the highest risk for dementia in these three age groups:

• Age < 60 years: elevated waist circumference (HR 1.39 [95% CI 1.07, 1.81]), low HDL-C, (HR 1.30 [95% CI 1.02, 1.66]), and elevated blood pressure (HR 1.34 [95% CI 1.09, 1.63]).
• Age 60-70 years: low HDL-C (HR 1.26 [95% CI 1.02, 1.57]) and elevated fasting glucose (HR 1.40 [95% CI 1.12, 1.74]).
• Age >70 years: elevated fasting glucose (HR 1.38 [95% CI 1.07, 1.79]).

The study found that the dementia risk was significantly high in study participants under age 60 who had at least one (HR 1.99 [95% CI 1.08, 3.66]) or two (HR 1.69 [95% CI 1.12, 2.56]) metabolic syndrome components even when they didn’t have CVD.

“The present study adds to the understanding of the association between metabolic syndrome and dementia due to three novel features,” Dr. Machado-Fragua said. “First, we tested alternative thresholds to define ‘high metabolic risk,’ and findings show increased risk of dementia to start with the presence of one metabolic syndrome component. Second, assessment of metabolic syndrome components in midlife and later life allowed the examination of the role of age at prevalence of metabolic risk for incident dementia at older ages. Third, our findings showed high dementia risk in those free of cardiovascular disease during follow-up, suggesting that the association between high metabolic risk and incident dementia is not fully explained by cardiovascular disease.”

Dr. Machado-Fragua added, “For now, a cure for dementia remains elusive, making it important to think of prevention strategies. Our findings support targeting the components of the metabolic syndrome in midlife, even in those who have fewer than three of the metabolic syndrome components.”

Applicability ‘confusing’

In an interview, Yehuda Handelsman, MD, questioned the applicability of the study findings in the clinic. “Metabolic syndrome is a clinical manifestation of insulin resistance,” he said. “The more metabolic syndrome criteria a person has, the more insulin resistant that person will be. There is literature that is [suggesting] that insulin resistance is an important cause of dementia.”

The finding of a higher dementia risk before age 70, compared to afterward, makes the applicability “even more confusing,” he said. The results are even more muddled for U.S. physicians, who have moved away from the term metabolic syndrome in favor of cardiometabolic syndrome, said Dr. Handelsman, medical director and principal investigator at the Metabolic Institute of America and president of the Diabetes CardioRenal & Metabolism Institute, both in Tarzana, Calif.

Confusion also surrounds one of the components of metabolic syndrome: Waist circumference, per the harmonized definition the study used, and body mass index, which the more traditional definition uses.

Nonetheless, metabolic syndrome can be used as “kind of a risk calculator” for CVD, diabetes, and dementia, he said. One strength of the study, Dr. Handelsman said, is its size and scope, following 28 years of data. But a weakness was its observational design. “It doesn’t evaluate any true intervention to modify risk,” he said.

Dr. Machado-Fragua and coauthors have no disclosures.

The more components of metabolic syndrome a person has in midlife seems to raise their risk of dementia, although that relationship seems to go away after age 70, a post hoc analysis of data from a major European cohort study has found.

A team of European researchers reported online in the journal Diabetes Care that the follow-up of the Whitehall II cohort study, a study of more than 10,000 civil servants in London that was established in the late 1980s, also found that cardiovascular disease (CVD) may only partially contribute to the risk of dementia in study participants.

They found that each additional metabolic syndrome component before age 60 years was linked to a 13% rise in the risk of dementia (hazard ratio, 1.13; 95% confidence interval [CI], 1.05-1.23) and, from age 60 to 70, the risk rose 8% (HR, 1.08; 95% CI, 1.00-1.16). However, in people aged 70 years and older, the relationship wasn’t statistically significant (HR, 1.04; 95% CI, 0.96-1.13]).

The study used “the latest harmonized definition” of metabolic syndrome; that is, participants were classified as having metabolic syndrome if they had three or more of the five components. As lead author Marcos D. Machado-Fragua, PhD, noted in an email interview, those components are abdominal obesity, high triglycerides, low HDL cholesterol levels, high blood pressure, and high fasting glucose.

“Our research question was on the association between metabolic syndrome and late-life dementia. We found that the presence of one metabolic syndrome component and the presence of metabolic risk before age 60, but not after, is associated with higher risk of dementia,” said Dr. Machado-Fragua, a post-doctoral researcher at the French Institute for Health and Medical Research in Paris.

The study cohort consisted of 10,308 London-based civil servants aged 35-55 years. Every 4-5 years after enrollment, from 1991 through 2016, they completed a questionnaire and had a clinical examination. The U.K. National Health Service electronic health record system tracked outcomes for all but 10 participants through March 2019.

The study identified the individual metabolic syndrome components that posed the highest risk for dementia in these three age groups:

• Age < 60 years: elevated waist circumference (HR 1.39 [95% CI 1.07, 1.81]), low HDL-C, (HR 1.30 [95% CI 1.02, 1.66]), and elevated blood pressure (HR 1.34 [95% CI 1.09, 1.63]).
• Age 60-70 years: low HDL-C (HR 1.26 [95% CI 1.02, 1.57]) and elevated fasting glucose (HR 1.40 [95% CI 1.12, 1.74]).
• Age >70 years: elevated fasting glucose (HR 1.38 [95% CI 1.07, 1.79]).

The study found that the dementia risk was significantly high in study participants under age 60 who had at least one (HR 1.99 [95% CI 1.08, 3.66]) or two (HR 1.69 [95% CI 1.12, 2.56]) metabolic syndrome components even when they didn’t have CVD.

“The present study adds to the understanding of the association between metabolic syndrome and dementia due to three novel features,” Dr. Machado-Fragua said. “First, we tested alternative thresholds to define ‘high metabolic risk,’ and findings show increased risk of dementia to start with the presence of one metabolic syndrome component. Second, assessment of metabolic syndrome components in midlife and later life allowed the examination of the role of age at prevalence of metabolic risk for incident dementia at older ages. Third, our findings showed high dementia risk in those free of cardiovascular disease during follow-up, suggesting that the association between high metabolic risk and incident dementia is not fully explained by cardiovascular disease.”

Dr. Machado-Fragua added, “For now, a cure for dementia remains elusive, making it important to think of prevention strategies. Our findings support targeting the components of the metabolic syndrome in midlife, even in those who have fewer than three of the metabolic syndrome components.”

Applicability ‘confusing’

In an interview, Yehuda Handelsman, MD, questioned the applicability of the study findings in the clinic. “Metabolic syndrome is a clinical manifestation of insulin resistance,” he said. “The more metabolic syndrome criteria a person has, the more insulin resistant that person will be. There is literature that is [suggesting] that insulin resistance is an important cause of dementia.”

The finding of a higher dementia risk before age 70, compared to afterward, makes the applicability “even more confusing,” he said. The results are even more muddled for U.S. physicians, who have moved away from the term metabolic syndrome in favor of cardiometabolic syndrome, said Dr. Handelsman, medical director and principal investigator at the Metabolic Institute of America and president of the Diabetes CardioRenal & Metabolism Institute, both in Tarzana, Calif.

Confusion also surrounds one of the components of metabolic syndrome: Waist circumference, per the harmonized definition the study used, and body mass index, which the more traditional definition uses.

Nonetheless, metabolic syndrome can be used as “kind of a risk calculator” for CVD, diabetes, and dementia, he said. One strength of the study, Dr. Handelsman said, is its size and scope, following 28 years of data. But a weakness was its observational design. “It doesn’t evaluate any true intervention to modify risk,” he said.

Dr. Machado-Fragua and coauthors have no disclosures.

The more components of metabolic syndrome a person has in midlife seems to raise their risk of dementia, although that relationship seems to go away after age 70, a post hoc analysis of data from a major European cohort study has found.

A team of European researchers reported online in the journal Diabetes Care that the follow-up of the Whitehall II cohort study, a study of more than 10,000 civil servants in London that was established in the late 1980s, also found that cardiovascular disease (CVD) may only partially contribute to the risk of dementia in study participants.

They found that each additional metabolic syndrome component before age 60 years was linked to a 13% rise in the risk of dementia (hazard ratio, 1.13; 95% confidence interval [CI], 1.05-1.23) and, from age 60 to 70, the risk rose 8% (HR, 1.08; 95% CI, 1.00-1.16). However, in people aged 70 years and older, the relationship wasn’t statistically significant (HR, 1.04; 95% CI, 0.96-1.13]).

The study used “the latest harmonized definition” of metabolic syndrome; that is, participants were classified as having metabolic syndrome if they had three or more of the five components. As lead author Marcos D. Machado-Fragua, PhD, noted in an email interview, those components are abdominal obesity, high triglycerides, low HDL cholesterol levels, high blood pressure, and high fasting glucose.

“Our research question was on the association between metabolic syndrome and late-life dementia. We found that the presence of one metabolic syndrome component and the presence of metabolic risk before age 60, but not after, is associated with higher risk of dementia,” said Dr. Machado-Fragua, a post-doctoral researcher at the French Institute for Health and Medical Research in Paris.

The study cohort consisted of 10,308 London-based civil servants aged 35-55 years. Every 4-5 years after enrollment, from 1991 through 2016, they completed a questionnaire and had a clinical examination. The U.K. National Health Service electronic health record system tracked outcomes for all but 10 participants through March 2019.

The study identified the individual metabolic syndrome components that posed the highest risk for dementia in these three age groups:

• Age < 60 years: elevated waist circumference (HR 1.39 [95% CI 1.07, 1.81]), low HDL-C, (HR 1.30 [95% CI 1.02, 1.66]), and elevated blood pressure (HR 1.34 [95% CI 1.09, 1.63]).
• Age 60-70 years: low HDL-C (HR 1.26 [95% CI 1.02, 1.57]) and elevated fasting glucose (HR 1.40 [95% CI 1.12, 1.74]).
• Age >70 years: elevated fasting glucose (HR 1.38 [95% CI 1.07, 1.79]).

The study found that the dementia risk was significantly high in study participants under age 60 who had at least one (HR 1.99 [95% CI 1.08, 3.66]) or two (HR 1.69 [95% CI 1.12, 2.56]) metabolic syndrome components even when they didn’t have CVD.

“The present study adds to the understanding of the association between metabolic syndrome and dementia due to three novel features,” Dr. Machado-Fragua said. “First, we tested alternative thresholds to define ‘high metabolic risk,’ and findings show increased risk of dementia to start with the presence of one metabolic syndrome component. Second, assessment of metabolic syndrome components in midlife and later life allowed the examination of the role of age at prevalence of metabolic risk for incident dementia at older ages. Third, our findings showed high dementia risk in those free of cardiovascular disease during follow-up, suggesting that the association between high metabolic risk and incident dementia is not fully explained by cardiovascular disease.”

Dr. Machado-Fragua added, “For now, a cure for dementia remains elusive, making it important to think of prevention strategies. Our findings support targeting the components of the metabolic syndrome in midlife, even in those who have fewer than three of the metabolic syndrome components.”

Applicability ‘confusing’

In an interview, Yehuda Handelsman, MD, questioned the applicability of the study findings in the clinic. “Metabolic syndrome is a clinical manifestation of insulin resistance,” he said. “The more metabolic syndrome criteria a person has, the more insulin resistant that person will be. There is literature that is [suggesting] that insulin resistance is an important cause of dementia.”

The finding of a higher dementia risk before age 70, compared to afterward, makes the applicability “even more confusing,” he said. The results are even more muddled for U.S. physicians, who have moved away from the term metabolic syndrome in favor of cardiometabolic syndrome, said Dr. Handelsman, medical director and principal investigator at the Metabolic Institute of America and president of the Diabetes CardioRenal & Metabolism Institute, both in Tarzana, Calif.

Confusion also surrounds one of the components of metabolic syndrome: Waist circumference, per the harmonized definition the study used, and body mass index, which the more traditional definition uses.

Nonetheless, metabolic syndrome can be used as “kind of a risk calculator” for CVD, diabetes, and dementia, he said. One strength of the study, Dr. Handelsman said, is its size and scope, following 28 years of data. But a weakness was its observational design. “It doesn’t evaluate any true intervention to modify risk,” he said.

Dr. Machado-Fragua and coauthors have no disclosures.

For the seventh consecutive year, the Mayo Clinic in Rochester, Minn., took the top spot in the annual honor roll of best hospitals, published July 26 by U.S. News & World Report.

The 2022 rankings, which marks the 33rd edition, showcase several methodology changes, including new ratings for ovarian, prostate, and uterine cancer surgeries that “provide patients ... with previously unavailable information to assist them in making a critical health care decision,” a news release from the publication explains.

Additional expanded health equity measures assess “which hospitals provide more care to low-income patients and which have racial disparities in certain surgical outcomes,” said the release. Finally, a new metric called “home time” determines how successfully each hospital helps patients return home.
 

Mayo Clinic remains No. 1

For the 2022-2023 rankings and ratings, U.S. News compared more than 4,500 medical centers across the country in 15 specialties and 20 procedures and conditions. Of these, 493 were recognized as Best Regional Hospitals as a result of their overall strong performance.

The list was then narrowed to the top 20 hospitals, outlined in the honor roll below, that deliver “exceptional treatment across multiple areas of care.”

Following Mayo Clinic in the annual ranking’s top spot, Cedars-Sinai Medical Center in Los Angeles rises from No. 6 to No. 2, and New York University Langone Hospitals finish third, up from eighth in 2021.

Cleveland Clinic in Ohio holds the No. 4 spot, down two from 2021, while Johns Hopkins Hospital in Baltimore and UCLA Medical Center in Los Angeles tie for fifth place. Rounding out the top 10, in order, are: New York–Presbyterian Hospital–Columbia and Cornell, New York; Massachusetts General Hospital, Boston; Northwestern Memorial Hospital, Chicago; Stanford (Calif.) Health Care–Stanford Hospital.

The following hospitals complete the top 20 in the United States:

• 11. Barnes-Jewish Hospital, St. Louis
• 12. UCSF Medical Center, San Francisco
• 13. Hospitals of the University of Pennsylvania–Penn Presbyterian, Philadelphia
• 14. Brigham and Women’s Hospital, Boston
• 15. Houston Methodist Hospital
• 16. Mount Sinai Hospital, New York
• 17. University of Michigan Health–Michigan Medicine, Ann Arbor
• 18. Mayo Clinic–Phoenix
• 19. Vanderbilt University Medical Center, Nashville, Tenn.
• 20. Rush University Medical Center, Chicago

For the specialty rankings, the University of Texas MD Anderson Cancer Center, Houston, remains No. 1 in cancer care, the Cleveland Clinic is No. 1 in cardiology and heart surgery, and the Hospital for Special Surgery in New York is No. 1 in orthopedics.
 

Top five for cancer

• 1. University of Texas MD Anderson Cancer Center, Houston
• 2. Memorial Sloan Kettering Cancer Center, New York
• 3. Mayo Clinic, Rochester, Minn.
• 4. Dana-Farber/Brigham and Women’s Cancer Center, Boston
• 5. UCLA Medical Center, Los Angeles

Top five for cardiology and heart surgery

• 1. Cleveland Clinic
• 2. Mayo Clinic, Rochester, Minn.
• 3. Cedars-Sinai Medical Center, Los Angeles
• 4. New York–Presbyterian Hospital–Columbia and Cornell, New York
• 5. New York University Langone Hospitals

Top five for orthopedics

• 1. Hospital for Special Surgery, New York
• 2. Mayo Clinic, Rochester, Minn.
• 3. Cedars-Sinai Medical Center, Los Angeles
• 4. New York University Langone Hospitals
• 5. (tie) Rush University Medical Center, Chicago
• 5. (tie) UCLA Medical Center, Los Angeles

According to the news release, the procedures and conditions ratings are based entirely on objective patient care measures like survival rates, patient experience, home time, and level of nursing care. The Best Hospitals rankings consider a variety of data provided by the Centers for Medicare & Medicaid Services, American Hospital Association, professional organizations, and medical specialists.

The full report is available online.

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

For the seventh consecutive year, the Mayo Clinic in Rochester, Minn., took the top spot in the annual honor roll of best hospitals, published July 26 by U.S. News & World Report.

The 2022 rankings, which marks the 33rd edition, showcase several methodology changes, including new ratings for ovarian, prostate, and uterine cancer surgeries that “provide patients ... with previously unavailable information to assist them in making a critical health care decision,” a news release from the publication explains.

Additional expanded health equity measures assess “which hospitals provide more care to low-income patients and which have racial disparities in certain surgical outcomes,” said the release. Finally, a new metric called “home time” determines how successfully each hospital helps patients return home.
 

Mayo Clinic remains No. 1

For the 2022-2023 rankings and ratings, U.S. News compared more than 4,500 medical centers across the country in 15 specialties and 20 procedures and conditions. Of these, 493 were recognized as Best Regional Hospitals as a result of their overall strong performance.

The list was then narrowed to the top 20 hospitals, outlined in the honor roll below, that deliver “exceptional treatment across multiple areas of care.”

Following Mayo Clinic in the annual ranking’s top spot, Cedars-Sinai Medical Center in Los Angeles rises from No. 6 to No. 2, and New York University Langone Hospitals finish third, up from eighth in 2021.

Cleveland Clinic in Ohio holds the No. 4 spot, down two from 2021, while Johns Hopkins Hospital in Baltimore and UCLA Medical Center in Los Angeles tie for fifth place. Rounding out the top 10, in order, are: New York–Presbyterian Hospital–Columbia and Cornell, New York; Massachusetts General Hospital, Boston; Northwestern Memorial Hospital, Chicago; Stanford (Calif.) Health Care–Stanford Hospital.

The following hospitals complete the top 20 in the United States:

• 11. Barnes-Jewish Hospital, St. Louis
• 12. UCSF Medical Center, San Francisco
• 13. Hospitals of the University of Pennsylvania–Penn Presbyterian, Philadelphia
• 14. Brigham and Women’s Hospital, Boston
• 15. Houston Methodist Hospital
• 16. Mount Sinai Hospital, New York
• 17. University of Michigan Health–Michigan Medicine, Ann Arbor
• 18. Mayo Clinic–Phoenix
• 19. Vanderbilt University Medical Center, Nashville, Tenn.
• 20. Rush University Medical Center, Chicago

For the specialty rankings, the University of Texas MD Anderson Cancer Center, Houston, remains No. 1 in cancer care, the Cleveland Clinic is No. 1 in cardiology and heart surgery, and the Hospital for Special Surgery in New York is No. 1 in orthopedics.
 

Top five for cancer

• 1. University of Texas MD Anderson Cancer Center, Houston
• 2. Memorial Sloan Kettering Cancer Center, New York
• 3. Mayo Clinic, Rochester, Minn.
• 4. Dana-Farber/Brigham and Women’s Cancer Center, Boston
• 5. UCLA Medical Center, Los Angeles

Top five for cardiology and heart surgery

• 1. Cleveland Clinic
• 2. Mayo Clinic, Rochester, Minn.
• 3. Cedars-Sinai Medical Center, Los Angeles
• 4. New York–Presbyterian Hospital–Columbia and Cornell, New York
• 5. New York University Langone Hospitals

Top five for orthopedics

• 1. Hospital for Special Surgery, New York
• 2. Mayo Clinic, Rochester, Minn.
• 3. Cedars-Sinai Medical Center, Los Angeles
• 4. New York University Langone Hospitals
• 5. (tie) Rush University Medical Center, Chicago
• 5. (tie) UCLA Medical Center, Los Angeles

According to the news release, the procedures and conditions ratings are based entirely on objective patient care measures like survival rates, patient experience, home time, and level of nursing care. The Best Hospitals rankings consider a variety of data provided by the Centers for Medicare & Medicaid Services, American Hospital Association, professional organizations, and medical specialists.

The full report is available online.

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

For the seventh consecutive year, the Mayo Clinic in Rochester, Minn., took the top spot in the annual honor roll of best hospitals, published July 26 by U.S. News & World Report.

The 2022 rankings, which marks the 33rd edition, showcase several methodology changes, including new ratings for ovarian, prostate, and uterine cancer surgeries that “provide patients ... with previously unavailable information to assist them in making a critical health care decision,” a news release from the publication explains.

Additional expanded health equity measures assess “which hospitals provide more care to low-income patients and which have racial disparities in certain surgical outcomes,” said the release. Finally, a new metric called “home time” determines how successfully each hospital helps patients return home.
 

Mayo Clinic remains No. 1

For the 2022-2023 rankings and ratings, U.S. News compared more than 4,500 medical centers across the country in 15 specialties and 20 procedures and conditions. Of these, 493 were recognized as Best Regional Hospitals as a result of their overall strong performance.

The list was then narrowed to the top 20 hospitals, outlined in the honor roll below, that deliver “exceptional treatment across multiple areas of care.”

Following Mayo Clinic in the annual ranking’s top spot, Cedars-Sinai Medical Center in Los Angeles rises from No. 6 to No. 2, and New York University Langone Hospitals finish third, up from eighth in 2021.

Cleveland Clinic in Ohio holds the No. 4 spot, down two from 2021, while Johns Hopkins Hospital in Baltimore and UCLA Medical Center in Los Angeles tie for fifth place. Rounding out the top 10, in order, are: New York–Presbyterian Hospital–Columbia and Cornell, New York; Massachusetts General Hospital, Boston; Northwestern Memorial Hospital, Chicago; Stanford (Calif.) Health Care–Stanford Hospital.

The following hospitals complete the top 20 in the United States:

• 11. Barnes-Jewish Hospital, St. Louis
• 12. UCSF Medical Center, San Francisco
• 13. Hospitals of the University of Pennsylvania–Penn Presbyterian, Philadelphia
• 14. Brigham and Women’s Hospital, Boston
• 15. Houston Methodist Hospital
• 16. Mount Sinai Hospital, New York
• 17. University of Michigan Health–Michigan Medicine, Ann Arbor
• 18. Mayo Clinic–Phoenix
• 19. Vanderbilt University Medical Center, Nashville, Tenn.
• 20. Rush University Medical Center, Chicago

For the specialty rankings, the University of Texas MD Anderson Cancer Center, Houston, remains No. 1 in cancer care, the Cleveland Clinic is No. 1 in cardiology and heart surgery, and the Hospital for Special Surgery in New York is No. 1 in orthopedics.
 

Top five for cancer

• 1. University of Texas MD Anderson Cancer Center, Houston
• 2. Memorial Sloan Kettering Cancer Center, New York
• 3. Mayo Clinic, Rochester, Minn.
• 4. Dana-Farber/Brigham and Women’s Cancer Center, Boston
• 5. UCLA Medical Center, Los Angeles

Top five for cardiology and heart surgery

• 1. Cleveland Clinic
• 2. Mayo Clinic, Rochester, Minn.
• 3. Cedars-Sinai Medical Center, Los Angeles
• 4. New York–Presbyterian Hospital–Columbia and Cornell, New York
• 5. New York University Langone Hospitals

Top five for orthopedics

• 1. Hospital for Special Surgery, New York
• 2. Mayo Clinic, Rochester, Minn.
• 3. Cedars-Sinai Medical Center, Los Angeles
• 4. New York University Langone Hospitals
• 5. (tie) Rush University Medical Center, Chicago
• 5. (tie) UCLA Medical Center, Los Angeles

According to the news release, the procedures and conditions ratings are based entirely on objective patient care measures like survival rates, patient experience, home time, and level of nursing care. The Best Hospitals rankings consider a variety of data provided by the Centers for Medicare & Medicaid Services, American Hospital Association, professional organizations, and medical specialists.

The full report is available online.

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