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Nine more minutes a day of vigorous exercise tied to better cognition
such as running and cycling, plays in brain health.
“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.
The findings were published online in the Journal of Epidemiology and Community Health.
Research gap
Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.
Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.
In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.
The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.
The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.
The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.
The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.
Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.
On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.
Researchers calculated an overall global score for verbal memory and executive function.
The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.
The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.
SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.
To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.
“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
Real cognitive change
There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.
Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”
The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.
On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.
The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”
Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
Important findings
In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.
“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”
She added that this seemed to be especially true for people who sit while at work.
The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.
“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”
She noted the study was cross-sectional, “so it is not possible to infer causation.”
The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
such as running and cycling, plays in brain health.
“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.
The findings were published online in the Journal of Epidemiology and Community Health.
Research gap
Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.
Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.
In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.
The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.
The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.
The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.
The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.
Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.
On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.
Researchers calculated an overall global score for verbal memory and executive function.
The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.
The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.
SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.
To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.
“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
Real cognitive change
There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.
Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”
The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.
On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.
The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”
Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
Important findings
In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.
“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”
She added that this seemed to be especially true for people who sit while at work.
The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.
“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”
She noted the study was cross-sectional, “so it is not possible to infer causation.”
The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
such as running and cycling, plays in brain health.
“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.
The findings were published online in the Journal of Epidemiology and Community Health.
Research gap
Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.
Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.
In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.
The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.
The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.
The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.
The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.
Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.
On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.
Researchers calculated an overall global score for verbal memory and executive function.
The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.
The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.
SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.
To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.
“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
Real cognitive change
There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.
Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”
The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.
On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.
The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”
Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
Important findings
In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.
“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”
She added that this seemed to be especially true for people who sit while at work.
The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.
“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”
She noted the study was cross-sectional, “so it is not possible to infer causation.”
The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH
Meet the JCOM Author with Dr. Barkoudah: Development of a Safety Awards Program at a VA Health Care System
Meet the JCOM Author with Dr. Barkoudah: Teaching Quality Improvement to Internal Medicine Residents
Flu, other common viruses linked to neurologic disease
People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows.
The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.
The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders.
“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”
For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.
Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.
Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.
“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”
The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.
The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.
A version of this article first appeared on WebMD.com.
People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows.
The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.
The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders.
“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”
For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.
Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.
Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.
“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”
The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.
The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.
A version of this article first appeared on WebMD.com.
People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows.
The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.
The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders.
“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”
For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.
Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.
Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.
“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”
The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.
The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.
A version of this article first appeared on WebMD.com.
FROM NEURON
My patient chose quality of life over treatment
Several decades ago, a new patient came to my office with her family. She was elderly, in good health, spoke no English, and her extended family translated for her. Their request: “Don’t tell her that she has cancer.” Sharing her diagnosis with her would cause too much stress, they said. Their mother would not be able to tolerate the bad news, they said. She would “give up.”
I asked her (through her family and an interpreter) how much she wanted to know about what was going on, or would she prefer I confine my remarks to her family? It turns out that she did want to know her diagnosis and prognosis, and after a thorough discussion in front of her family about her treatment options, she decided she did not want to proceed with additional therapy. She wanted to focus on quality of life. I did not get the impression that this is what her family would have opted for.
The patient’s voice can take multiple directions, such as making informed decisions about their own care. When empowered, patients can and will express their wants, needs, feelings, and priorities to their providers, and they’ll participate in directing their own care. There is a growing body of evidence that shows patients who are more engaged and share decision-making with their health care professionals have better health outcomes and care experiences. Engaged patients feel more empowered and are more motivated to take action. They’re also more likely to follow treatment plans, take their medications, and heed their provider’s recommendations. By virtue of better treatments for lung cancer, many patients are living longer and better lives. Some of these patients even become “experts” on their own care, often bringing questions about research and clinical trials to the attention of their providers.
The patient’s voice in research and advocacy
The patient’s perspective is also key to a meaningful, successful clinical research project. Rather than being carried out to, about, or for the patient, patient involvement means research being carried out with or by patients. A patient and researcher may have different research goals. For example, patients may value being able to work, be with family, and live without pain, whereas a clinical researcher’s goal may be inducing responses. Patient involvement is important in both laboratory research and clinical research. The best-designed projects involve patient advocates from the beginning of the project to help make research relevant and meaningful to patients and include these perspectives through project completion.
More and more pharmaceutical companies are actively involving patients at all levels of protocol development, including protocol design and selection of relevant outcomes to patients. Benefits of engaging patients as partners in research include inclusion of real-world data, increased study enrollment, and translation of results to the cancer community in an understandable and accessible manner.
Accelerated research
Advocating for accelerated research is another area where the patient’s voice is important. Patients can and do identify research priorities for researchers, funding agencies, and pharma. Patients who support research advocacy are frequently part of meetings and panel discussions with researchers, the Food and Drug Administration, and the National Cancer Institute. And, they serve on advisory boards for pharmaceutical companies. They participate in grant reviews and institutional review boards, review manuscripts, and are active members of the cooperative groups and other professional societies. In fact, patient-led advocacy groups are raising money to help fund research they feel is most important to them. In lung cancer, for example, there are many groups organized around biomarkers, including the EGFR Resisters, ALK Positive, ROS1ders, MET Crusaders, and KRAS Kickers, who have raised hundreds of thousands of dollars to fund investigator-led translational research that would not have occurred without their involvement.
It is important to recognize that all patients are different and have different values and motivations that are important to them and influence their life decisions. Some patients want to know more about their condition and their preferences should be respected. Similarly, it’s critical to understand that not every patient is an advocate and not every advocate is a research advocate. Research advocates have more in-depth knowledge about the science of lung cancer and focus on representing the patient perspective for all lung cancer patients.
So, getting back to my original story: Did my patient “give up” by choosing palliative care without chemotherapy? Perhaps, but I don’t think she considered her decision “giving up.” Instead, she made the best decision possible for herself. What would have happened had she not been told of her diagnosis? She probably would not have spent extra quality time with her family, as they tried to ignore the obvious. And, after all, quality time with her family was all she wanted.
Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation. Ivy Elkins, cofounder of EGFR Resisters, a patient, survivor, and caregiver advocacy group, contributed to this article.
Several decades ago, a new patient came to my office with her family. She was elderly, in good health, spoke no English, and her extended family translated for her. Their request: “Don’t tell her that she has cancer.” Sharing her diagnosis with her would cause too much stress, they said. Their mother would not be able to tolerate the bad news, they said. She would “give up.”
I asked her (through her family and an interpreter) how much she wanted to know about what was going on, or would she prefer I confine my remarks to her family? It turns out that she did want to know her diagnosis and prognosis, and after a thorough discussion in front of her family about her treatment options, she decided she did not want to proceed with additional therapy. She wanted to focus on quality of life. I did not get the impression that this is what her family would have opted for.
The patient’s voice can take multiple directions, such as making informed decisions about their own care. When empowered, patients can and will express their wants, needs, feelings, and priorities to their providers, and they’ll participate in directing their own care. There is a growing body of evidence that shows patients who are more engaged and share decision-making with their health care professionals have better health outcomes and care experiences. Engaged patients feel more empowered and are more motivated to take action. They’re also more likely to follow treatment plans, take their medications, and heed their provider’s recommendations. By virtue of better treatments for lung cancer, many patients are living longer and better lives. Some of these patients even become “experts” on their own care, often bringing questions about research and clinical trials to the attention of their providers.
The patient’s voice in research and advocacy
The patient’s perspective is also key to a meaningful, successful clinical research project. Rather than being carried out to, about, or for the patient, patient involvement means research being carried out with or by patients. A patient and researcher may have different research goals. For example, patients may value being able to work, be with family, and live without pain, whereas a clinical researcher’s goal may be inducing responses. Patient involvement is important in both laboratory research and clinical research. The best-designed projects involve patient advocates from the beginning of the project to help make research relevant and meaningful to patients and include these perspectives through project completion.
More and more pharmaceutical companies are actively involving patients at all levels of protocol development, including protocol design and selection of relevant outcomes to patients. Benefits of engaging patients as partners in research include inclusion of real-world data, increased study enrollment, and translation of results to the cancer community in an understandable and accessible manner.
Accelerated research
Advocating for accelerated research is another area where the patient’s voice is important. Patients can and do identify research priorities for researchers, funding agencies, and pharma. Patients who support research advocacy are frequently part of meetings and panel discussions with researchers, the Food and Drug Administration, and the National Cancer Institute. And, they serve on advisory boards for pharmaceutical companies. They participate in grant reviews and institutional review boards, review manuscripts, and are active members of the cooperative groups and other professional societies. In fact, patient-led advocacy groups are raising money to help fund research they feel is most important to them. In lung cancer, for example, there are many groups organized around biomarkers, including the EGFR Resisters, ALK Positive, ROS1ders, MET Crusaders, and KRAS Kickers, who have raised hundreds of thousands of dollars to fund investigator-led translational research that would not have occurred without their involvement.
It is important to recognize that all patients are different and have different values and motivations that are important to them and influence their life decisions. Some patients want to know more about their condition and their preferences should be respected. Similarly, it’s critical to understand that not every patient is an advocate and not every advocate is a research advocate. Research advocates have more in-depth knowledge about the science of lung cancer and focus on representing the patient perspective for all lung cancer patients.
So, getting back to my original story: Did my patient “give up” by choosing palliative care without chemotherapy? Perhaps, but I don’t think she considered her decision “giving up.” Instead, she made the best decision possible for herself. What would have happened had she not been told of her diagnosis? She probably would not have spent extra quality time with her family, as they tried to ignore the obvious. And, after all, quality time with her family was all she wanted.
Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation. Ivy Elkins, cofounder of EGFR Resisters, a patient, survivor, and caregiver advocacy group, contributed to this article.
Several decades ago, a new patient came to my office with her family. She was elderly, in good health, spoke no English, and her extended family translated for her. Their request: “Don’t tell her that she has cancer.” Sharing her diagnosis with her would cause too much stress, they said. Their mother would not be able to tolerate the bad news, they said. She would “give up.”
I asked her (through her family and an interpreter) how much she wanted to know about what was going on, or would she prefer I confine my remarks to her family? It turns out that she did want to know her diagnosis and prognosis, and after a thorough discussion in front of her family about her treatment options, she decided she did not want to proceed with additional therapy. She wanted to focus on quality of life. I did not get the impression that this is what her family would have opted for.
The patient’s voice can take multiple directions, such as making informed decisions about their own care. When empowered, patients can and will express their wants, needs, feelings, and priorities to their providers, and they’ll participate in directing their own care. There is a growing body of evidence that shows patients who are more engaged and share decision-making with their health care professionals have better health outcomes and care experiences. Engaged patients feel more empowered and are more motivated to take action. They’re also more likely to follow treatment plans, take their medications, and heed their provider’s recommendations. By virtue of better treatments for lung cancer, many patients are living longer and better lives. Some of these patients even become “experts” on their own care, often bringing questions about research and clinical trials to the attention of their providers.
The patient’s voice in research and advocacy
The patient’s perspective is also key to a meaningful, successful clinical research project. Rather than being carried out to, about, or for the patient, patient involvement means research being carried out with or by patients. A patient and researcher may have different research goals. For example, patients may value being able to work, be with family, and live without pain, whereas a clinical researcher’s goal may be inducing responses. Patient involvement is important in both laboratory research and clinical research. The best-designed projects involve patient advocates from the beginning of the project to help make research relevant and meaningful to patients and include these perspectives through project completion.
More and more pharmaceutical companies are actively involving patients at all levels of protocol development, including protocol design and selection of relevant outcomes to patients. Benefits of engaging patients as partners in research include inclusion of real-world data, increased study enrollment, and translation of results to the cancer community in an understandable and accessible manner.
Accelerated research
Advocating for accelerated research is another area where the patient’s voice is important. Patients can and do identify research priorities for researchers, funding agencies, and pharma. Patients who support research advocacy are frequently part of meetings and panel discussions with researchers, the Food and Drug Administration, and the National Cancer Institute. And, they serve on advisory boards for pharmaceutical companies. They participate in grant reviews and institutional review boards, review manuscripts, and are active members of the cooperative groups and other professional societies. In fact, patient-led advocacy groups are raising money to help fund research they feel is most important to them. In lung cancer, for example, there are many groups organized around biomarkers, including the EGFR Resisters, ALK Positive, ROS1ders, MET Crusaders, and KRAS Kickers, who have raised hundreds of thousands of dollars to fund investigator-led translational research that would not have occurred without their involvement.
It is important to recognize that all patients are different and have different values and motivations that are important to them and influence their life decisions. Some patients want to know more about their condition and their preferences should be respected. Similarly, it’s critical to understand that not every patient is an advocate and not every advocate is a research advocate. Research advocates have more in-depth knowledge about the science of lung cancer and focus on representing the patient perspective for all lung cancer patients.
So, getting back to my original story: Did my patient “give up” by choosing palliative care without chemotherapy? Perhaps, but I don’t think she considered her decision “giving up.” Instead, she made the best decision possible for herself. What would have happened had she not been told of her diagnosis? She probably would not have spent extra quality time with her family, as they tried to ignore the obvious. And, after all, quality time with her family was all she wanted.
Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation. Ivy Elkins, cofounder of EGFR Resisters, a patient, survivor, and caregiver advocacy group, contributed to this article.
High HDL-C levels linked to increased fracture risk
High levels of high-density lipoprotein cholesterol (HDL-C) in older adults are associated with a higher risk of sustaining a fracture than lower HDL-C levels, a new study suggests.
“Two animal studies showing that HDL-C reduces bone mineral density by reducing osteoblast number and function provide a plausible explanation for why high HDL-C may increase the risk of fractures,” Monira Hussain, MBBS, MPH, PhD, of Monash University in Melbourne, told this news organization. “So, it was not surprising when our analyses provided evidence that amongst those in the highest quintile of HDL-C (> 74 mg/dL), there was a [33%] increased risk of fractures.”
After adjustment, one standard deviation increment in HDL-C level was associated with a 14% higher risk of fracture during a 4-year follow-up.
Based on this and other studies, Dr. Hussain said, “I believe that the finding of a very high HDL-C [should] alert clinicians to a higher risk of mortality, fractures, and possibly other threats to their patient’s health.”
The study was published online in JAMA Cardiology.
Independent risk factor
For this report, the researchers conducted a post hoc analysis of data from the Aspirin in Reducing Events in the Elderly (ASPREE) clinical trial and the ASPREE-Fracture substudy.
ASPREE was a double-blind, randomized, placebo-controlled primary prevention trial of aspirin. Participants were 16,703 community-dwelling Australians and 2,411 individuals from the United States with a mean age of 75 and without evident cardiovascular disease, dementia, physical disability, or life-limiting chronic illness.
The ASPREE-Fracture substudy collected data on fractures reported post randomization from the Australian participants. Fractures were confirmed by imaging and adjudicated by an expert panel and included both traumatic and minimal trauma fractures.
Of the 16,262 participants who had a plasma HDL-C measurement at baseline (55% women), 1,659 (10.2%) experienced at least one fracture over a median of 4 years. This included 711 minimal trauma fractures (for example, falls from standing height) and 948 other trauma fractures, mainly falls on stairs, ladders, or stools.
Higher rates of fractures occurred in the highest quintile of HDL-C level where the mean level was 89 mg/dL. At baseline, participants in that quintile had a lower BMI, a high prevalence of current/former smoking and current alcohol use, 12 years or longer of school, more physical activity, and higher use of antiosteoporosis medication. They also had less chronic kidney disease, diabetes, prefrailty/frailty, or treatment with lipid-lowering drugs.
In a fully adjusted model, each standard deviation increment in HDL-C level was associated with a 14% higher risk of fractures (hazard ratio, 1.14). When analyzed in quintiles, compared with participants in Q1, those in Q5 had a 33% higher risk for fracture (HR, 1.33).
Prevalence rates were similar between the sexes. The increase in fracture risk appeared to be independent of traditional risk factors for fractures, including age, sex, physical activity, alcohol use, frailty, BMI, smoking status, diabetes, chronic kidney disease, use of lipid-lowering or antiosteoporosis drugs, and education, the authors note.
The results persisted in sensitivity analyses in restricted subgroups of interest and in stratified analyses – including, for example, only minimal fractures; participants not taking antiosteoporosis drugs or statins; never smokers; nondrinkers; and those engaging in minimal physical activity (walking less than 30 minutes per day).
No association was observed between non–HDL-C levels and fractures.
The authors conclude that the study “provides robust evidence that higher levels of HDL-C are associated with incident fractures in both male and female individuals, independent of conventional risk factors.”
Clinically useful?
Commenting on the study for this news organization, Marilyn Tan, MD, clinic chief of the Endocrine Clinic and clinical associate professor of medicine at Stanford (Calif.) University, said, “I certainly would not recommend anyone do anything to actively lower their HDL levels. HDL levels are largely determined by genetics, diet, and lifestyle, with some effects from certain medications/supplements. Studies have demonstrated that moderately higher HDL levels may be protective for atherosclerosis.”
In the current study, she said, “Causation has not been proven, and importantly there is no evidence that reducing HDL levels reduces fracture risk. Also, this association between raised HDL levels and fracture risk has not been demonstrated consistently in other studies.”
Furthermore, she noted, the preclinical trials on which the authors based their hypothesis – that is, an association between HDL and a reduction in the number and function of osteoblasts – “has not been demonstrated widely in human subjects.”
“We have a large armamentarium of FDA-approved treatments for osteoporosis that have been clinically proven to reduce fracture risk very significantly, and these are the tools [in addition to lifestyle changes] we should use to reduce fracture risk,” Dr. Tan concluded.
John Wilkins, MD, of Northwestern University, Chicago, and Anand Rohatgi, MD, MSCS, of UT Southwestern Medical Center, Dallas, also point out some limitations of the study in a related editorial.
They note the inclusion of predominantly healthy adults with a mean age of 75, a population that could yield different findings from middle-aged cohorts with chronic illnesses, as well as a lack of clarity regarding the possible role of alcohol intake among the study participants.
Furthermore, the editorialists write, although significant associations were shown in this study, “models were not adjusted for detailed measures of exercise/activity, triglycerides, or any other lipids, including other HDL compositional measures such as HDL-P or ApoA-I levels. There was no assessment of whether HDL-C improved discrimination, reclassification, or any other validated measures of risk prediction performance.
“Taken together,” they conclude, “this study alone leaves several unanswered questions as to whether high HDL-C could be a useful biomarker to detect fracture risk.”
No commercial funding was disclosed. The authors report no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
High levels of high-density lipoprotein cholesterol (HDL-C) in older adults are associated with a higher risk of sustaining a fracture than lower HDL-C levels, a new study suggests.
“Two animal studies showing that HDL-C reduces bone mineral density by reducing osteoblast number and function provide a plausible explanation for why high HDL-C may increase the risk of fractures,” Monira Hussain, MBBS, MPH, PhD, of Monash University in Melbourne, told this news organization. “So, it was not surprising when our analyses provided evidence that amongst those in the highest quintile of HDL-C (> 74 mg/dL), there was a [33%] increased risk of fractures.”
After adjustment, one standard deviation increment in HDL-C level was associated with a 14% higher risk of fracture during a 4-year follow-up.
Based on this and other studies, Dr. Hussain said, “I believe that the finding of a very high HDL-C [should] alert clinicians to a higher risk of mortality, fractures, and possibly other threats to their patient’s health.”
The study was published online in JAMA Cardiology.
Independent risk factor
For this report, the researchers conducted a post hoc analysis of data from the Aspirin in Reducing Events in the Elderly (ASPREE) clinical trial and the ASPREE-Fracture substudy.
ASPREE was a double-blind, randomized, placebo-controlled primary prevention trial of aspirin. Participants were 16,703 community-dwelling Australians and 2,411 individuals from the United States with a mean age of 75 and without evident cardiovascular disease, dementia, physical disability, or life-limiting chronic illness.
The ASPREE-Fracture substudy collected data on fractures reported post randomization from the Australian participants. Fractures were confirmed by imaging and adjudicated by an expert panel and included both traumatic and minimal trauma fractures.
Of the 16,262 participants who had a plasma HDL-C measurement at baseline (55% women), 1,659 (10.2%) experienced at least one fracture over a median of 4 years. This included 711 minimal trauma fractures (for example, falls from standing height) and 948 other trauma fractures, mainly falls on stairs, ladders, or stools.
Higher rates of fractures occurred in the highest quintile of HDL-C level where the mean level was 89 mg/dL. At baseline, participants in that quintile had a lower BMI, a high prevalence of current/former smoking and current alcohol use, 12 years or longer of school, more physical activity, and higher use of antiosteoporosis medication. They also had less chronic kidney disease, diabetes, prefrailty/frailty, or treatment with lipid-lowering drugs.
In a fully adjusted model, each standard deviation increment in HDL-C level was associated with a 14% higher risk of fractures (hazard ratio, 1.14). When analyzed in quintiles, compared with participants in Q1, those in Q5 had a 33% higher risk for fracture (HR, 1.33).
Prevalence rates were similar between the sexes. The increase in fracture risk appeared to be independent of traditional risk factors for fractures, including age, sex, physical activity, alcohol use, frailty, BMI, smoking status, diabetes, chronic kidney disease, use of lipid-lowering or antiosteoporosis drugs, and education, the authors note.
The results persisted in sensitivity analyses in restricted subgroups of interest and in stratified analyses – including, for example, only minimal fractures; participants not taking antiosteoporosis drugs or statins; never smokers; nondrinkers; and those engaging in minimal physical activity (walking less than 30 minutes per day).
No association was observed between non–HDL-C levels and fractures.
The authors conclude that the study “provides robust evidence that higher levels of HDL-C are associated with incident fractures in both male and female individuals, independent of conventional risk factors.”
Clinically useful?
Commenting on the study for this news organization, Marilyn Tan, MD, clinic chief of the Endocrine Clinic and clinical associate professor of medicine at Stanford (Calif.) University, said, “I certainly would not recommend anyone do anything to actively lower their HDL levels. HDL levels are largely determined by genetics, diet, and lifestyle, with some effects from certain medications/supplements. Studies have demonstrated that moderately higher HDL levels may be protective for atherosclerosis.”
In the current study, she said, “Causation has not been proven, and importantly there is no evidence that reducing HDL levels reduces fracture risk. Also, this association between raised HDL levels and fracture risk has not been demonstrated consistently in other studies.”
Furthermore, she noted, the preclinical trials on which the authors based their hypothesis – that is, an association between HDL and a reduction in the number and function of osteoblasts – “has not been demonstrated widely in human subjects.”
“We have a large armamentarium of FDA-approved treatments for osteoporosis that have been clinically proven to reduce fracture risk very significantly, and these are the tools [in addition to lifestyle changes] we should use to reduce fracture risk,” Dr. Tan concluded.
John Wilkins, MD, of Northwestern University, Chicago, and Anand Rohatgi, MD, MSCS, of UT Southwestern Medical Center, Dallas, also point out some limitations of the study in a related editorial.
They note the inclusion of predominantly healthy adults with a mean age of 75, a population that could yield different findings from middle-aged cohorts with chronic illnesses, as well as a lack of clarity regarding the possible role of alcohol intake among the study participants.
Furthermore, the editorialists write, although significant associations were shown in this study, “models were not adjusted for detailed measures of exercise/activity, triglycerides, or any other lipids, including other HDL compositional measures such as HDL-P or ApoA-I levels. There was no assessment of whether HDL-C improved discrimination, reclassification, or any other validated measures of risk prediction performance.
“Taken together,” they conclude, “this study alone leaves several unanswered questions as to whether high HDL-C could be a useful biomarker to detect fracture risk.”
No commercial funding was disclosed. The authors report no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
High levels of high-density lipoprotein cholesterol (HDL-C) in older adults are associated with a higher risk of sustaining a fracture than lower HDL-C levels, a new study suggests.
“Two animal studies showing that HDL-C reduces bone mineral density by reducing osteoblast number and function provide a plausible explanation for why high HDL-C may increase the risk of fractures,” Monira Hussain, MBBS, MPH, PhD, of Monash University in Melbourne, told this news organization. “So, it was not surprising when our analyses provided evidence that amongst those in the highest quintile of HDL-C (> 74 mg/dL), there was a [33%] increased risk of fractures.”
After adjustment, one standard deviation increment in HDL-C level was associated with a 14% higher risk of fracture during a 4-year follow-up.
Based on this and other studies, Dr. Hussain said, “I believe that the finding of a very high HDL-C [should] alert clinicians to a higher risk of mortality, fractures, and possibly other threats to their patient’s health.”
The study was published online in JAMA Cardiology.
Independent risk factor
For this report, the researchers conducted a post hoc analysis of data from the Aspirin in Reducing Events in the Elderly (ASPREE) clinical trial and the ASPREE-Fracture substudy.
ASPREE was a double-blind, randomized, placebo-controlled primary prevention trial of aspirin. Participants were 16,703 community-dwelling Australians and 2,411 individuals from the United States with a mean age of 75 and without evident cardiovascular disease, dementia, physical disability, or life-limiting chronic illness.
The ASPREE-Fracture substudy collected data on fractures reported post randomization from the Australian participants. Fractures were confirmed by imaging and adjudicated by an expert panel and included both traumatic and minimal trauma fractures.
Of the 16,262 participants who had a plasma HDL-C measurement at baseline (55% women), 1,659 (10.2%) experienced at least one fracture over a median of 4 years. This included 711 minimal trauma fractures (for example, falls from standing height) and 948 other trauma fractures, mainly falls on stairs, ladders, or stools.
Higher rates of fractures occurred in the highest quintile of HDL-C level where the mean level was 89 mg/dL. At baseline, participants in that quintile had a lower BMI, a high prevalence of current/former smoking and current alcohol use, 12 years or longer of school, more physical activity, and higher use of antiosteoporosis medication. They also had less chronic kidney disease, diabetes, prefrailty/frailty, or treatment with lipid-lowering drugs.
In a fully adjusted model, each standard deviation increment in HDL-C level was associated with a 14% higher risk of fractures (hazard ratio, 1.14). When analyzed in quintiles, compared with participants in Q1, those in Q5 had a 33% higher risk for fracture (HR, 1.33).
Prevalence rates were similar between the sexes. The increase in fracture risk appeared to be independent of traditional risk factors for fractures, including age, sex, physical activity, alcohol use, frailty, BMI, smoking status, diabetes, chronic kidney disease, use of lipid-lowering or antiosteoporosis drugs, and education, the authors note.
The results persisted in sensitivity analyses in restricted subgroups of interest and in stratified analyses – including, for example, only minimal fractures; participants not taking antiosteoporosis drugs or statins; never smokers; nondrinkers; and those engaging in minimal physical activity (walking less than 30 minutes per day).
No association was observed between non–HDL-C levels and fractures.
The authors conclude that the study “provides robust evidence that higher levels of HDL-C are associated with incident fractures in both male and female individuals, independent of conventional risk factors.”
Clinically useful?
Commenting on the study for this news organization, Marilyn Tan, MD, clinic chief of the Endocrine Clinic and clinical associate professor of medicine at Stanford (Calif.) University, said, “I certainly would not recommend anyone do anything to actively lower their HDL levels. HDL levels are largely determined by genetics, diet, and lifestyle, with some effects from certain medications/supplements. Studies have demonstrated that moderately higher HDL levels may be protective for atherosclerosis.”
In the current study, she said, “Causation has not been proven, and importantly there is no evidence that reducing HDL levels reduces fracture risk. Also, this association between raised HDL levels and fracture risk has not been demonstrated consistently in other studies.”
Furthermore, she noted, the preclinical trials on which the authors based their hypothesis – that is, an association between HDL and a reduction in the number and function of osteoblasts – “has not been demonstrated widely in human subjects.”
“We have a large armamentarium of FDA-approved treatments for osteoporosis that have been clinically proven to reduce fracture risk very significantly, and these are the tools [in addition to lifestyle changes] we should use to reduce fracture risk,” Dr. Tan concluded.
John Wilkins, MD, of Northwestern University, Chicago, and Anand Rohatgi, MD, MSCS, of UT Southwestern Medical Center, Dallas, also point out some limitations of the study in a related editorial.
They note the inclusion of predominantly healthy adults with a mean age of 75, a population that could yield different findings from middle-aged cohorts with chronic illnesses, as well as a lack of clarity regarding the possible role of alcohol intake among the study participants.
Furthermore, the editorialists write, although significant associations were shown in this study, “models were not adjusted for detailed measures of exercise/activity, triglycerides, or any other lipids, including other HDL compositional measures such as HDL-P or ApoA-I levels. There was no assessment of whether HDL-C improved discrimination, reclassification, or any other validated measures of risk prediction performance.
“Taken together,” they conclude, “this study alone leaves several unanswered questions as to whether high HDL-C could be a useful biomarker to detect fracture risk.”
No commercial funding was disclosed. The authors report no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Medicare policy tweak on LVADs may reduce access to transplant
A recent change in Medicare policy designed to increase access to left ventricular assist devices (LVADs) may have had the unintended consequence of increasing inequalities in access to heart transplant for patients with advanced heart failure.
In December 2020, the Centers for Medicare & Medicaid Services relaxed restrictions on centers that implant LVADs but don’t perform heart transplants. Specifically, they dropped the requirement that LVAD-only centers obtain permission from a Medicare-approved heart transplant center authorizing LVAD implantation with “bridge-to-transplant” (BTT) intent, meaning the patient is a transplant candidate.
While the relaxed requirement has the potential to increase access to LVADs for appropriate patients, a look back at 22,221 LVAD recipients found that patients who received LVADs at transplant-capable centers had a 79% higher likelihood of receiving a BTT LVAD designation.
The 2-year heart transplant rate following LVAD implant was 25.6% for patients who received an LVAD at a heart transplant center, compared with 11.9% at LVAD-only centers.
Thomas Cascino, MD, with University of Michigan Health Frankel Cardiovascular Center, Ann Arbor, and colleagues reported their findings in JAMA Network Open.
Differential assessment?
Nontransplant LVAD centers are increasing in number in the United States now that the CMS has made establishing an LVAD-only center easier.
“Although there should be enthusiasm for the potential of LVAD-only centers to increase access to LVAD, it appears that receiving an LVAD at a center that does not perform transplants results in differential assessment of transplant eligibility at the time of LVAD implant and inequities in receipt of transplant,” Dr. Cascino and colleagues said.
“Being cared for at a center that does not perform heart transplant should not result in a lesser chance to receive a heart transplant,” Dr. Cascino added in a university news release. “Our study shows that this disparity existed before the policy change, and we think it will likely grow larger now that there is less collaboration.”
The CMS policy will likely “further challenge equity in access to transplant for patients seeking care at nontransplant centers and may have the unintended consequence of contributing to increasing inequities in access to transplants, as has been feared,” the researchers wrote.
They also note that recent changes in the adult heart allocation system under the United Network for Organ Sharing have significantly reduced the likelihood of transplant after durable LVAD implant unless candidates are listed as being at higher urgency status owing to an LVAD complication or clinical deterioration.
“The reality is that durable LVADs are much less likely to be a bridge to the best therapy (that is, transplant) in the current allocation system. As a result, there is a critical need to select appropriate durable LVAD and transplant candidates at the initial evaluation,” the authors said.
“This puts the onus on the transplant community to select appropriate LVAD and transplant candidates during the initial evaluation. We need a system in which any patient can walk into the same hospital and get the right therapy for them,” Dr. Cascino added in the news release.
The research was supported in part through funding from the University of Michigan Health department of cardiac surgery and the National Institutes of Health, National Heart, Lung, and Blood Institute. Dr. Cascino has received grants from Johnson & Johnson.
A version of this article first appeared on Medscape.com.
A recent change in Medicare policy designed to increase access to left ventricular assist devices (LVADs) may have had the unintended consequence of increasing inequalities in access to heart transplant for patients with advanced heart failure.
In December 2020, the Centers for Medicare & Medicaid Services relaxed restrictions on centers that implant LVADs but don’t perform heart transplants. Specifically, they dropped the requirement that LVAD-only centers obtain permission from a Medicare-approved heart transplant center authorizing LVAD implantation with “bridge-to-transplant” (BTT) intent, meaning the patient is a transplant candidate.
While the relaxed requirement has the potential to increase access to LVADs for appropriate patients, a look back at 22,221 LVAD recipients found that patients who received LVADs at transplant-capable centers had a 79% higher likelihood of receiving a BTT LVAD designation.
The 2-year heart transplant rate following LVAD implant was 25.6% for patients who received an LVAD at a heart transplant center, compared with 11.9% at LVAD-only centers.
Thomas Cascino, MD, with University of Michigan Health Frankel Cardiovascular Center, Ann Arbor, and colleagues reported their findings in JAMA Network Open.
Differential assessment?
Nontransplant LVAD centers are increasing in number in the United States now that the CMS has made establishing an LVAD-only center easier.
“Although there should be enthusiasm for the potential of LVAD-only centers to increase access to LVAD, it appears that receiving an LVAD at a center that does not perform transplants results in differential assessment of transplant eligibility at the time of LVAD implant and inequities in receipt of transplant,” Dr. Cascino and colleagues said.
“Being cared for at a center that does not perform heart transplant should not result in a lesser chance to receive a heart transplant,” Dr. Cascino added in a university news release. “Our study shows that this disparity existed before the policy change, and we think it will likely grow larger now that there is less collaboration.”
The CMS policy will likely “further challenge equity in access to transplant for patients seeking care at nontransplant centers and may have the unintended consequence of contributing to increasing inequities in access to transplants, as has been feared,” the researchers wrote.
They also note that recent changes in the adult heart allocation system under the United Network for Organ Sharing have significantly reduced the likelihood of transplant after durable LVAD implant unless candidates are listed as being at higher urgency status owing to an LVAD complication or clinical deterioration.
“The reality is that durable LVADs are much less likely to be a bridge to the best therapy (that is, transplant) in the current allocation system. As a result, there is a critical need to select appropriate durable LVAD and transplant candidates at the initial evaluation,” the authors said.
“This puts the onus on the transplant community to select appropriate LVAD and transplant candidates during the initial evaluation. We need a system in which any patient can walk into the same hospital and get the right therapy for them,” Dr. Cascino added in the news release.
The research was supported in part through funding from the University of Michigan Health department of cardiac surgery and the National Institutes of Health, National Heart, Lung, and Blood Institute. Dr. Cascino has received grants from Johnson & Johnson.
A version of this article first appeared on Medscape.com.
A recent change in Medicare policy designed to increase access to left ventricular assist devices (LVADs) may have had the unintended consequence of increasing inequalities in access to heart transplant for patients with advanced heart failure.
In December 2020, the Centers for Medicare & Medicaid Services relaxed restrictions on centers that implant LVADs but don’t perform heart transplants. Specifically, they dropped the requirement that LVAD-only centers obtain permission from a Medicare-approved heart transplant center authorizing LVAD implantation with “bridge-to-transplant” (BTT) intent, meaning the patient is a transplant candidate.
While the relaxed requirement has the potential to increase access to LVADs for appropriate patients, a look back at 22,221 LVAD recipients found that patients who received LVADs at transplant-capable centers had a 79% higher likelihood of receiving a BTT LVAD designation.
The 2-year heart transplant rate following LVAD implant was 25.6% for patients who received an LVAD at a heart transplant center, compared with 11.9% at LVAD-only centers.
Thomas Cascino, MD, with University of Michigan Health Frankel Cardiovascular Center, Ann Arbor, and colleagues reported their findings in JAMA Network Open.
Differential assessment?
Nontransplant LVAD centers are increasing in number in the United States now that the CMS has made establishing an LVAD-only center easier.
“Although there should be enthusiasm for the potential of LVAD-only centers to increase access to LVAD, it appears that receiving an LVAD at a center that does not perform transplants results in differential assessment of transplant eligibility at the time of LVAD implant and inequities in receipt of transplant,” Dr. Cascino and colleagues said.
“Being cared for at a center that does not perform heart transplant should not result in a lesser chance to receive a heart transplant,” Dr. Cascino added in a university news release. “Our study shows that this disparity existed before the policy change, and we think it will likely grow larger now that there is less collaboration.”
The CMS policy will likely “further challenge equity in access to transplant for patients seeking care at nontransplant centers and may have the unintended consequence of contributing to increasing inequities in access to transplants, as has been feared,” the researchers wrote.
They also note that recent changes in the adult heart allocation system under the United Network for Organ Sharing have significantly reduced the likelihood of transplant after durable LVAD implant unless candidates are listed as being at higher urgency status owing to an LVAD complication or clinical deterioration.
“The reality is that durable LVADs are much less likely to be a bridge to the best therapy (that is, transplant) in the current allocation system. As a result, there is a critical need to select appropriate durable LVAD and transplant candidates at the initial evaluation,” the authors said.
“This puts the onus on the transplant community to select appropriate LVAD and transplant candidates during the initial evaluation. We need a system in which any patient can walk into the same hospital and get the right therapy for them,” Dr. Cascino added in the news release.
The research was supported in part through funding from the University of Michigan Health department of cardiac surgery and the National Institutes of Health, National Heart, Lung, and Blood Institute. Dr. Cascino has received grants from Johnson & Johnson.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
If we care about cancer patients, we must care about climate change
Because we care about our patients, we need to get involved in the climate change movement. If we want to help prevent cancer and deliver the best possible care to our patients, we need to stop burning fossil fuels. As addressed in an earlier version of this column, burning fossil fuels results in the release of particulate matter and particles measuring 2.5 micrometers in diameter (PM2.5), are classified as group 1 carcinogens by the International Association of Research and Cancer.
Fossil fuels also release greenhouse gases (carbon dioxide, methane, nitrous oxide, and fluorinated gases) which trap solar radiation that would otherwise have been reflected back into space after hitting the earth’s surface. Instead, it is redirected back to earth as infrared radiation warming the planet by 1.1° C since preindustrial times.
Climate change has a number of consequences, including more extreme weather events, rising sea levels, warming seas, environmental degradation, and affects water and food quality, supply, and production. A global increase of 1.5° C above the preindustrial average risks catastrophic harm to health that will be impossible to reverse, prompting the editors of over 260 health journals to call for emergency action to limit global temperature increases, restore biodiversity, and protect health.
In October, the 2022 version of the Lancet Countdown on health and climate change was issued and the findings are not good. “After 30 years of UNFCCC negotiations, the Lancet Countdown indicators show that countries and companies continue to make choices that threaten the health and survival of people in every part of the world. As countries devise ways to recover from the coexisting crises, the evidence is unequivocal. At this critical juncture, an immediate, health-centered response can still secure a future in which world populations can not only survive, but thrive,” the authors wrote. Governments and companies continue to prioritize fossil fuels over people’s health.
Among the key findings from the report, Marina Romanello, PhD, of the Institute for Global Health at University College London, and her colleagues, call for “A health-centered response to the coexisting climate, energy, and cost-of-living crises provides an opportunity to deliver a healthy, low-carbon future. The associated reduction in the burden of disease will in turn reduce the strain on overwhelmed health care providers, and enable better care.”
The authors also state that “Well-prepared health systems are essential to protect populations from the health impacts of climate change. However, global health systems have been drastically weakened by the effects of the COVID-19 pandemic, and the funds available for climate action decreased in 239 (30%) of 798 cities, with health systems increasingly being affected by extreme weather events and supply chain disruptions.”
And, the authors are concerned that health systems have left themselves vulnerable to climate change–related health hazards because they have not adapted their operations for climate-related changes. “Only 48 of 95 countries have assessed their climate change adaptation needs and only 63% of countries reported high to very high implementation status for health emergency management in 2021. Increasing adaptation to climate change has the potential to simultaneously improve the capacity of health systems to manage both future infectious disease outbreaks and other health emergencies.”
There is roughly a 50% chance that the 1.5° C threshold proposed in the Paris Agreement will be exceeded within 5 years. The carbon intensity of the global energy system has been reduced by less than 1% from 1992 levels, when the United Nations Framework Convention on Climate Change was adopted. At our current pace, global emissions could be 13.7% above 2010 levels by 2030 and fully decarbonizing the energy system would take 150 years. Clearly, we are nowhere near meeting the goals of the Paris Agreement signed in 2015 by 192 countries and the European Union. Participants pledged to decrease their carbon footprint by 50% by 2030, and net zero by the end of the century.
The effect of increasing greenhouse gases in our atmosphere will have a massive impact on the prevention and care of cancer patients. Air pollution is responsible for about 14% of lung cancer deaths throughout the world. Rising temperatures lead to extreme weather events which disrupts infrastructure and the ability to access health care, leading to delays in treatment, increased morbidity, and death. Screening rates for cancer go down, which leads to more patients presenting with advanced cancer in the future.
As oncologists who care deeply about their patients, we need to get actively involved. It is our responsibility to our current and future patients to do whatever we can to prevent cancer and reduce its complications.
Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation.
Because we care about our patients, we need to get involved in the climate change movement. If we want to help prevent cancer and deliver the best possible care to our patients, we need to stop burning fossil fuels. As addressed in an earlier version of this column, burning fossil fuels results in the release of particulate matter and particles measuring 2.5 micrometers in diameter (PM2.5), are classified as group 1 carcinogens by the International Association of Research and Cancer.
Fossil fuels also release greenhouse gases (carbon dioxide, methane, nitrous oxide, and fluorinated gases) which trap solar radiation that would otherwise have been reflected back into space after hitting the earth’s surface. Instead, it is redirected back to earth as infrared radiation warming the planet by 1.1° C since preindustrial times.
Climate change has a number of consequences, including more extreme weather events, rising sea levels, warming seas, environmental degradation, and affects water and food quality, supply, and production. A global increase of 1.5° C above the preindustrial average risks catastrophic harm to health that will be impossible to reverse, prompting the editors of over 260 health journals to call for emergency action to limit global temperature increases, restore biodiversity, and protect health.
In October, the 2022 version of the Lancet Countdown on health and climate change was issued and the findings are not good. “After 30 years of UNFCCC negotiations, the Lancet Countdown indicators show that countries and companies continue to make choices that threaten the health and survival of people in every part of the world. As countries devise ways to recover from the coexisting crises, the evidence is unequivocal. At this critical juncture, an immediate, health-centered response can still secure a future in which world populations can not only survive, but thrive,” the authors wrote. Governments and companies continue to prioritize fossil fuels over people’s health.
Among the key findings from the report, Marina Romanello, PhD, of the Institute for Global Health at University College London, and her colleagues, call for “A health-centered response to the coexisting climate, energy, and cost-of-living crises provides an opportunity to deliver a healthy, low-carbon future. The associated reduction in the burden of disease will in turn reduce the strain on overwhelmed health care providers, and enable better care.”
The authors also state that “Well-prepared health systems are essential to protect populations from the health impacts of climate change. However, global health systems have been drastically weakened by the effects of the COVID-19 pandemic, and the funds available for climate action decreased in 239 (30%) of 798 cities, with health systems increasingly being affected by extreme weather events and supply chain disruptions.”
And, the authors are concerned that health systems have left themselves vulnerable to climate change–related health hazards because they have not adapted their operations for climate-related changes. “Only 48 of 95 countries have assessed their climate change adaptation needs and only 63% of countries reported high to very high implementation status for health emergency management in 2021. Increasing adaptation to climate change has the potential to simultaneously improve the capacity of health systems to manage both future infectious disease outbreaks and other health emergencies.”
There is roughly a 50% chance that the 1.5° C threshold proposed in the Paris Agreement will be exceeded within 5 years. The carbon intensity of the global energy system has been reduced by less than 1% from 1992 levels, when the United Nations Framework Convention on Climate Change was adopted. At our current pace, global emissions could be 13.7% above 2010 levels by 2030 and fully decarbonizing the energy system would take 150 years. Clearly, we are nowhere near meeting the goals of the Paris Agreement signed in 2015 by 192 countries and the European Union. Participants pledged to decrease their carbon footprint by 50% by 2030, and net zero by the end of the century.
The effect of increasing greenhouse gases in our atmosphere will have a massive impact on the prevention and care of cancer patients. Air pollution is responsible for about 14% of lung cancer deaths throughout the world. Rising temperatures lead to extreme weather events which disrupts infrastructure and the ability to access health care, leading to delays in treatment, increased morbidity, and death. Screening rates for cancer go down, which leads to more patients presenting with advanced cancer in the future.
As oncologists who care deeply about their patients, we need to get actively involved. It is our responsibility to our current and future patients to do whatever we can to prevent cancer and reduce its complications.
Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation.
Because we care about our patients, we need to get involved in the climate change movement. If we want to help prevent cancer and deliver the best possible care to our patients, we need to stop burning fossil fuels. As addressed in an earlier version of this column, burning fossil fuels results in the release of particulate matter and particles measuring 2.5 micrometers in diameter (PM2.5), are classified as group 1 carcinogens by the International Association of Research and Cancer.
Fossil fuels also release greenhouse gases (carbon dioxide, methane, nitrous oxide, and fluorinated gases) which trap solar radiation that would otherwise have been reflected back into space after hitting the earth’s surface. Instead, it is redirected back to earth as infrared radiation warming the planet by 1.1° C since preindustrial times.
Climate change has a number of consequences, including more extreme weather events, rising sea levels, warming seas, environmental degradation, and affects water and food quality, supply, and production. A global increase of 1.5° C above the preindustrial average risks catastrophic harm to health that will be impossible to reverse, prompting the editors of over 260 health journals to call for emergency action to limit global temperature increases, restore biodiversity, and protect health.
In October, the 2022 version of the Lancet Countdown on health and climate change was issued and the findings are not good. “After 30 years of UNFCCC negotiations, the Lancet Countdown indicators show that countries and companies continue to make choices that threaten the health and survival of people in every part of the world. As countries devise ways to recover from the coexisting crises, the evidence is unequivocal. At this critical juncture, an immediate, health-centered response can still secure a future in which world populations can not only survive, but thrive,” the authors wrote. Governments and companies continue to prioritize fossil fuels over people’s health.
Among the key findings from the report, Marina Romanello, PhD, of the Institute for Global Health at University College London, and her colleagues, call for “A health-centered response to the coexisting climate, energy, and cost-of-living crises provides an opportunity to deliver a healthy, low-carbon future. The associated reduction in the burden of disease will in turn reduce the strain on overwhelmed health care providers, and enable better care.”
The authors also state that “Well-prepared health systems are essential to protect populations from the health impacts of climate change. However, global health systems have been drastically weakened by the effects of the COVID-19 pandemic, and the funds available for climate action decreased in 239 (30%) of 798 cities, with health systems increasingly being affected by extreme weather events and supply chain disruptions.”
And, the authors are concerned that health systems have left themselves vulnerable to climate change–related health hazards because they have not adapted their operations for climate-related changes. “Only 48 of 95 countries have assessed their climate change adaptation needs and only 63% of countries reported high to very high implementation status for health emergency management in 2021. Increasing adaptation to climate change has the potential to simultaneously improve the capacity of health systems to manage both future infectious disease outbreaks and other health emergencies.”
There is roughly a 50% chance that the 1.5° C threshold proposed in the Paris Agreement will be exceeded within 5 years. The carbon intensity of the global energy system has been reduced by less than 1% from 1992 levels, when the United Nations Framework Convention on Climate Change was adopted. At our current pace, global emissions could be 13.7% above 2010 levels by 2030 and fully decarbonizing the energy system would take 150 years. Clearly, we are nowhere near meeting the goals of the Paris Agreement signed in 2015 by 192 countries and the European Union. Participants pledged to decrease their carbon footprint by 50% by 2030, and net zero by the end of the century.
The effect of increasing greenhouse gases in our atmosphere will have a massive impact on the prevention and care of cancer patients. Air pollution is responsible for about 14% of lung cancer deaths throughout the world. Rising temperatures lead to extreme weather events which disrupts infrastructure and the ability to access health care, leading to delays in treatment, increased morbidity, and death. Screening rates for cancer go down, which leads to more patients presenting with advanced cancer in the future.
As oncologists who care deeply about their patients, we need to get actively involved. It is our responsibility to our current and future patients to do whatever we can to prevent cancer and reduce its complications.
Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation.
Eye check important before starting semaglutide for diabetes
A small potential increased risk of retinopathy worsening at 1 year with injected semaglutide (Ozempic, Novo Nordisk), a glucagon-like peptide 1 (GLP-1) agonist approved for type 2 diabetes, doesn’t outweigh the drug’s cardiovascular benefits but does highlight the need for baseline ophthalmologic evaluation before initiating treatment and ongoing retinal monitoring, researchers say.
That conclusion was based on data from a meta-analysis of the seven major cardiovascular outcomes trials of GLP-1 agonists currently on the market.
The findings were recently published in Diabetes & Metabolic Syndrome: Clinical Research & Reviews, by Stewart G. Albert, MD, and colleagues.
Concerns about retinopathy worsening with the GLP-1 agonist drug class first arose from the SUSTAIN-6 cardiovascular outcomes trial for injectable semaglutide, although a subsequent analysis of data from that trial appeared to suggest the problem is likely due to rapid glucose-lowering in already vulnerable patients rather than a drug-specific effect. This effect had been previously reported, most notably in the landmark Diabetes Control and Complications Trial.
In this new meta-analysis, “we showed that with improvements in A1c there were correlations with decreases in the rate of cardiovascular events but increases in the rate of retinopathy,” Dr. Albert, of St. Louis University, told this news organization.
“As a class of drugs, we did not find an increased rate of retinopathy. The effect of GLP-1 agonists on retinopathy did not appear to be due to an immediate direct toxic effect of the drug. The worsening of the rate of retinopathy was seen with semaglutide after 1 year of therapy and when there was a decrease in A1c of 1%,” he explained.
He noted that because the increased risk was seen primarily among those who already had retinopathy at baseline, “it would seem prudent to know the level of retinopathy either before or plan for close ophthalmologic monitoring around the time of drug initiation ... We routinely evaluate patients with known type 2 diabetes mellitus at yearly intervals for retinopathy. From our data, we saw worsening at 1 year of drug exposure, but we do not know the exact time when the changes occurred during that year.”
The Ozempic label advises that “patients with a history of diabetic retinopathy should be monitored for progression of diabetic retinopathy” but doesn’t specifically mention baseline assessment at the time of drug initiation.
No increase in retinopathy risk for GLP-1 agonist class overall
The seven trials in the meta-analysis comprised 56,004 participants, with baseline retinopathy prevalence ranging from 9% to 31%.
For the GLP-1 agonist class overall, there was no significant increase in the relative rate (RR) of retinopathy (RR, 1.09; P = .36), while there were significant reductions in relative rates of major adverse cardiac events, overall deaths, and cardiovascular deaths (all P < .001 or P = .001).
The increased retinopathy risk was seen only in the subcutaneous semaglutide group (RR, 1.73; P = .02).
The overall number needed to harm was 1,000 and the number to treat was 77. For semaglutide, those values were 77 and 43, respectively.
There was a significant correlation between a decrease in major adverse cardiac events and a decrease in A1c (P = .014), while for retinopathy, the risk increased with improved A1c (P = .076).
Semaglutide subanalysis finds increased retinopathy worsening
Dr. Albert and colleagues conducted a separate subanalysis of 11 studies of semaglutide that enrolled 11,894 patients, of which 6 studies (n = 5,610) were of oral semaglutide (Rybelsus) and 5 studies were of subcutaneous semaglutide (Ozempic; n = 6,284).
In the subanalysis, there was an overall increase in relative rates of new or worsening retinopathy (RR, 1.218; P = .049).
The change in relative rate of retinopathy was predominantly found for subcutaneous semaglutide given for longer than 1 year (RR, 1.559; P = .022) and decreases in A1c of more than 1.0% (RR, 1.590; P = .016). No such differences were seen with oral semaglutide.
A further evaluation of the data without the SUSTAIN 6 trial showed no effect on retinopathy but the analysis lacked power.
Dr. Albert told this news organization: “We did not find an immediate toxic effect of any drug. However, we cannot rule out that there was a cumulative effect of the dose over longer times.”
No disclosures were given.
A version of this article first appeared on Medscape.com.
A small potential increased risk of retinopathy worsening at 1 year with injected semaglutide (Ozempic, Novo Nordisk), a glucagon-like peptide 1 (GLP-1) agonist approved for type 2 diabetes, doesn’t outweigh the drug’s cardiovascular benefits but does highlight the need for baseline ophthalmologic evaluation before initiating treatment and ongoing retinal monitoring, researchers say.
That conclusion was based on data from a meta-analysis of the seven major cardiovascular outcomes trials of GLP-1 agonists currently on the market.
The findings were recently published in Diabetes & Metabolic Syndrome: Clinical Research & Reviews, by Stewart G. Albert, MD, and colleagues.
Concerns about retinopathy worsening with the GLP-1 agonist drug class first arose from the SUSTAIN-6 cardiovascular outcomes trial for injectable semaglutide, although a subsequent analysis of data from that trial appeared to suggest the problem is likely due to rapid glucose-lowering in already vulnerable patients rather than a drug-specific effect. This effect had been previously reported, most notably in the landmark Diabetes Control and Complications Trial.
In this new meta-analysis, “we showed that with improvements in A1c there were correlations with decreases in the rate of cardiovascular events but increases in the rate of retinopathy,” Dr. Albert, of St. Louis University, told this news organization.
“As a class of drugs, we did not find an increased rate of retinopathy. The effect of GLP-1 agonists on retinopathy did not appear to be due to an immediate direct toxic effect of the drug. The worsening of the rate of retinopathy was seen with semaglutide after 1 year of therapy and when there was a decrease in A1c of 1%,” he explained.
He noted that because the increased risk was seen primarily among those who already had retinopathy at baseline, “it would seem prudent to know the level of retinopathy either before or plan for close ophthalmologic monitoring around the time of drug initiation ... We routinely evaluate patients with known type 2 diabetes mellitus at yearly intervals for retinopathy. From our data, we saw worsening at 1 year of drug exposure, but we do not know the exact time when the changes occurred during that year.”
The Ozempic label advises that “patients with a history of diabetic retinopathy should be monitored for progression of diabetic retinopathy” but doesn’t specifically mention baseline assessment at the time of drug initiation.
No increase in retinopathy risk for GLP-1 agonist class overall
The seven trials in the meta-analysis comprised 56,004 participants, with baseline retinopathy prevalence ranging from 9% to 31%.
For the GLP-1 agonist class overall, there was no significant increase in the relative rate (RR) of retinopathy (RR, 1.09; P = .36), while there were significant reductions in relative rates of major adverse cardiac events, overall deaths, and cardiovascular deaths (all P < .001 or P = .001).
The increased retinopathy risk was seen only in the subcutaneous semaglutide group (RR, 1.73; P = .02).
The overall number needed to harm was 1,000 and the number to treat was 77. For semaglutide, those values were 77 and 43, respectively.
There was a significant correlation between a decrease in major adverse cardiac events and a decrease in A1c (P = .014), while for retinopathy, the risk increased with improved A1c (P = .076).
Semaglutide subanalysis finds increased retinopathy worsening
Dr. Albert and colleagues conducted a separate subanalysis of 11 studies of semaglutide that enrolled 11,894 patients, of which 6 studies (n = 5,610) were of oral semaglutide (Rybelsus) and 5 studies were of subcutaneous semaglutide (Ozempic; n = 6,284).
In the subanalysis, there was an overall increase in relative rates of new or worsening retinopathy (RR, 1.218; P = .049).
The change in relative rate of retinopathy was predominantly found for subcutaneous semaglutide given for longer than 1 year (RR, 1.559; P = .022) and decreases in A1c of more than 1.0% (RR, 1.590; P = .016). No such differences were seen with oral semaglutide.
A further evaluation of the data without the SUSTAIN 6 trial showed no effect on retinopathy but the analysis lacked power.
Dr. Albert told this news organization: “We did not find an immediate toxic effect of any drug. However, we cannot rule out that there was a cumulative effect of the dose over longer times.”
No disclosures were given.
A version of this article first appeared on Medscape.com.
A small potential increased risk of retinopathy worsening at 1 year with injected semaglutide (Ozempic, Novo Nordisk), a glucagon-like peptide 1 (GLP-1) agonist approved for type 2 diabetes, doesn’t outweigh the drug’s cardiovascular benefits but does highlight the need for baseline ophthalmologic evaluation before initiating treatment and ongoing retinal monitoring, researchers say.
That conclusion was based on data from a meta-analysis of the seven major cardiovascular outcomes trials of GLP-1 agonists currently on the market.
The findings were recently published in Diabetes & Metabolic Syndrome: Clinical Research & Reviews, by Stewart G. Albert, MD, and colleagues.
Concerns about retinopathy worsening with the GLP-1 agonist drug class first arose from the SUSTAIN-6 cardiovascular outcomes trial for injectable semaglutide, although a subsequent analysis of data from that trial appeared to suggest the problem is likely due to rapid glucose-lowering in already vulnerable patients rather than a drug-specific effect. This effect had been previously reported, most notably in the landmark Diabetes Control and Complications Trial.
In this new meta-analysis, “we showed that with improvements in A1c there were correlations with decreases in the rate of cardiovascular events but increases in the rate of retinopathy,” Dr. Albert, of St. Louis University, told this news organization.
“As a class of drugs, we did not find an increased rate of retinopathy. The effect of GLP-1 agonists on retinopathy did not appear to be due to an immediate direct toxic effect of the drug. The worsening of the rate of retinopathy was seen with semaglutide after 1 year of therapy and when there was a decrease in A1c of 1%,” he explained.
He noted that because the increased risk was seen primarily among those who already had retinopathy at baseline, “it would seem prudent to know the level of retinopathy either before or plan for close ophthalmologic monitoring around the time of drug initiation ... We routinely evaluate patients with known type 2 diabetes mellitus at yearly intervals for retinopathy. From our data, we saw worsening at 1 year of drug exposure, but we do not know the exact time when the changes occurred during that year.”
The Ozempic label advises that “patients with a history of diabetic retinopathy should be monitored for progression of diabetic retinopathy” but doesn’t specifically mention baseline assessment at the time of drug initiation.
No increase in retinopathy risk for GLP-1 agonist class overall
The seven trials in the meta-analysis comprised 56,004 participants, with baseline retinopathy prevalence ranging from 9% to 31%.
For the GLP-1 agonist class overall, there was no significant increase in the relative rate (RR) of retinopathy (RR, 1.09; P = .36), while there were significant reductions in relative rates of major adverse cardiac events, overall deaths, and cardiovascular deaths (all P < .001 or P = .001).
The increased retinopathy risk was seen only in the subcutaneous semaglutide group (RR, 1.73; P = .02).
The overall number needed to harm was 1,000 and the number to treat was 77. For semaglutide, those values were 77 and 43, respectively.
There was a significant correlation between a decrease in major adverse cardiac events and a decrease in A1c (P = .014), while for retinopathy, the risk increased with improved A1c (P = .076).
Semaglutide subanalysis finds increased retinopathy worsening
Dr. Albert and colleagues conducted a separate subanalysis of 11 studies of semaglutide that enrolled 11,894 patients, of which 6 studies (n = 5,610) were of oral semaglutide (Rybelsus) and 5 studies were of subcutaneous semaglutide (Ozempic; n = 6,284).
In the subanalysis, there was an overall increase in relative rates of new or worsening retinopathy (RR, 1.218; P = .049).
The change in relative rate of retinopathy was predominantly found for subcutaneous semaglutide given for longer than 1 year (RR, 1.559; P = .022) and decreases in A1c of more than 1.0% (RR, 1.590; P = .016). No such differences were seen with oral semaglutide.
A further evaluation of the data without the SUSTAIN 6 trial showed no effect on retinopathy but the analysis lacked power.
Dr. Albert told this news organization: “We did not find an immediate toxic effect of any drug. However, we cannot rule out that there was a cumulative effect of the dose over longer times.”
No disclosures were given.
A version of this article first appeared on Medscape.com.
FROM DIABETES & METABOLIC SYNDROME: CLINICAL RESEARCH & REVIEWS
FDA okays Tidepool Loop app to help guide insulin delivery
The Food and Drug Administration has cleared the Tidepool Loop, a mobile application for use with compatible continuous glucose monitors (CGMs) and insulin pumps to enable automated insulin delivery.
Indicated for people with type 1 diabetes ages 6 years and up, the app algorithm was developed by the diabetes startup Tidepool, which already hosts a cloud-based platform for users to download and review data from different glucose meters, insulin pumps, and CGM systems. The Tidepool Loop project arose from patient-led, open-source initiatives to enable interoperability between the devices.
“The [FDA] authorization of the Tidepool Loop is a huge win for the type 1 diabetes (T1D) community and is a vital step towards a world where people with T1D can choose the pump, CGM, and algorithm that are best for them – and have all three work together seamlessly,” Aaron Kowalski, PhD, CEO of the advocacy organization JDRF, said in a statement.
JDRF helped support preclinical and clinical research in the development of the Loop algorithm, along with The Leona M. and Harry B. Helmsley Charitable Trust, the Tullman Foundation, and partnerships with device makers and donations from the T1D community.
Available by prescription only, the Tidepool app is for single patient use. It works with designated “integrated CGMs” and “alternate controller enabled pumps” to automatically increase, decrease, or suspend insulin delivery, based on the glucose readings and predicted values. The app can also recommend correction doses, which the user can confirm.
According to an FDA statement:“Tidepool Loop’s algorithm technology is designed to be compatible with other individual interoperable devices that meet prespecified acceptance criteria set forth in a validation and integration plan provided by the sponsor and cleared by the FDA as part of the premarket submission.”
Tidepool is finalizing agreements with the various device manufacturers “to create a seamless experience for both physicians prescribing Tidepool Loop and the patients using it,” according to a company statement.
Tidepool’s initial launch device partners have not yet been announced, but the company “has a development partnership with Dexcom and other yet-to-be-named medical device companies for future inclusion of their components with the Tidepool Loop platform,” the statement says.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration has cleared the Tidepool Loop, a mobile application for use with compatible continuous glucose monitors (CGMs) and insulin pumps to enable automated insulin delivery.
Indicated for people with type 1 diabetes ages 6 years and up, the app algorithm was developed by the diabetes startup Tidepool, which already hosts a cloud-based platform for users to download and review data from different glucose meters, insulin pumps, and CGM systems. The Tidepool Loop project arose from patient-led, open-source initiatives to enable interoperability between the devices.
“The [FDA] authorization of the Tidepool Loop is a huge win for the type 1 diabetes (T1D) community and is a vital step towards a world where people with T1D can choose the pump, CGM, and algorithm that are best for them – and have all three work together seamlessly,” Aaron Kowalski, PhD, CEO of the advocacy organization JDRF, said in a statement.
JDRF helped support preclinical and clinical research in the development of the Loop algorithm, along with The Leona M. and Harry B. Helmsley Charitable Trust, the Tullman Foundation, and partnerships with device makers and donations from the T1D community.
Available by prescription only, the Tidepool app is for single patient use. It works with designated “integrated CGMs” and “alternate controller enabled pumps” to automatically increase, decrease, or suspend insulin delivery, based on the glucose readings and predicted values. The app can also recommend correction doses, which the user can confirm.
According to an FDA statement:“Tidepool Loop’s algorithm technology is designed to be compatible with other individual interoperable devices that meet prespecified acceptance criteria set forth in a validation and integration plan provided by the sponsor and cleared by the FDA as part of the premarket submission.”
Tidepool is finalizing agreements with the various device manufacturers “to create a seamless experience for both physicians prescribing Tidepool Loop and the patients using it,” according to a company statement.
Tidepool’s initial launch device partners have not yet been announced, but the company “has a development partnership with Dexcom and other yet-to-be-named medical device companies for future inclusion of their components with the Tidepool Loop platform,” the statement says.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration has cleared the Tidepool Loop, a mobile application for use with compatible continuous glucose monitors (CGMs) and insulin pumps to enable automated insulin delivery.
Indicated for people with type 1 diabetes ages 6 years and up, the app algorithm was developed by the diabetes startup Tidepool, which already hosts a cloud-based platform for users to download and review data from different glucose meters, insulin pumps, and CGM systems. The Tidepool Loop project arose from patient-led, open-source initiatives to enable interoperability between the devices.
“The [FDA] authorization of the Tidepool Loop is a huge win for the type 1 diabetes (T1D) community and is a vital step towards a world where people with T1D can choose the pump, CGM, and algorithm that are best for them – and have all three work together seamlessly,” Aaron Kowalski, PhD, CEO of the advocacy organization JDRF, said in a statement.
JDRF helped support preclinical and clinical research in the development of the Loop algorithm, along with The Leona M. and Harry B. Helmsley Charitable Trust, the Tullman Foundation, and partnerships with device makers and donations from the T1D community.
Available by prescription only, the Tidepool app is for single patient use. It works with designated “integrated CGMs” and “alternate controller enabled pumps” to automatically increase, decrease, or suspend insulin delivery, based on the glucose readings and predicted values. The app can also recommend correction doses, which the user can confirm.
According to an FDA statement:“Tidepool Loop’s algorithm technology is designed to be compatible with other individual interoperable devices that meet prespecified acceptance criteria set forth in a validation and integration plan provided by the sponsor and cleared by the FDA as part of the premarket submission.”
Tidepool is finalizing agreements with the various device manufacturers “to create a seamless experience for both physicians prescribing Tidepool Loop and the patients using it,” according to a company statement.
Tidepool’s initial launch device partners have not yet been announced, but the company “has a development partnership with Dexcom and other yet-to-be-named medical device companies for future inclusion of their components with the Tidepool Loop platform,” the statement says.
A version of this article first appeared on Medscape.com.