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AHA flags differing CVD risk in Asian American subgroups
Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.
“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.
The statement was published online in the journal Circulation.
Impact on health outcomes
Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).
Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.
Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.
For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.
However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).
Available data on T2D among Asian American subgroups also show varied prevalence and risk.
A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.
Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.
“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.
“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.
The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.
On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.
Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
Filling in the gaps
The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.
Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.
“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.
“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.
The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
A version of this article first appeared on Medscape.com.
Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.
“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.
The statement was published online in the journal Circulation.
Impact on health outcomes
Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).
Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.
Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.
For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.
However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).
Available data on T2D among Asian American subgroups also show varied prevalence and risk.
A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.
Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.
“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.
“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.
The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.
On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.
Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
Filling in the gaps
The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.
Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.
“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.
“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.
The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
A version of this article first appeared on Medscape.com.
Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.
“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.
The statement was published online in the journal Circulation.
Impact on health outcomes
Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).
Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.
Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.
For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.
However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).
Available data on T2D among Asian American subgroups also show varied prevalence and risk.
A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.
Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.
“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.
“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.
The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.
On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.
Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
Filling in the gaps
The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.
Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.
“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.
“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.
The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
A version of this article first appeared on Medscape.com.
FROM CIRCULATION
Young men at highest schizophrenia risk from cannabis abuse
A new study confirms the robust link between cannabis use and schizophrenia among men and women but suggests that young men may be especially susceptible to schizophrenia from cannabis abuse.
Of note, 
“The entanglement of substance use disorders and mental illnesses is a major public health issue, requiring urgent action and support for people who need it,” study coauthor Nora Volkow, MD, director of the National Institute on Drug Abuse, said in a news release.
“As access to potent cannabis products continues to expand, it is crucial that we also expand prevention, screening, and treatment for people who may experience mental illnesses associated with cannabis use,” Dr. Volkow added.
The study was published online in Psychological Medicine.
A modifiable risk factor
The researchers analyzed Danish registry data spanning 5 decades and representing more than 6.9 million people in Denmark to estimate the population-level percentage of schizophrenia cases attributable to CUD.
A total of 60,563 participants were diagnosed with CUD. Three-quarters of cases were in men; there were 45,327 incident cases of schizophrenia during the study period.
The overall adjusted hazard ratio for CUD on schizophrenia was slightly higher among males than females (aHR, 2.42 vs. 2.02); however, among those aged 16 to 20 years, the adjusted incidence risk ratio for males was more than twice that for females (aIRR, 3.84 vs. 1.81).
The researchers estimate that, in 2021, about 15% of schizophrenia cases among males aged 16-49 could have been avoided by preventing CUD, compared with 4% among females in this age range.
For young men aged 21-30, the proportion of preventable schizophrenia cases related to CUD may be as high as 30%, the authors reported.
“Alongside the increasing evidence that CUD is a modifiable risk factor for schizophrenia, our findings underscore the importance of evidence-based strategies to regulate cannabis use and to effectively prevent, screen for, and treat CUD as well as schizophrenia,” the researchers wrote.
Legalization sends the wrong message
In a press statement, lead investigator Carsten Hjorthøj, PhD, with the University of Copenhagen, noted that “increases in the legalization of cannabis over the past few decades have made it one of the most frequently used psychoactive substances in the world, while also decreasing the public’s perception of its harm. This study adds to our growing understanding that cannabis use is not harmless, and that risks are not fixed at one point in time.”
In a prior study, Dr. Hjorthøj and colleagues found that the proportion of new schizophrenia cases attributable to CUD has consistently increased over the past 20 years.
“In my view, the association is most likely causative, at least to a large extent,” Dr. Hjorthøj said at the time this research was published.
“It is of course nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” Dr. Hjorthøj added.
The study received no specific funding. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study confirms the robust link between cannabis use and schizophrenia among men and women but suggests that young men may be especially susceptible to schizophrenia from cannabis abuse.
Of note,
“The entanglement of substance use disorders and mental illnesses is a major public health issue, requiring urgent action and support for people who need it,” study coauthor Nora Volkow, MD, director of the National Institute on Drug Abuse, said in a news release.
“As access to potent cannabis products continues to expand, it is crucial that we also expand prevention, screening, and treatment for people who may experience mental illnesses associated with cannabis use,” Dr. Volkow added.
The study was published online in Psychological Medicine.
A modifiable risk factor
The researchers analyzed Danish registry data spanning 5 decades and representing more than 6.9 million people in Denmark to estimate the population-level percentage of schizophrenia cases attributable to CUD.
A total of 60,563 participants were diagnosed with CUD. Three-quarters of cases were in men; there were 45,327 incident cases of schizophrenia during the study period.
The overall adjusted hazard ratio for CUD on schizophrenia was slightly higher among males than females (aHR, 2.42 vs. 2.02); however, among those aged 16 to 20 years, the adjusted incidence risk ratio for males was more than twice that for females (aIRR, 3.84 vs. 1.81).
The researchers estimate that, in 2021, about 15% of schizophrenia cases among males aged 16-49 could have been avoided by preventing CUD, compared with 4% among females in this age range.
For young men aged 21-30, the proportion of preventable schizophrenia cases related to CUD may be as high as 30%, the authors reported.
“Alongside the increasing evidence that CUD is a modifiable risk factor for schizophrenia, our findings underscore the importance of evidence-based strategies to regulate cannabis use and to effectively prevent, screen for, and treat CUD as well as schizophrenia,” the researchers wrote.
Legalization sends the wrong message
In a press statement, lead investigator Carsten Hjorthøj, PhD, with the University of Copenhagen, noted that “increases in the legalization of cannabis over the past few decades have made it one of the most frequently used psychoactive substances in the world, while also decreasing the public’s perception of its harm. This study adds to our growing understanding that cannabis use is not harmless, and that risks are not fixed at one point in time.”
In a prior study, Dr. Hjorthøj and colleagues found that the proportion of new schizophrenia cases attributable to CUD has consistently increased over the past 20 years.
“In my view, the association is most likely causative, at least to a large extent,” Dr. Hjorthøj said at the time this research was published.
“It is of course nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” Dr. Hjorthøj added.
The study received no specific funding. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study confirms the robust link between cannabis use and schizophrenia among men and women but suggests that young men may be especially susceptible to schizophrenia from cannabis abuse.
Of note,
“The entanglement of substance use disorders and mental illnesses is a major public health issue, requiring urgent action and support for people who need it,” study coauthor Nora Volkow, MD, director of the National Institute on Drug Abuse, said in a news release.
“As access to potent cannabis products continues to expand, it is crucial that we also expand prevention, screening, and treatment for people who may experience mental illnesses associated with cannabis use,” Dr. Volkow added.
The study was published online in Psychological Medicine.
A modifiable risk factor
The researchers analyzed Danish registry data spanning 5 decades and representing more than 6.9 million people in Denmark to estimate the population-level percentage of schizophrenia cases attributable to CUD.
A total of 60,563 participants were diagnosed with CUD. Three-quarters of cases were in men; there were 45,327 incident cases of schizophrenia during the study period.
The overall adjusted hazard ratio for CUD on schizophrenia was slightly higher among males than females (aHR, 2.42 vs. 2.02); however, among those aged 16 to 20 years, the adjusted incidence risk ratio for males was more than twice that for females (aIRR, 3.84 vs. 1.81).
The researchers estimate that, in 2021, about 15% of schizophrenia cases among males aged 16-49 could have been avoided by preventing CUD, compared with 4% among females in this age range.
For young men aged 21-30, the proportion of preventable schizophrenia cases related to CUD may be as high as 30%, the authors reported.
“Alongside the increasing evidence that CUD is a modifiable risk factor for schizophrenia, our findings underscore the importance of evidence-based strategies to regulate cannabis use and to effectively prevent, screen for, and treat CUD as well as schizophrenia,” the researchers wrote.
Legalization sends the wrong message
In a press statement, lead investigator Carsten Hjorthøj, PhD, with the University of Copenhagen, noted that “increases in the legalization of cannabis over the past few decades have made it one of the most frequently used psychoactive substances in the world, while also decreasing the public’s perception of its harm. This study adds to our growing understanding that cannabis use is not harmless, and that risks are not fixed at one point in time.”
In a prior study, Dr. Hjorthøj and colleagues found that the proportion of new schizophrenia cases attributable to CUD has consistently increased over the past 20 years.
“In my view, the association is most likely causative, at least to a large extent,” Dr. Hjorthøj said at the time this research was published.
“It is of course nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” Dr. Hjorthøj added.
The study received no specific funding. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM PSYCHOLOGICAL MEDICINE
Asthma tied to increased risk for multiple cancers
People with asthma have an elevated risk for a variety of cancers other than lung cancer, including melanoma as well as blood, kidney, and ovarian cancers, new research suggests.
But, the authors found, treatment with an inhaled steroid may lower that risk, perhaps by keeping inflammation in check.
“Using real-world data, our study is the first to provide evidence of a positive association between asthma and cancer risk in United States patients,” Yi Guo, PhD, with the University of Florida, Gainesville, said in a news release.
The study was published online in Cancer Medicine.
The relationship between chronic inflammation and cancer remains a key area of exploration in cancer etiology. Data show that the risk for developing cancer is higher in patients with chronic inflammatory diseases, and patients with asthma have complex and chronic inflammation. However, prior studies exploring a possible link between asthma and cancer have yielded mixed results.
To investigate further, Dr. Guo and colleagues analyzed electronic health records and claims data in the OneFlorida+ clinical research network for roughly 90,000 adults with asthma and a matched cohort of about 270,000 adults without asthma.
Multivariable analysis revealed that adults with asthma were more likely to develop cancer, compared with peers without asthma (hazard ratio, 1.36), the investigators found.
Adults with asthma had an elevated cancer risk for five of the 13 cancers assessed, including melanoma (HR, 1.98), ovarian cancer (HR, 1.88), lung cancer (HR, 1.56), kidney cancer (HR, 1.48), and blood cancer (HR, 1.26).
Compared with adults without asthma, those with asthma who did not treat it with an inhaled steroid had a more pronounced overall cancer risk, compared with those who were on an inhaled steroid (HR, 1.60 vs. 1.11).
For specific cancer types, the risk was elevated for nine of 13 cancers in patients with asthma not taking an inhaled steroid: prostate (HR, 1.50), lung (HR, 1.74), colorectal (HR, 1.51), blood (HR, 1.44), melanoma (HR, 2.05), corpus uteri (HR, 1.76), kidney (HR, 1.52), ovarian (HR, 2.31), and cervical (HR, 1.46).
In contrast, in patients with asthma who did use an inhaled steroid, an elevated cancer risk was observed for only two cancers, lung cancer (HR, 1.39) and melanoma (HR, 1.92), suggesting a potential protective effect of inhaled steroid use on cancer, the researchers said.
Although prior studies have shown a protective effect of inhaled steroid use on some cancers, potentially by reducing inflammation, the “speculative nature of chronic inflammation (asthma as a common example) as a driver for pan-cancer development requires more investigation,” Dr. Guo and colleagues cautioned.
And because of the observational nature of the current study, Dr. Guo’s team stressed that these findings do not prove a causal relationship between asthma and cancer.
“More in-depth studies using real-word data are needed to further explore the causal mechanisms of asthma on cancer risk,” the researchers concluded.
Funding for the study was provided in part by grants to the researchers from the National Institutes of Health, National Cancer Institute, National Institute on Aging, and the Centers for Disease Control and Prevention. This project was supported by the Cancer Informatics Shared Resource in the University of Florida Health Cancer Center. The authors have disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
People with asthma have an elevated risk for a variety of cancers other than lung cancer, including melanoma as well as blood, kidney, and ovarian cancers, new research suggests.
But, the authors found, treatment with an inhaled steroid may lower that risk, perhaps by keeping inflammation in check.
“Using real-world data, our study is the first to provide evidence of a positive association between asthma and cancer risk in United States patients,” Yi Guo, PhD, with the University of Florida, Gainesville, said in a news release.
The study was published online in Cancer Medicine.
The relationship between chronic inflammation and cancer remains a key area of exploration in cancer etiology. Data show that the risk for developing cancer is higher in patients with chronic inflammatory diseases, and patients with asthma have complex and chronic inflammation. However, prior studies exploring a possible link between asthma and cancer have yielded mixed results.
To investigate further, Dr. Guo and colleagues analyzed electronic health records and claims data in the OneFlorida+ clinical research network for roughly 90,000 adults with asthma and a matched cohort of about 270,000 adults without asthma.
Multivariable analysis revealed that adults with asthma were more likely to develop cancer, compared with peers without asthma (hazard ratio, 1.36), the investigators found.
Adults with asthma had an elevated cancer risk for five of the 13 cancers assessed, including melanoma (HR, 1.98), ovarian cancer (HR, 1.88), lung cancer (HR, 1.56), kidney cancer (HR, 1.48), and blood cancer (HR, 1.26).
Compared with adults without asthma, those with asthma who did not treat it with an inhaled steroid had a more pronounced overall cancer risk, compared with those who were on an inhaled steroid (HR, 1.60 vs. 1.11).
For specific cancer types, the risk was elevated for nine of 13 cancers in patients with asthma not taking an inhaled steroid: prostate (HR, 1.50), lung (HR, 1.74), colorectal (HR, 1.51), blood (HR, 1.44), melanoma (HR, 2.05), corpus uteri (HR, 1.76), kidney (HR, 1.52), ovarian (HR, 2.31), and cervical (HR, 1.46).
In contrast, in patients with asthma who did use an inhaled steroid, an elevated cancer risk was observed for only two cancers, lung cancer (HR, 1.39) and melanoma (HR, 1.92), suggesting a potential protective effect of inhaled steroid use on cancer, the researchers said.
Although prior studies have shown a protective effect of inhaled steroid use on some cancers, potentially by reducing inflammation, the “speculative nature of chronic inflammation (asthma as a common example) as a driver for pan-cancer development requires more investigation,” Dr. Guo and colleagues cautioned.
And because of the observational nature of the current study, Dr. Guo’s team stressed that these findings do not prove a causal relationship between asthma and cancer.
“More in-depth studies using real-word data are needed to further explore the causal mechanisms of asthma on cancer risk,” the researchers concluded.
Funding for the study was provided in part by grants to the researchers from the National Institutes of Health, National Cancer Institute, National Institute on Aging, and the Centers for Disease Control and Prevention. This project was supported by the Cancer Informatics Shared Resource in the University of Florida Health Cancer Center. The authors have disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
People with asthma have an elevated risk for a variety of cancers other than lung cancer, including melanoma as well as blood, kidney, and ovarian cancers, new research suggests.
But, the authors found, treatment with an inhaled steroid may lower that risk, perhaps by keeping inflammation in check.
“Using real-world data, our study is the first to provide evidence of a positive association between asthma and cancer risk in United States patients,” Yi Guo, PhD, with the University of Florida, Gainesville, said in a news release.
The study was published online in Cancer Medicine.
The relationship between chronic inflammation and cancer remains a key area of exploration in cancer etiology. Data show that the risk for developing cancer is higher in patients with chronic inflammatory diseases, and patients with asthma have complex and chronic inflammation. However, prior studies exploring a possible link between asthma and cancer have yielded mixed results.
To investigate further, Dr. Guo and colleagues analyzed electronic health records and claims data in the OneFlorida+ clinical research network for roughly 90,000 adults with asthma and a matched cohort of about 270,000 adults without asthma.
Multivariable analysis revealed that adults with asthma were more likely to develop cancer, compared with peers without asthma (hazard ratio, 1.36), the investigators found.
Adults with asthma had an elevated cancer risk for five of the 13 cancers assessed, including melanoma (HR, 1.98), ovarian cancer (HR, 1.88), lung cancer (HR, 1.56), kidney cancer (HR, 1.48), and blood cancer (HR, 1.26).
Compared with adults without asthma, those with asthma who did not treat it with an inhaled steroid had a more pronounced overall cancer risk, compared with those who were on an inhaled steroid (HR, 1.60 vs. 1.11).
For specific cancer types, the risk was elevated for nine of 13 cancers in patients with asthma not taking an inhaled steroid: prostate (HR, 1.50), lung (HR, 1.74), colorectal (HR, 1.51), blood (HR, 1.44), melanoma (HR, 2.05), corpus uteri (HR, 1.76), kidney (HR, 1.52), ovarian (HR, 2.31), and cervical (HR, 1.46).
In contrast, in patients with asthma who did use an inhaled steroid, an elevated cancer risk was observed for only two cancers, lung cancer (HR, 1.39) and melanoma (HR, 1.92), suggesting a potential protective effect of inhaled steroid use on cancer, the researchers said.
Although prior studies have shown a protective effect of inhaled steroid use on some cancers, potentially by reducing inflammation, the “speculative nature of chronic inflammation (asthma as a common example) as a driver for pan-cancer development requires more investigation,” Dr. Guo and colleagues cautioned.
And because of the observational nature of the current study, Dr. Guo’s team stressed that these findings do not prove a causal relationship between asthma and cancer.
“More in-depth studies using real-word data are needed to further explore the causal mechanisms of asthma on cancer risk,” the researchers concluded.
Funding for the study was provided in part by grants to the researchers from the National Institutes of Health, National Cancer Institute, National Institute on Aging, and the Centers for Disease Control and Prevention. This project was supported by the Cancer Informatics Shared Resource in the University of Florida Health Cancer Center. The authors have disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
Pausing endocrine therapy to attempt pregnancy is safe
The results provide the “strongest evidence to date on the short-term safety of this choice,” Sharon Giordano, MD, MPH, with University of Texas M.D. Anderson Cancer Center, Houston, wrote in an editorial accompanying the study.
“Physicians should now incorporate these positive data into their shared decision-making process with patients,” Dr. Giordano said.
The POSITIVE trial findings were published online in The New England Journal of Medicine.
Before the analysis, the risks associated with taking a break from endocrine therapy among young women with hormone receptor (HR)–positive breast cancer remained unclear.
In the current trial, Ann Partridge, MD, MPH, and colleagues sought prospective data on the safety associated with taking a temporary break from therapy to attempt pregnancy.
The single-group trial enrolled more than 500 premenopausal women who had received 18-30 months of endocrine therapy for mostly stage I or II HR-positive breast cancer. After a 3-month washout, the women were given 2 years to conceive, deliver, and breastfeed, if desired, before resuming treatment. Breast cancer events – the primary outcome – were defined as local, regional, or distant recurrence of invasive breast cancer or new contralateral invasive breast cancer.
The results, initially reported at San Antonio Breast Cancer Symposium (SABCS) 2022, showed that a temporary interruption of therapy to attempt pregnancy did not appear to lead to worse breast cancer outcomes.
Among 497 women who were followed for pregnancy status, 368 (74%) had at least one pregnancy, and 317 (64%) had at least one live birth.
After a median follow-up of 3.4 years, 44 women had had a breast cancer event – a result that was close to, but did not exceed, the safety threshold of 46 breast cancer events.
The 3-year incidence of breast cancer events was 8.9% (95% confidence interval [CI], 6.3-11.6) in the treatment-interruption group compared with 9.2% (95% CI, 7.6-10.8) among historical controls, which included women who would have met the entry criteria for the trial.
“These results suggest that although endocrine therapy for a period of 5-10 years substantially improves disease outcomes in patients with hormone receptor–positive early breast cancer, a temporary interruption of therapy to attempt pregnancy does not appear to have an appreciable negative short-term effect,” wrote Dr. Partridge, vice chair of medical oncology at Dana-Farber Cancer Institute and professor of medicine at Harvard Medical School, Boston, and colleagues.
The authors cautioned, however, that the median follow-up was only 3.4 years and that 10-year follow-up data will be “critical” to confirm the safety of interruption of adjuvant endocrine therapy.
Dr. Giordano agreed, noting that “recurrences of breast cancer are reported to occur at a steady rate for up to 20 years after diagnosis among patients with hormone receptor–positive disease; the protocol-specified 10-year follow-up data will be essential to establish longer-term safety.”
The study was supported by the International Breast Cancer Study Group and by the Alliance for Clinical Trials in Oncology in North America in collaboration with the Breast International Group (BIG). Disclosures for authors and editorial writer are available at NEJM.org.
A version of this article first appeared on Medscape.com.
The results provide the “strongest evidence to date on the short-term safety of this choice,” Sharon Giordano, MD, MPH, with University of Texas M.D. Anderson Cancer Center, Houston, wrote in an editorial accompanying the study.
“Physicians should now incorporate these positive data into their shared decision-making process with patients,” Dr. Giordano said.
The POSITIVE trial findings were published online in The New England Journal of Medicine.
Before the analysis, the risks associated with taking a break from endocrine therapy among young women with hormone receptor (HR)–positive breast cancer remained unclear.
In the current trial, Ann Partridge, MD, MPH, and colleagues sought prospective data on the safety associated with taking a temporary break from therapy to attempt pregnancy.
The single-group trial enrolled more than 500 premenopausal women who had received 18-30 months of endocrine therapy for mostly stage I or II HR-positive breast cancer. After a 3-month washout, the women were given 2 years to conceive, deliver, and breastfeed, if desired, before resuming treatment. Breast cancer events – the primary outcome – were defined as local, regional, or distant recurrence of invasive breast cancer or new contralateral invasive breast cancer.
The results, initially reported at San Antonio Breast Cancer Symposium (SABCS) 2022, showed that a temporary interruption of therapy to attempt pregnancy did not appear to lead to worse breast cancer outcomes.
Among 497 women who were followed for pregnancy status, 368 (74%) had at least one pregnancy, and 317 (64%) had at least one live birth.
After a median follow-up of 3.4 years, 44 women had had a breast cancer event – a result that was close to, but did not exceed, the safety threshold of 46 breast cancer events.
The 3-year incidence of breast cancer events was 8.9% (95% confidence interval [CI], 6.3-11.6) in the treatment-interruption group compared with 9.2% (95% CI, 7.6-10.8) among historical controls, which included women who would have met the entry criteria for the trial.
“These results suggest that although endocrine therapy for a period of 5-10 years substantially improves disease outcomes in patients with hormone receptor–positive early breast cancer, a temporary interruption of therapy to attempt pregnancy does not appear to have an appreciable negative short-term effect,” wrote Dr. Partridge, vice chair of medical oncology at Dana-Farber Cancer Institute and professor of medicine at Harvard Medical School, Boston, and colleagues.
The authors cautioned, however, that the median follow-up was only 3.4 years and that 10-year follow-up data will be “critical” to confirm the safety of interruption of adjuvant endocrine therapy.
Dr. Giordano agreed, noting that “recurrences of breast cancer are reported to occur at a steady rate for up to 20 years after diagnosis among patients with hormone receptor–positive disease; the protocol-specified 10-year follow-up data will be essential to establish longer-term safety.”
The study was supported by the International Breast Cancer Study Group and by the Alliance for Clinical Trials in Oncology in North America in collaboration with the Breast International Group (BIG). Disclosures for authors and editorial writer are available at NEJM.org.
A version of this article first appeared on Medscape.com.
The results provide the “strongest evidence to date on the short-term safety of this choice,” Sharon Giordano, MD, MPH, with University of Texas M.D. Anderson Cancer Center, Houston, wrote in an editorial accompanying the study.
“Physicians should now incorporate these positive data into their shared decision-making process with patients,” Dr. Giordano said.
The POSITIVE trial findings were published online in The New England Journal of Medicine.
Before the analysis, the risks associated with taking a break from endocrine therapy among young women with hormone receptor (HR)–positive breast cancer remained unclear.
In the current trial, Ann Partridge, MD, MPH, and colleagues sought prospective data on the safety associated with taking a temporary break from therapy to attempt pregnancy.
The single-group trial enrolled more than 500 premenopausal women who had received 18-30 months of endocrine therapy for mostly stage I or II HR-positive breast cancer. After a 3-month washout, the women were given 2 years to conceive, deliver, and breastfeed, if desired, before resuming treatment. Breast cancer events – the primary outcome – were defined as local, regional, or distant recurrence of invasive breast cancer or new contralateral invasive breast cancer.
The results, initially reported at San Antonio Breast Cancer Symposium (SABCS) 2022, showed that a temporary interruption of therapy to attempt pregnancy did not appear to lead to worse breast cancer outcomes.
Among 497 women who were followed for pregnancy status, 368 (74%) had at least one pregnancy, and 317 (64%) had at least one live birth.
After a median follow-up of 3.4 years, 44 women had had a breast cancer event – a result that was close to, but did not exceed, the safety threshold of 46 breast cancer events.
The 3-year incidence of breast cancer events was 8.9% (95% confidence interval [CI], 6.3-11.6) in the treatment-interruption group compared with 9.2% (95% CI, 7.6-10.8) among historical controls, which included women who would have met the entry criteria for the trial.
“These results suggest that although endocrine therapy for a period of 5-10 years substantially improves disease outcomes in patients with hormone receptor–positive early breast cancer, a temporary interruption of therapy to attempt pregnancy does not appear to have an appreciable negative short-term effect,” wrote Dr. Partridge, vice chair of medical oncology at Dana-Farber Cancer Institute and professor of medicine at Harvard Medical School, Boston, and colleagues.
The authors cautioned, however, that the median follow-up was only 3.4 years and that 10-year follow-up data will be “critical” to confirm the safety of interruption of adjuvant endocrine therapy.
Dr. Giordano agreed, noting that “recurrences of breast cancer are reported to occur at a steady rate for up to 20 years after diagnosis among patients with hormone receptor–positive disease; the protocol-specified 10-year follow-up data will be essential to establish longer-term safety.”
The study was supported by the International Breast Cancer Study Group and by the Alliance for Clinical Trials in Oncology in North America in collaboration with the Breast International Group (BIG). Disclosures for authors and editorial writer are available at NEJM.org.
A version of this article first appeared on Medscape.com.
FROM NEJM
H. pylori eradication therapy curbs risk for stomach cancer
People with H. pylori who were treated had about a 63% lower risk of developing noncardia gastric adenocarcinoma (NCGA) after 8 years of follow-up, compared with peers with H. pylori who were not treated.
The U.S. data align with previous studies, conducted mostly in Asia, that found that treating the infection can reduce stomach cancer incidence.
The KPNC study shows the “potential for stomach cancer prevention in U.S. populations through H. pylori screening and treatment,” study investigator Dan Li, MD, gastroenterologist with the Kaiser Permanente Medical Group and Kaiser Permanente Division of Research in Oakland, Calif., said in an interview.
Judith Kim, MD, a gastroenterologist at NYU Langone Health in New York, who wasn’t involved in the research, said that the study is significant because “it is the first to show this effect in a large, diverse population in the U.S., where gastric cancer incidence is lower.”
The study was published online in Gastroenterology.
Top risk factor
About 30% of people in the United States are infected with H. pylori, which is the No. 1 known risk factor for stomach cancer, Dr. Li said.
The study cohort included 716,567 KPNC members who underwent H. pylori testing and/or treatment between 1997 and 2015.
Among H. pylori–infected individuals (based on positive nonserology test results), the subdistribution hazard ratio was 6.07 for untreated individuals and 2.68 for treated individuals, compared with H. pylori–negative individuals.
It’s not surprising that people who were treated for the infection still had a higher risk of NCGA than people who had never had the infection, Dr. Li said.
“This is likely because many people with chronic H. pylori infection had already developed some precancerous changes in their stomach before they were treated. This finding suggests that H. pylori ideally should be treated before precancerous changes develop,” he said.
When compared directly with H. pylori–positive/untreated individuals, the risk for NCGA in H. pylori–positive/treated individuals was somewhat lower at less than 8 years follow-up (sHR, 0.95) and significantly lower at 8+ years of follow-up (sHR, 0.37).
“After 7-10 years of follow-up, people with H. pylori who received treatment had nearly half the risk of developing stomach cancer as the general population,” Dr. Li said. “This is likely because most people infected with H. pylori in the general population are not screened nor treated. This highlights the impact screening and treatment can have.”
The data also show that cumulative incidence curves for H. pylori–positive/untreated and H. pylori–positive/treated largely overlapped during the first 7 years of follow-up and started to separate after 8 years.
At 10 years, cumulative NCGA incidence rates for H. pylori–positive/untreated, H. pylori–positive/treated, and H. pylori negative were 31.0, 19.7, and 3.5 per 10,000 persons, respectively (P < .0001).
This study shows that treating H. pylori reduces stomach cancer incidence in the United States, thus “filling an important research and knowledge gap,” Dr. Li said.
In the United States, Asian, Black, and Hispanic adults are much more likely to be infected with H. pylori, and they have a two- to threefold higher risk of developing stomach cancer, he noted.
“This suggests it may be reasonable to consider targeted screening and treatment in these high-risk groups. However, the optimal strategy for population-based H. pylori screening has not been established, and more research is needed to determine who should be screened for H. pylori and at what age screening should begin,” Dr. Li said.
Strong data, jury out on universal screening
For additional comment, this news organization reached out to Aaron Glatt, MD, a spokesperson for the Infectious Diseases Society of America and chief of infectious diseases and hospital epidemiologist at Mount Sinai South Nassau in Oceanside, N.Y.
The study shows that the treatment of H. pylori “absolutely will decrease your risk of certain types of gastric carcinoma down the line. It does take a while to show that, 7 years, but this study shows that very clearly,” Dr. Glatt said.
“People who have definitely been shown to have H. pylori should be treated,” Dr. Glatt said.
“I don’t think this study yet supports that everybody should be screened, but it does make sense that people who have upper GI symptoms consistent with H. pylori should be checked for H. pylori and then appropriately treated, he noted.
Routine screening for H. pylori is recommended in countries with high incidence of gastric cancer, but not in the United States, Dr. Kim noted.
“Given the risk reduction of cancer with H. pylori treatment, consideration should be made in the U.S. for asymptomatic individuals with a family history of gastric cancer or immigrants from high-incidence countries,” she added.
The study was funded by the Kaiser Permanente Northern California Community Health Research Grants Program, the Permanente Medical Group Delivery Science & Applied Research Program, and the Permanente Medical Group. Dr. Li, Dr. Glatt, and Dr. Kim have declared no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
People with H. pylori who were treated had about a 63% lower risk of developing noncardia gastric adenocarcinoma (NCGA) after 8 years of follow-up, compared with peers with H. pylori who were not treated.
The U.S. data align with previous studies, conducted mostly in Asia, that found that treating the infection can reduce stomach cancer incidence.
The KPNC study shows the “potential for stomach cancer prevention in U.S. populations through H. pylori screening and treatment,” study investigator Dan Li, MD, gastroenterologist with the Kaiser Permanente Medical Group and Kaiser Permanente Division of Research in Oakland, Calif., said in an interview.
Judith Kim, MD, a gastroenterologist at NYU Langone Health in New York, who wasn’t involved in the research, said that the study is significant because “it is the first to show this effect in a large, diverse population in the U.S., where gastric cancer incidence is lower.”
The study was published online in Gastroenterology.
Top risk factor
About 30% of people in the United States are infected with H. pylori, which is the No. 1 known risk factor for stomach cancer, Dr. Li said.
The study cohort included 716,567 KPNC members who underwent H. pylori testing and/or treatment between 1997 and 2015.
Among H. pylori–infected individuals (based on positive nonserology test results), the subdistribution hazard ratio was 6.07 for untreated individuals and 2.68 for treated individuals, compared with H. pylori–negative individuals.
It’s not surprising that people who were treated for the infection still had a higher risk of NCGA than people who had never had the infection, Dr. Li said.
“This is likely because many people with chronic H. pylori infection had already developed some precancerous changes in their stomach before they were treated. This finding suggests that H. pylori ideally should be treated before precancerous changes develop,” he said.
When compared directly with H. pylori–positive/untreated individuals, the risk for NCGA in H. pylori–positive/treated individuals was somewhat lower at less than 8 years follow-up (sHR, 0.95) and significantly lower at 8+ years of follow-up (sHR, 0.37).
“After 7-10 years of follow-up, people with H. pylori who received treatment had nearly half the risk of developing stomach cancer as the general population,” Dr. Li said. “This is likely because most people infected with H. pylori in the general population are not screened nor treated. This highlights the impact screening and treatment can have.”
The data also show that cumulative incidence curves for H. pylori–positive/untreated and H. pylori–positive/treated largely overlapped during the first 7 years of follow-up and started to separate after 8 years.
At 10 years, cumulative NCGA incidence rates for H. pylori–positive/untreated, H. pylori–positive/treated, and H. pylori negative were 31.0, 19.7, and 3.5 per 10,000 persons, respectively (P < .0001).
This study shows that treating H. pylori reduces stomach cancer incidence in the United States, thus “filling an important research and knowledge gap,” Dr. Li said.
In the United States, Asian, Black, and Hispanic adults are much more likely to be infected with H. pylori, and they have a two- to threefold higher risk of developing stomach cancer, he noted.
“This suggests it may be reasonable to consider targeted screening and treatment in these high-risk groups. However, the optimal strategy for population-based H. pylori screening has not been established, and more research is needed to determine who should be screened for H. pylori and at what age screening should begin,” Dr. Li said.
Strong data, jury out on universal screening
For additional comment, this news organization reached out to Aaron Glatt, MD, a spokesperson for the Infectious Diseases Society of America and chief of infectious diseases and hospital epidemiologist at Mount Sinai South Nassau in Oceanside, N.Y.
The study shows that the treatment of H. pylori “absolutely will decrease your risk of certain types of gastric carcinoma down the line. It does take a while to show that, 7 years, but this study shows that very clearly,” Dr. Glatt said.
“People who have definitely been shown to have H. pylori should be treated,” Dr. Glatt said.
“I don’t think this study yet supports that everybody should be screened, but it does make sense that people who have upper GI symptoms consistent with H. pylori should be checked for H. pylori and then appropriately treated, he noted.
Routine screening for H. pylori is recommended in countries with high incidence of gastric cancer, but not in the United States, Dr. Kim noted.
“Given the risk reduction of cancer with H. pylori treatment, consideration should be made in the U.S. for asymptomatic individuals with a family history of gastric cancer or immigrants from high-incidence countries,” she added.
The study was funded by the Kaiser Permanente Northern California Community Health Research Grants Program, the Permanente Medical Group Delivery Science & Applied Research Program, and the Permanente Medical Group. Dr. Li, Dr. Glatt, and Dr. Kim have declared no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
People with H. pylori who were treated had about a 63% lower risk of developing noncardia gastric adenocarcinoma (NCGA) after 8 years of follow-up, compared with peers with H. pylori who were not treated.
The U.S. data align with previous studies, conducted mostly in Asia, that found that treating the infection can reduce stomach cancer incidence.
The KPNC study shows the “potential for stomach cancer prevention in U.S. populations through H. pylori screening and treatment,” study investigator Dan Li, MD, gastroenterologist with the Kaiser Permanente Medical Group and Kaiser Permanente Division of Research in Oakland, Calif., said in an interview.
Judith Kim, MD, a gastroenterologist at NYU Langone Health in New York, who wasn’t involved in the research, said that the study is significant because “it is the first to show this effect in a large, diverse population in the U.S., where gastric cancer incidence is lower.”
The study was published online in Gastroenterology.
Top risk factor
About 30% of people in the United States are infected with H. pylori, which is the No. 1 known risk factor for stomach cancer, Dr. Li said.
The study cohort included 716,567 KPNC members who underwent H. pylori testing and/or treatment between 1997 and 2015.
Among H. pylori–infected individuals (based on positive nonserology test results), the subdistribution hazard ratio was 6.07 for untreated individuals and 2.68 for treated individuals, compared with H. pylori–negative individuals.
It’s not surprising that people who were treated for the infection still had a higher risk of NCGA than people who had never had the infection, Dr. Li said.
“This is likely because many people with chronic H. pylori infection had already developed some precancerous changes in their stomach before they were treated. This finding suggests that H. pylori ideally should be treated before precancerous changes develop,” he said.
When compared directly with H. pylori–positive/untreated individuals, the risk for NCGA in H. pylori–positive/treated individuals was somewhat lower at less than 8 years follow-up (sHR, 0.95) and significantly lower at 8+ years of follow-up (sHR, 0.37).
“After 7-10 years of follow-up, people with H. pylori who received treatment had nearly half the risk of developing stomach cancer as the general population,” Dr. Li said. “This is likely because most people infected with H. pylori in the general population are not screened nor treated. This highlights the impact screening and treatment can have.”
The data also show that cumulative incidence curves for H. pylori–positive/untreated and H. pylori–positive/treated largely overlapped during the first 7 years of follow-up and started to separate after 8 years.
At 10 years, cumulative NCGA incidence rates for H. pylori–positive/untreated, H. pylori–positive/treated, and H. pylori negative were 31.0, 19.7, and 3.5 per 10,000 persons, respectively (P < .0001).
This study shows that treating H. pylori reduces stomach cancer incidence in the United States, thus “filling an important research and knowledge gap,” Dr. Li said.
In the United States, Asian, Black, and Hispanic adults are much more likely to be infected with H. pylori, and they have a two- to threefold higher risk of developing stomach cancer, he noted.
“This suggests it may be reasonable to consider targeted screening and treatment in these high-risk groups. However, the optimal strategy for population-based H. pylori screening has not been established, and more research is needed to determine who should be screened for H. pylori and at what age screening should begin,” Dr. Li said.
Strong data, jury out on universal screening
For additional comment, this news organization reached out to Aaron Glatt, MD, a spokesperson for the Infectious Diseases Society of America and chief of infectious diseases and hospital epidemiologist at Mount Sinai South Nassau in Oceanside, N.Y.
The study shows that the treatment of H. pylori “absolutely will decrease your risk of certain types of gastric carcinoma down the line. It does take a while to show that, 7 years, but this study shows that very clearly,” Dr. Glatt said.
“People who have definitely been shown to have H. pylori should be treated,” Dr. Glatt said.
“I don’t think this study yet supports that everybody should be screened, but it does make sense that people who have upper GI symptoms consistent with H. pylori should be checked for H. pylori and then appropriately treated, he noted.
Routine screening for H. pylori is recommended in countries with high incidence of gastric cancer, but not in the United States, Dr. Kim noted.
“Given the risk reduction of cancer with H. pylori treatment, consideration should be made in the U.S. for asymptomatic individuals with a family history of gastric cancer or immigrants from high-incidence countries,” she added.
The study was funded by the Kaiser Permanente Northern California Community Health Research Grants Program, the Permanente Medical Group Delivery Science & Applied Research Program, and the Permanente Medical Group. Dr. Li, Dr. Glatt, and Dr. Kim have declared no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM GASTROENTEROLOGY
Hearing aids are a ‘powerful’ tool for reducing dementia risk
, new research confirms. A large observational study from the United Kingdom showed a 42% increased risk for dementia in people with hearing loss compared with their peers with no hearing trouble. In addition, there was no increased risk in those with hearing loss who used hearing aids.
“The evidence is building that hearing loss may be the most impactful modifiable risk factor for dementia in mid-life, but the effectiveness of hearing aid use on reducing the risk of dementia in the real world has remained unclear,” Dongshan Zhu, PhD, with Shandong University, Jinan, China, said in a news release.
“Our study provides the best evidence to date to suggest that hearing aids could be a minimally invasive, cost-effective treatment to mitigate the potential impact of hearing loss on dementia,” Dr. Zhu said.
The study, which was published online in Lancet Public Health, comes on the heels of the 2020 Lancet Commission report on dementia, which suggested hearing loss may be linked to approximately 8% of worldwide dementia cases.
‘Compelling’ evidence
For the study, investigators analyzed longitudinal data on 437,704 individuals, most of whom were White, from the UK Biobank (54% female; mean age at baseline, 56 years). Roughly three quarters of the cohort had no hearing loss and one quarter had some level of hearing loss, with 12% of these individuals using hearing aids.
After the researchers controlled for relevant cofactors, compared with people without hearing loss, those with hearing loss who were not using hearing aids had an increased risk for all-cause dementia (hazard ratio [HR], 1.42; 95% confidence interval [CI], 1.29-1.56).
No increased risk was seen in people with hearing loss who were using hearing aids (HR, 1.04; 95% CI, 0.98-1.10).
The positive association of hearing aid use was observed in all-cause dementia and cause-specific dementia subtypes, including Alzheimer’s disease, vascular dementia, and non–Alzheimer’s disease nonvascular dementia.
The data also suggest that the protection against dementia conferred by hearing aid use most likely stems from direct effects from hearing aids rather than indirect mediators, such as social isolation, loneliness, and low mood.
Dr. Zhu said the findings highlight the “urgent need” for the early use of hearing aids when an individual starts having trouble hearing.
“A group effort from across society is necessary, including raising awareness of hearing loss and the potential links with dementia; increasing accessibility to hearing aids by reducing cost; and more support for primary care workers to screen for hearing impairment, raise awareness, and deliver treatment such as fitting hearing aids,” Dr. Zhu said.
Writing in a linked comment, Gill Livingston, MD, and Sergi Costafreda, MD, PhD, with University College London, noted that with addition of this study, “the evidence that hearing aids are a powerful tool to reduce the risk of dementia in people with hearing loss, is as good as possible without randomized controlled trials, which might not be practically possible or ethical because people with hearing loss should not be stopped from using effective treatments.”
“The evidence is compelling that treating hearing loss is a promising way of reducing dementia risk. This is the time to increase awareness of and detection of hearing loss, as well as the acceptability and usability of hearing aids,” Dr. Livingston and Dr. Costafreda added.
High-quality evidence – with caveats
Several experts offered perspective on the analysis in a statement from the U.K.-based nonprofit Science Media Centre, which was not involved with the conduct of this study. Charles Marshall, MRCP, PhD, with Queen Mary University of London, said that the study provides “high-quality evidence” that those with hearing loss who use hearing aids are at lower risk for dementia than are those with hearing loss who do not use hearing aids.
“This raises the possibility that a proportion of dementia cases could be prevented by using hearing aids to correct hearing loss. However, the observational nature of this study makes it difficult to be sure that hearing aids are actually causing the reduced risk of dementia,” Dr. Marshall added.
“Hearing aids produce slightly distorted sound, and the brain has to adapt to this in order for hearing aids to be helpful,” he said. “People who are at risk of developing dementia in the future may have early changes in their brain that impair this adaptation, and this may lead to them choosing to not use hearing aids. This would confound the association, creating the appearance that hearing aids were reducing dementia risk, when actually their use was just identifying people with relatively healthy brains,” Dr. Marshall added.
Tara Spires-Jones, PhD, with the University of Edinburgh, said this “well-conducted” study confirms previous similar studies showing an association between hearing loss and dementia risk.
Echoing Dr. Marshall, Dr. Spires-Jones noted that this type of study cannot prove conclusively that hearing loss causes dementia.
“For example,” she said, “it is possible that people who are already in the very early stages of disease are less likely to seek help for hearing loss. However, on balance, this study and the rest of the data in the field indicate that keeping your brain healthy and engaged reduces dementia risk.”
Dr. Spires-Jones said that she agrees with the investigators that it’s “important to help people with hearing loss to get effective hearing aids to help keep their brains engaged through allowing richer social interactions.”
This study was funded by the National Natural Science Foundation of China and Shandong Province, Taishan Scholars Project, China Medical Board, and China Postdoctoral Science Foundation. Dr. Zhu, Dr. Livingston, Dr. Costafreda, Dr. Marshall, and Dr. Spires-Jones have no relevant disclosures.
A version of this article originally appeared on Medscape.com.
, new research confirms. A large observational study from the United Kingdom showed a 42% increased risk for dementia in people with hearing loss compared with their peers with no hearing trouble. In addition, there was no increased risk in those with hearing loss who used hearing aids.
“The evidence is building that hearing loss may be the most impactful modifiable risk factor for dementia in mid-life, but the effectiveness of hearing aid use on reducing the risk of dementia in the real world has remained unclear,” Dongshan Zhu, PhD, with Shandong University, Jinan, China, said in a news release.
“Our study provides the best evidence to date to suggest that hearing aids could be a minimally invasive, cost-effective treatment to mitigate the potential impact of hearing loss on dementia,” Dr. Zhu said.
The study, which was published online in Lancet Public Health, comes on the heels of the 2020 Lancet Commission report on dementia, which suggested hearing loss may be linked to approximately 8% of worldwide dementia cases.
‘Compelling’ evidence
For the study, investigators analyzed longitudinal data on 437,704 individuals, most of whom were White, from the UK Biobank (54% female; mean age at baseline, 56 years). Roughly three quarters of the cohort had no hearing loss and one quarter had some level of hearing loss, with 12% of these individuals using hearing aids.
After the researchers controlled for relevant cofactors, compared with people without hearing loss, those with hearing loss who were not using hearing aids had an increased risk for all-cause dementia (hazard ratio [HR], 1.42; 95% confidence interval [CI], 1.29-1.56).
No increased risk was seen in people with hearing loss who were using hearing aids (HR, 1.04; 95% CI, 0.98-1.10).
The positive association of hearing aid use was observed in all-cause dementia and cause-specific dementia subtypes, including Alzheimer’s disease, vascular dementia, and non–Alzheimer’s disease nonvascular dementia.
The data also suggest that the protection against dementia conferred by hearing aid use most likely stems from direct effects from hearing aids rather than indirect mediators, such as social isolation, loneliness, and low mood.
Dr. Zhu said the findings highlight the “urgent need” for the early use of hearing aids when an individual starts having trouble hearing.
“A group effort from across society is necessary, including raising awareness of hearing loss and the potential links with dementia; increasing accessibility to hearing aids by reducing cost; and more support for primary care workers to screen for hearing impairment, raise awareness, and deliver treatment such as fitting hearing aids,” Dr. Zhu said.
Writing in a linked comment, Gill Livingston, MD, and Sergi Costafreda, MD, PhD, with University College London, noted that with addition of this study, “the evidence that hearing aids are a powerful tool to reduce the risk of dementia in people with hearing loss, is as good as possible without randomized controlled trials, which might not be practically possible or ethical because people with hearing loss should not be stopped from using effective treatments.”
“The evidence is compelling that treating hearing loss is a promising way of reducing dementia risk. This is the time to increase awareness of and detection of hearing loss, as well as the acceptability and usability of hearing aids,” Dr. Livingston and Dr. Costafreda added.
High-quality evidence – with caveats
Several experts offered perspective on the analysis in a statement from the U.K.-based nonprofit Science Media Centre, which was not involved with the conduct of this study. Charles Marshall, MRCP, PhD, with Queen Mary University of London, said that the study provides “high-quality evidence” that those with hearing loss who use hearing aids are at lower risk for dementia than are those with hearing loss who do not use hearing aids.
“This raises the possibility that a proportion of dementia cases could be prevented by using hearing aids to correct hearing loss. However, the observational nature of this study makes it difficult to be sure that hearing aids are actually causing the reduced risk of dementia,” Dr. Marshall added.
“Hearing aids produce slightly distorted sound, and the brain has to adapt to this in order for hearing aids to be helpful,” he said. “People who are at risk of developing dementia in the future may have early changes in their brain that impair this adaptation, and this may lead to them choosing to not use hearing aids. This would confound the association, creating the appearance that hearing aids were reducing dementia risk, when actually their use was just identifying people with relatively healthy brains,” Dr. Marshall added.
Tara Spires-Jones, PhD, with the University of Edinburgh, said this “well-conducted” study confirms previous similar studies showing an association between hearing loss and dementia risk.
Echoing Dr. Marshall, Dr. Spires-Jones noted that this type of study cannot prove conclusively that hearing loss causes dementia.
“For example,” she said, “it is possible that people who are already in the very early stages of disease are less likely to seek help for hearing loss. However, on balance, this study and the rest of the data in the field indicate that keeping your brain healthy and engaged reduces dementia risk.”
Dr. Spires-Jones said that she agrees with the investigators that it’s “important to help people with hearing loss to get effective hearing aids to help keep their brains engaged through allowing richer social interactions.”
This study was funded by the National Natural Science Foundation of China and Shandong Province, Taishan Scholars Project, China Medical Board, and China Postdoctoral Science Foundation. Dr. Zhu, Dr. Livingston, Dr. Costafreda, Dr. Marshall, and Dr. Spires-Jones have no relevant disclosures.
A version of this article originally appeared on Medscape.com.
, new research confirms. A large observational study from the United Kingdom showed a 42% increased risk for dementia in people with hearing loss compared with their peers with no hearing trouble. In addition, there was no increased risk in those with hearing loss who used hearing aids.
“The evidence is building that hearing loss may be the most impactful modifiable risk factor for dementia in mid-life, but the effectiveness of hearing aid use on reducing the risk of dementia in the real world has remained unclear,” Dongshan Zhu, PhD, with Shandong University, Jinan, China, said in a news release.
“Our study provides the best evidence to date to suggest that hearing aids could be a minimally invasive, cost-effective treatment to mitigate the potential impact of hearing loss on dementia,” Dr. Zhu said.
The study, which was published online in Lancet Public Health, comes on the heels of the 2020 Lancet Commission report on dementia, which suggested hearing loss may be linked to approximately 8% of worldwide dementia cases.
‘Compelling’ evidence
For the study, investigators analyzed longitudinal data on 437,704 individuals, most of whom were White, from the UK Biobank (54% female; mean age at baseline, 56 years). Roughly three quarters of the cohort had no hearing loss and one quarter had some level of hearing loss, with 12% of these individuals using hearing aids.
After the researchers controlled for relevant cofactors, compared with people without hearing loss, those with hearing loss who were not using hearing aids had an increased risk for all-cause dementia (hazard ratio [HR], 1.42; 95% confidence interval [CI], 1.29-1.56).
No increased risk was seen in people with hearing loss who were using hearing aids (HR, 1.04; 95% CI, 0.98-1.10).
The positive association of hearing aid use was observed in all-cause dementia and cause-specific dementia subtypes, including Alzheimer’s disease, vascular dementia, and non–Alzheimer’s disease nonvascular dementia.
The data also suggest that the protection against dementia conferred by hearing aid use most likely stems from direct effects from hearing aids rather than indirect mediators, such as social isolation, loneliness, and low mood.
Dr. Zhu said the findings highlight the “urgent need” for the early use of hearing aids when an individual starts having trouble hearing.
“A group effort from across society is necessary, including raising awareness of hearing loss and the potential links with dementia; increasing accessibility to hearing aids by reducing cost; and more support for primary care workers to screen for hearing impairment, raise awareness, and deliver treatment such as fitting hearing aids,” Dr. Zhu said.
Writing in a linked comment, Gill Livingston, MD, and Sergi Costafreda, MD, PhD, with University College London, noted that with addition of this study, “the evidence that hearing aids are a powerful tool to reduce the risk of dementia in people with hearing loss, is as good as possible without randomized controlled trials, which might not be practically possible or ethical because people with hearing loss should not be stopped from using effective treatments.”
“The evidence is compelling that treating hearing loss is a promising way of reducing dementia risk. This is the time to increase awareness of and detection of hearing loss, as well as the acceptability and usability of hearing aids,” Dr. Livingston and Dr. Costafreda added.
High-quality evidence – with caveats
Several experts offered perspective on the analysis in a statement from the U.K.-based nonprofit Science Media Centre, which was not involved with the conduct of this study. Charles Marshall, MRCP, PhD, with Queen Mary University of London, said that the study provides “high-quality evidence” that those with hearing loss who use hearing aids are at lower risk for dementia than are those with hearing loss who do not use hearing aids.
“This raises the possibility that a proportion of dementia cases could be prevented by using hearing aids to correct hearing loss. However, the observational nature of this study makes it difficult to be sure that hearing aids are actually causing the reduced risk of dementia,” Dr. Marshall added.
“Hearing aids produce slightly distorted sound, and the brain has to adapt to this in order for hearing aids to be helpful,” he said. “People who are at risk of developing dementia in the future may have early changes in their brain that impair this adaptation, and this may lead to them choosing to not use hearing aids. This would confound the association, creating the appearance that hearing aids were reducing dementia risk, when actually their use was just identifying people with relatively healthy brains,” Dr. Marshall added.
Tara Spires-Jones, PhD, with the University of Edinburgh, said this “well-conducted” study confirms previous similar studies showing an association between hearing loss and dementia risk.
Echoing Dr. Marshall, Dr. Spires-Jones noted that this type of study cannot prove conclusively that hearing loss causes dementia.
“For example,” she said, “it is possible that people who are already in the very early stages of disease are less likely to seek help for hearing loss. However, on balance, this study and the rest of the data in the field indicate that keeping your brain healthy and engaged reduces dementia risk.”
Dr. Spires-Jones said that she agrees with the investigators that it’s “important to help people with hearing loss to get effective hearing aids to help keep their brains engaged through allowing richer social interactions.”
This study was funded by the National Natural Science Foundation of China and Shandong Province, Taishan Scholars Project, China Medical Board, and China Postdoctoral Science Foundation. Dr. Zhu, Dr. Livingston, Dr. Costafreda, Dr. Marshall, and Dr. Spires-Jones have no relevant disclosures.
A version of this article originally appeared on Medscape.com.
New clues to how air pollution fuels lung cancer in nonsmokers
“This work adds to our understanding of the mechanism by which air pollutants promote the earliest stages of lung cancer, particularly in people who have never smoked,” William Hill, PhD, co–first author and postdoctoral researcher at the Francis Crick Institute, London, told this news organization.
The study, which assessed human lung samples and mouse cancer models, was published online in Nature.
Although smoking remains the chief risk factor for lung cancer, outdoor air pollution causes roughly 1 in 10 cases of lung cancer in the United Kingdom, according to Cancer Research UK. In 2019, about 300,000 lung cancer deaths around the world were attributed to exposure to ambient particulate matter measuring ≤ 2.5 mcm (PM2.5).
While the link between air pollution and lung cancer is well known, the mechanism that explains this link has been harder to pinpoint.
One theory is that environmental carcinogens such as tobacco smoke and UV light cause mutations by damaging DNA directly. However, recent data have hinted that that may not be the case.
In the current study, Dr. Hill and colleagues proposed that, rather than act on DNA directly, air pollutants might promote inflammatory changes in the lung tissue that wake up inactive cancer-causing mutations, which accumulate naturally in these cells as people age. This idea lines up with a decades-old theory of cancer promotion, according to which tumorigenesis is a two-step process: The initial step induces mutations in healthy cells, after which a promoter step triggers cancer development.
The study team focused on epidermal growth factor receptor (EGFR)–driven lung cancer, which is more common in never-smokers and light smokers, and on environmental particulate matter measuring ≤ 2.5 mcm (PM2.5), which is fine enough to travel into the lungs and is associated with lung cancer risk.
Dr. Hill and colleagues analyzed data from over 400,000 people in three countries. They compared rates of EGFR-mutant lung cancer cases in areas with different levels of PM2.5 pollution. The team found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in England, South Korea, and Taiwan.
The researchers then studied genetically engineered mouse models of lung adenocarcinoma to determine whether particulate matter exposure could trigger the development of lung tumors. In these functional mouse models, air pollutants led to an influx of macrophages in the lung and the release of interleukin-1beta, a key mediator of the inflammatory response.
This process ultimately “fuels tumorigenesis,” the study team concluded.
The team also found that treatment with an anti-interleukin-1beta antibody during PM2.5 exposure reduced lung cancer promotion by air pollutants.
A detailed mutational profiling of histologically normal lung tissue from 295 individuals revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively.
Overall, “our data suggest a mechanistic and causative link between air pollutants and lung cancer,” the study team wrote.
The study demonstrates that air pollution rouses cells in the lung that carry cancer-causing mutations, “encouraging them to grow and potentially form tumors,” Dr. Hill said. “Understanding the biology could help identify high-risk individuals and, in the future, may open avenues to prevent cancer caused by breathing polluted air.”
In a related article in Nature, Allan Balmain, PhD, of the University of California, San Francisco, said these results have “major implications for how to think about cancer prevention.”
“There is presently nothing that can be done to remove the mutated cells that accumulate in normal tissues, but if there is a promotion stage that influences the rate of cancer development, then inhibition of this stage might be an effective way to prevent cancer,” Dr. Balmain said.
Another prevention option, Dr. Hill noted, is to reduce the levels of air pollution. “Our study provides a mandate for the reduction of PM2.5 emissions globally,” he said.
Dr. Hill also believes the findings may extend beyond lung cancer.
“It’s possible that this inflammatory pathway could be involved in other types of cancer and that it could be triggered by other environmental carcinogens,” he said. “But further research is needed to find out which other environmental carcinogens might trigger this pathway, as well as which other parts of the body this may occur in.”
Funding for the study was provided by Cancer Research UK, the European Research Council, the Francis Crick Institute, the Mark Foundation, the Lung Cancer Research Foundation, Rosetrees Trust, and the Ruth Strauss Foundation. A complete list of author disclosures is available with the original article. Dr. Balmain has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“This work adds to our understanding of the mechanism by which air pollutants promote the earliest stages of lung cancer, particularly in people who have never smoked,” William Hill, PhD, co–first author and postdoctoral researcher at the Francis Crick Institute, London, told this news organization.
The study, which assessed human lung samples and mouse cancer models, was published online in Nature.
Although smoking remains the chief risk factor for lung cancer, outdoor air pollution causes roughly 1 in 10 cases of lung cancer in the United Kingdom, according to Cancer Research UK. In 2019, about 300,000 lung cancer deaths around the world were attributed to exposure to ambient particulate matter measuring ≤ 2.5 mcm (PM2.5).
While the link between air pollution and lung cancer is well known, the mechanism that explains this link has been harder to pinpoint.
One theory is that environmental carcinogens such as tobacco smoke and UV light cause mutations by damaging DNA directly. However, recent data have hinted that that may not be the case.
In the current study, Dr. Hill and colleagues proposed that, rather than act on DNA directly, air pollutants might promote inflammatory changes in the lung tissue that wake up inactive cancer-causing mutations, which accumulate naturally in these cells as people age. This idea lines up with a decades-old theory of cancer promotion, according to which tumorigenesis is a two-step process: The initial step induces mutations in healthy cells, after which a promoter step triggers cancer development.
The study team focused on epidermal growth factor receptor (EGFR)–driven lung cancer, which is more common in never-smokers and light smokers, and on environmental particulate matter measuring ≤ 2.5 mcm (PM2.5), which is fine enough to travel into the lungs and is associated with lung cancer risk.
Dr. Hill and colleagues analyzed data from over 400,000 people in three countries. They compared rates of EGFR-mutant lung cancer cases in areas with different levels of PM2.5 pollution. The team found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in England, South Korea, and Taiwan.
The researchers then studied genetically engineered mouse models of lung adenocarcinoma to determine whether particulate matter exposure could trigger the development of lung tumors. In these functional mouse models, air pollutants led to an influx of macrophages in the lung and the release of interleukin-1beta, a key mediator of the inflammatory response.
This process ultimately “fuels tumorigenesis,” the study team concluded.
The team also found that treatment with an anti-interleukin-1beta antibody during PM2.5 exposure reduced lung cancer promotion by air pollutants.
A detailed mutational profiling of histologically normal lung tissue from 295 individuals revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively.
Overall, “our data suggest a mechanistic and causative link between air pollutants and lung cancer,” the study team wrote.
The study demonstrates that air pollution rouses cells in the lung that carry cancer-causing mutations, “encouraging them to grow and potentially form tumors,” Dr. Hill said. “Understanding the biology could help identify high-risk individuals and, in the future, may open avenues to prevent cancer caused by breathing polluted air.”
In a related article in Nature, Allan Balmain, PhD, of the University of California, San Francisco, said these results have “major implications for how to think about cancer prevention.”
“There is presently nothing that can be done to remove the mutated cells that accumulate in normal tissues, but if there is a promotion stage that influences the rate of cancer development, then inhibition of this stage might be an effective way to prevent cancer,” Dr. Balmain said.
Another prevention option, Dr. Hill noted, is to reduce the levels of air pollution. “Our study provides a mandate for the reduction of PM2.5 emissions globally,” he said.
Dr. Hill also believes the findings may extend beyond lung cancer.
“It’s possible that this inflammatory pathway could be involved in other types of cancer and that it could be triggered by other environmental carcinogens,” he said. “But further research is needed to find out which other environmental carcinogens might trigger this pathway, as well as which other parts of the body this may occur in.”
Funding for the study was provided by Cancer Research UK, the European Research Council, the Francis Crick Institute, the Mark Foundation, the Lung Cancer Research Foundation, Rosetrees Trust, and the Ruth Strauss Foundation. A complete list of author disclosures is available with the original article. Dr. Balmain has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“This work adds to our understanding of the mechanism by which air pollutants promote the earliest stages of lung cancer, particularly in people who have never smoked,” William Hill, PhD, co–first author and postdoctoral researcher at the Francis Crick Institute, London, told this news organization.
The study, which assessed human lung samples and mouse cancer models, was published online in Nature.
Although smoking remains the chief risk factor for lung cancer, outdoor air pollution causes roughly 1 in 10 cases of lung cancer in the United Kingdom, according to Cancer Research UK. In 2019, about 300,000 lung cancer deaths around the world were attributed to exposure to ambient particulate matter measuring ≤ 2.5 mcm (PM2.5).
While the link between air pollution and lung cancer is well known, the mechanism that explains this link has been harder to pinpoint.
One theory is that environmental carcinogens such as tobacco smoke and UV light cause mutations by damaging DNA directly. However, recent data have hinted that that may not be the case.
In the current study, Dr. Hill and colleagues proposed that, rather than act on DNA directly, air pollutants might promote inflammatory changes in the lung tissue that wake up inactive cancer-causing mutations, which accumulate naturally in these cells as people age. This idea lines up with a decades-old theory of cancer promotion, according to which tumorigenesis is a two-step process: The initial step induces mutations in healthy cells, after which a promoter step triggers cancer development.
The study team focused on epidermal growth factor receptor (EGFR)–driven lung cancer, which is more common in never-smokers and light smokers, and on environmental particulate matter measuring ≤ 2.5 mcm (PM2.5), which is fine enough to travel into the lungs and is associated with lung cancer risk.
Dr. Hill and colleagues analyzed data from over 400,000 people in three countries. They compared rates of EGFR-mutant lung cancer cases in areas with different levels of PM2.5 pollution. The team found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in England, South Korea, and Taiwan.
The researchers then studied genetically engineered mouse models of lung adenocarcinoma to determine whether particulate matter exposure could trigger the development of lung tumors. In these functional mouse models, air pollutants led to an influx of macrophages in the lung and the release of interleukin-1beta, a key mediator of the inflammatory response.
This process ultimately “fuels tumorigenesis,” the study team concluded.
The team also found that treatment with an anti-interleukin-1beta antibody during PM2.5 exposure reduced lung cancer promotion by air pollutants.
A detailed mutational profiling of histologically normal lung tissue from 295 individuals revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively.
Overall, “our data suggest a mechanistic and causative link between air pollutants and lung cancer,” the study team wrote.
The study demonstrates that air pollution rouses cells in the lung that carry cancer-causing mutations, “encouraging them to grow and potentially form tumors,” Dr. Hill said. “Understanding the biology could help identify high-risk individuals and, in the future, may open avenues to prevent cancer caused by breathing polluted air.”
In a related article in Nature, Allan Balmain, PhD, of the University of California, San Francisco, said these results have “major implications for how to think about cancer prevention.”
“There is presently nothing that can be done to remove the mutated cells that accumulate in normal tissues, but if there is a promotion stage that influences the rate of cancer development, then inhibition of this stage might be an effective way to prevent cancer,” Dr. Balmain said.
Another prevention option, Dr. Hill noted, is to reduce the levels of air pollution. “Our study provides a mandate for the reduction of PM2.5 emissions globally,” he said.
Dr. Hill also believes the findings may extend beyond lung cancer.
“It’s possible that this inflammatory pathway could be involved in other types of cancer and that it could be triggered by other environmental carcinogens,” he said. “But further research is needed to find out which other environmental carcinogens might trigger this pathway, as well as which other parts of the body this may occur in.”
Funding for the study was provided by Cancer Research UK, the European Research Council, the Francis Crick Institute, the Mark Foundation, the Lung Cancer Research Foundation, Rosetrees Trust, and the Ruth Strauss Foundation. A complete list of author disclosures is available with the original article. Dr. Balmain has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
10 popular diets for heart health ranked
An evidence-based analysis of 10 popular dietary patterns shows that some promote heart health better than others.
A new American Heart Association scientific statement concludes that the Mediterranean, Dietary Approach to Stop Hypertension (DASH), pescatarian, and vegetarian eating patterns most strongly align with heart-healthy eating guidelines issued by the AHA in 2021, whereas the popular paleolithic (paleo) and ketogenic (keto) diets fall short.
“The good news for the public and their clinicians is that there are several dietary patterns that allow for substantial flexibility for following a heart healthy diet – DASH, Mediterranean, vegetarian,” writing-group chair Christopher Gardner, PhD, with Stanford (Calif.) University, told this news organization.
“However, some of the popular diets – particularly paleo and keto – are so strictly restrictive of specific food groups that when these diets are followed as intended by their proponents, they are not aligned with the scientific evidence for a heart-healthy diet,” Dr. Gardner said.
The statement was published online in Circulation.
A tool for clinicians
“The number of different, popular dietary patterns has proliferated in recent years, and the amount of misinformation about them on social media has reached critical levels,” Dr. Gardner said in a news release.
“The public – and even many health care professionals – may rightfully be confused about heart-healthy eating, and they may feel that they don’t have the time or the training to evaluate the different diets. We hope this statement serves as a tool for clinicians and the public to understand which diets promote good cardiometabolic health,” he noted.
The writing group rated on a scale of 1-100 how well 10 popular diets or eating patterns align with AHA dietary advice for heart-healthy eating.
That advice includes consuming a wide variety of fruits and vegetables; choosing mostly whole grains instead of refined grains; using liquid plant oils rather than tropical oils; eating healthy sources of protein, such as from plants, seafood, or lean meats; minimizing added sugars and salt; limiting alcohol; choosing minimally processed foods instead of ultraprocessed foods; and following this guidance wherever food is prepared or consumed.
The 10 diets/dietary patterns were DASH, Mediterranean-style, pescatarian, ovo-lacto vegetarian, vegan, low-fat, very low–fat, low-carbohydrate, paleo, and very low–carbohydrate/keto patterns.
The diets were divided into four tiers on the basis of their scores, which ranged from a low of 31 to a high of 100.
Only the DASH eating plan got a perfect score of 100. This eating pattern is low in salt, added sugar, tropical oil, alcohol, and processed foods and high in nonstarchy vegetables, fruits, whole grains, and legumes. Proteins are mostly plant-based, such as legumes, beans, or nuts, along with fish or seafood, lean poultry and meats, and low-fat or fat-free dairy products.
The Mediterranean eating pattern achieved a slightly lower score of 89 because unlike DASH, it allows for moderate alcohol consumption and does not address added salt.
The other two top tier eating patterns were pescatarian, with a score of 92, and vegetarian, with a score of 86.
“If implemented as intended, the top-tier dietary patterns align best with the American Heart Association’s guidance and may be adapted to respect cultural practices, food preferences and budgets to enable people to always eat this way, for the long term,” Dr. Gardner said in the release.
Vegan and low-fat diets (each with a score of 78) fell into the second tier.
Though these diets emphasize fruits, vegetables, whole grains, legumes, and nuts while limiting alcohol and added sugars, the vegan diet is so restrictive that it could be challenging to follow long-term or when eating out and may increase the risk for vitamin B12 deficiency, which can lead to anemia, the writing group notes.
There also are concerns that low-fat diets treat all fats equally, whereas the AHA guidance calls for replacing saturated fats with healthier fats, they point out.
The third tier includes the very low–fat diet (score 72) and low-carb diet (score 64), whereas the paleo and very low–carb/keto diets fall into the fourth tier, with the lowest scores of 53 and 31, respectively.
Dr. Gardner said that it’s important to note that all 10 diet patterns “share four positive characteristics: more veggies, more whole foods, less added sugars, less refined grains.”
“These are all areas for which Americans have substantial room for improvement, and these are all things that we could work on together. Progress across these aspects would make a large difference in the heart-healthiness of the U.S. diet,” he told this news organization.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Lifestyle and Cardiometabolic Health, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, and the Council on Peripheral Vascular Disease.
A version of this article first appeared on Medscape.com.
An evidence-based analysis of 10 popular dietary patterns shows that some promote heart health better than others.
A new American Heart Association scientific statement concludes that the Mediterranean, Dietary Approach to Stop Hypertension (DASH), pescatarian, and vegetarian eating patterns most strongly align with heart-healthy eating guidelines issued by the AHA in 2021, whereas the popular paleolithic (paleo) and ketogenic (keto) diets fall short.
“The good news for the public and their clinicians is that there are several dietary patterns that allow for substantial flexibility for following a heart healthy diet – DASH, Mediterranean, vegetarian,” writing-group chair Christopher Gardner, PhD, with Stanford (Calif.) University, told this news organization.
“However, some of the popular diets – particularly paleo and keto – are so strictly restrictive of specific food groups that when these diets are followed as intended by their proponents, they are not aligned with the scientific evidence for a heart-healthy diet,” Dr. Gardner said.
The statement was published online in Circulation.
A tool for clinicians
“The number of different, popular dietary patterns has proliferated in recent years, and the amount of misinformation about them on social media has reached critical levels,” Dr. Gardner said in a news release.
“The public – and even many health care professionals – may rightfully be confused about heart-healthy eating, and they may feel that they don’t have the time or the training to evaluate the different diets. We hope this statement serves as a tool for clinicians and the public to understand which diets promote good cardiometabolic health,” he noted.
The writing group rated on a scale of 1-100 how well 10 popular diets or eating patterns align with AHA dietary advice for heart-healthy eating.
That advice includes consuming a wide variety of fruits and vegetables; choosing mostly whole grains instead of refined grains; using liquid plant oils rather than tropical oils; eating healthy sources of protein, such as from plants, seafood, or lean meats; minimizing added sugars and salt; limiting alcohol; choosing minimally processed foods instead of ultraprocessed foods; and following this guidance wherever food is prepared or consumed.
The 10 diets/dietary patterns were DASH, Mediterranean-style, pescatarian, ovo-lacto vegetarian, vegan, low-fat, very low–fat, low-carbohydrate, paleo, and very low–carbohydrate/keto patterns.
The diets were divided into four tiers on the basis of their scores, which ranged from a low of 31 to a high of 100.
Only the DASH eating plan got a perfect score of 100. This eating pattern is low in salt, added sugar, tropical oil, alcohol, and processed foods and high in nonstarchy vegetables, fruits, whole grains, and legumes. Proteins are mostly plant-based, such as legumes, beans, or nuts, along with fish or seafood, lean poultry and meats, and low-fat or fat-free dairy products.
The Mediterranean eating pattern achieved a slightly lower score of 89 because unlike DASH, it allows for moderate alcohol consumption and does not address added salt.
The other two top tier eating patterns were pescatarian, with a score of 92, and vegetarian, with a score of 86.
“If implemented as intended, the top-tier dietary patterns align best with the American Heart Association’s guidance and may be adapted to respect cultural practices, food preferences and budgets to enable people to always eat this way, for the long term,” Dr. Gardner said in the release.
Vegan and low-fat diets (each with a score of 78) fell into the second tier.
Though these diets emphasize fruits, vegetables, whole grains, legumes, and nuts while limiting alcohol and added sugars, the vegan diet is so restrictive that it could be challenging to follow long-term or when eating out and may increase the risk for vitamin B12 deficiency, which can lead to anemia, the writing group notes.
There also are concerns that low-fat diets treat all fats equally, whereas the AHA guidance calls for replacing saturated fats with healthier fats, they point out.
The third tier includes the very low–fat diet (score 72) and low-carb diet (score 64), whereas the paleo and very low–carb/keto diets fall into the fourth tier, with the lowest scores of 53 and 31, respectively.
Dr. Gardner said that it’s important to note that all 10 diet patterns “share four positive characteristics: more veggies, more whole foods, less added sugars, less refined grains.”
“These are all areas for which Americans have substantial room for improvement, and these are all things that we could work on together. Progress across these aspects would make a large difference in the heart-healthiness of the U.S. diet,” he told this news organization.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Lifestyle and Cardiometabolic Health, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, and the Council on Peripheral Vascular Disease.
A version of this article first appeared on Medscape.com.
An evidence-based analysis of 10 popular dietary patterns shows that some promote heart health better than others.
A new American Heart Association scientific statement concludes that the Mediterranean, Dietary Approach to Stop Hypertension (DASH), pescatarian, and vegetarian eating patterns most strongly align with heart-healthy eating guidelines issued by the AHA in 2021, whereas the popular paleolithic (paleo) and ketogenic (keto) diets fall short.
“The good news for the public and their clinicians is that there are several dietary patterns that allow for substantial flexibility for following a heart healthy diet – DASH, Mediterranean, vegetarian,” writing-group chair Christopher Gardner, PhD, with Stanford (Calif.) University, told this news organization.
“However, some of the popular diets – particularly paleo and keto – are so strictly restrictive of specific food groups that when these diets are followed as intended by their proponents, they are not aligned with the scientific evidence for a heart-healthy diet,” Dr. Gardner said.
The statement was published online in Circulation.
A tool for clinicians
“The number of different, popular dietary patterns has proliferated in recent years, and the amount of misinformation about them on social media has reached critical levels,” Dr. Gardner said in a news release.
“The public – and even many health care professionals – may rightfully be confused about heart-healthy eating, and they may feel that they don’t have the time or the training to evaluate the different diets. We hope this statement serves as a tool for clinicians and the public to understand which diets promote good cardiometabolic health,” he noted.
The writing group rated on a scale of 1-100 how well 10 popular diets or eating patterns align with AHA dietary advice for heart-healthy eating.
That advice includes consuming a wide variety of fruits and vegetables; choosing mostly whole grains instead of refined grains; using liquid plant oils rather than tropical oils; eating healthy sources of protein, such as from plants, seafood, or lean meats; minimizing added sugars and salt; limiting alcohol; choosing minimally processed foods instead of ultraprocessed foods; and following this guidance wherever food is prepared or consumed.
The 10 diets/dietary patterns were DASH, Mediterranean-style, pescatarian, ovo-lacto vegetarian, vegan, low-fat, very low–fat, low-carbohydrate, paleo, and very low–carbohydrate/keto patterns.
The diets were divided into four tiers on the basis of their scores, which ranged from a low of 31 to a high of 100.
Only the DASH eating plan got a perfect score of 100. This eating pattern is low in salt, added sugar, tropical oil, alcohol, and processed foods and high in nonstarchy vegetables, fruits, whole grains, and legumes. Proteins are mostly plant-based, such as legumes, beans, or nuts, along with fish or seafood, lean poultry and meats, and low-fat or fat-free dairy products.
The Mediterranean eating pattern achieved a slightly lower score of 89 because unlike DASH, it allows for moderate alcohol consumption and does not address added salt.
The other two top tier eating patterns were pescatarian, with a score of 92, and vegetarian, with a score of 86.
“If implemented as intended, the top-tier dietary patterns align best with the American Heart Association’s guidance and may be adapted to respect cultural practices, food preferences and budgets to enable people to always eat this way, for the long term,” Dr. Gardner said in the release.
Vegan and low-fat diets (each with a score of 78) fell into the second tier.
Though these diets emphasize fruits, vegetables, whole grains, legumes, and nuts while limiting alcohol and added sugars, the vegan diet is so restrictive that it could be challenging to follow long-term or when eating out and may increase the risk for vitamin B12 deficiency, which can lead to anemia, the writing group notes.
There also are concerns that low-fat diets treat all fats equally, whereas the AHA guidance calls for replacing saturated fats with healthier fats, they point out.
The third tier includes the very low–fat diet (score 72) and low-carb diet (score 64), whereas the paleo and very low–carb/keto diets fall into the fourth tier, with the lowest scores of 53 and 31, respectively.
Dr. Gardner said that it’s important to note that all 10 diet patterns “share four positive characteristics: more veggies, more whole foods, less added sugars, less refined grains.”
“These are all areas for which Americans have substantial room for improvement, and these are all things that we could work on together. Progress across these aspects would make a large difference in the heart-healthiness of the U.S. diet,” he told this news organization.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Lifestyle and Cardiometabolic Health, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, and the Council on Peripheral Vascular Disease.
A version of this article first appeared on Medscape.com.
AHA backs screening for cognitive impairment after stroke
Screening for cognitive impairment should be part of multidisciplinary care for stroke survivors, the American Heart Association says in a new scientific statement.
“Cognitive impairment after stroke is very common, is associated with other post-stroke outcomes, and often has significant impact on the quality of life,” Nada El Husseini, MD, MHSc, chair of the scientific statement writing group, told this news organization.
“It is important to screen stroke survivors for cognitive impairment as well as for associated comorbidities such as mood and sleep disorders,” said Dr. El Husseini, associate professor of neurology at Duke University Medical Center in Durham, N.C.
The scientific statement was published online in Stroke. It’s the first to specifically focus on the cognitive impairment resulting from an overt stroke (ischemic or hemorrhagic).
‘Actionable’ considerations for care
The writing group performed a “scoping” review of the literature on the prevalence, diagnosis, and management of poststroke cognitive impairment (PSCI) to provide a framework for “actionable considerations” for clinical practice as well as to highlight gaps needing additional studies, Dr. El Husseini explained.
PSCI, ranging from mild to severe, occurs in up to 60% of stroke survivors in the first year after stroke; yet, it is often underreported and underdiagnosed, the writing group notes.
Up to 20% of stroke survivors who experience mild cognitive impairment fully recover cognitive function, and cognitive recovery is most likely within the first 6 months after a stroke.
However, improvement in cognitive impairment without return to prestroke levels is more frequent than is complete recovery. As many as one in three stroke survivors may develop dementia within 5 years of stroke.
The writing group also notes that PSCI is often associated with other conditions, including physical disability, sleep disorders, behavioral and personality changes, depression, and other neuropsychological changes – each of which may contribute to lower quality of life.
Currently, there is no “gold standard” for cognitive screening following stroke, but several brief cognitive screening tests, including the Mini–Mental State Examination and the Montreal Cognitive Assessment, are widely used to identify cognitive impairment after stroke.
The statement also highlights the importance of assessing cognitive changes over time after stroke. Stroke survivors who experience unexplained difficulties with cognitive-related activities of daily living, following care instructions, or providing a reliable health history may be candidates for additional cognitive screening.
Manage risk factors to prevent repeat stroke
“Anticipatory guidance regarding home and driving safety and, return to work (if applicable) along with interdisciplinary collaboration among different medical and ancillary specialists in the diagnosis and management of cognitive impairment is key for the holistic care of stroke survivors,” Dr. El Husseini told this news organization.
The multidisciplinary poststroke health care team could include neurologists, occupational therapists, speech therapists, nurses, neuropsychologists, gerontologists, and primary care providers.
“Because recurrent stroke is strongly associated with the development of cognitive impairment and dementia, prevention of recurrent strokes should be sought to decrease that risk,” Dr. El Husseini said. This includes addressing stroke risk factors, including high blood pressure, high cholesterol, type 2 diabetes, and atrial fibrillation.
The writing group says research is needed in the future to determine how cognitive impairment develops after stroke and the impact of nonbrain factors, including infection, frailty, and social factors.
Further research is also needed to determine best practices for cognitive screening after stroke, including the development and use of screening instruments that consider demographic, cultural, and linguistic factors in determining “normal” function.
“Perhaps the most pressing need, however, is the development of effective and culturally relevant treatments for poststroke cognitive impairment,” Dr. El Husseini said in a news release.
“We hope to see big enough clinical trials that assess various techniques, medications, and lifestyle changes in diverse groups of patients that may help improve cognitive function,” she added.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular Radiology and Intervention, the Council on Hypertension, and the Council on Lifestyle and Cardiometabolic Health.
Screening for cognitive impairment should be part of multidisciplinary care for stroke survivors, the American Heart Association says in a new scientific statement.
“Cognitive impairment after stroke is very common, is associated with other post-stroke outcomes, and often has significant impact on the quality of life,” Nada El Husseini, MD, MHSc, chair of the scientific statement writing group, told this news organization.
“It is important to screen stroke survivors for cognitive impairment as well as for associated comorbidities such as mood and sleep disorders,” said Dr. El Husseini, associate professor of neurology at Duke University Medical Center in Durham, N.C.
The scientific statement was published online in Stroke. It’s the first to specifically focus on the cognitive impairment resulting from an overt stroke (ischemic or hemorrhagic).
‘Actionable’ considerations for care
The writing group performed a “scoping” review of the literature on the prevalence, diagnosis, and management of poststroke cognitive impairment (PSCI) to provide a framework for “actionable considerations” for clinical practice as well as to highlight gaps needing additional studies, Dr. El Husseini explained.
PSCI, ranging from mild to severe, occurs in up to 60% of stroke survivors in the first year after stroke; yet, it is often underreported and underdiagnosed, the writing group notes.
Up to 20% of stroke survivors who experience mild cognitive impairment fully recover cognitive function, and cognitive recovery is most likely within the first 6 months after a stroke.
However, improvement in cognitive impairment without return to prestroke levels is more frequent than is complete recovery. As many as one in three stroke survivors may develop dementia within 5 years of stroke.
The writing group also notes that PSCI is often associated with other conditions, including physical disability, sleep disorders, behavioral and personality changes, depression, and other neuropsychological changes – each of which may contribute to lower quality of life.
Currently, there is no “gold standard” for cognitive screening following stroke, but several brief cognitive screening tests, including the Mini–Mental State Examination and the Montreal Cognitive Assessment, are widely used to identify cognitive impairment after stroke.
The statement also highlights the importance of assessing cognitive changes over time after stroke. Stroke survivors who experience unexplained difficulties with cognitive-related activities of daily living, following care instructions, or providing a reliable health history may be candidates for additional cognitive screening.
Manage risk factors to prevent repeat stroke
“Anticipatory guidance regarding home and driving safety and, return to work (if applicable) along with interdisciplinary collaboration among different medical and ancillary specialists in the diagnosis and management of cognitive impairment is key for the holistic care of stroke survivors,” Dr. El Husseini told this news organization.
The multidisciplinary poststroke health care team could include neurologists, occupational therapists, speech therapists, nurses, neuropsychologists, gerontologists, and primary care providers.
“Because recurrent stroke is strongly associated with the development of cognitive impairment and dementia, prevention of recurrent strokes should be sought to decrease that risk,” Dr. El Husseini said. This includes addressing stroke risk factors, including high blood pressure, high cholesterol, type 2 diabetes, and atrial fibrillation.
The writing group says research is needed in the future to determine how cognitive impairment develops after stroke and the impact of nonbrain factors, including infection, frailty, and social factors.
Further research is also needed to determine best practices for cognitive screening after stroke, including the development and use of screening instruments that consider demographic, cultural, and linguistic factors in determining “normal” function.
“Perhaps the most pressing need, however, is the development of effective and culturally relevant treatments for poststroke cognitive impairment,” Dr. El Husseini said in a news release.
“We hope to see big enough clinical trials that assess various techniques, medications, and lifestyle changes in diverse groups of patients that may help improve cognitive function,” she added.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular Radiology and Intervention, the Council on Hypertension, and the Council on Lifestyle and Cardiometabolic Health.
Screening for cognitive impairment should be part of multidisciplinary care for stroke survivors, the American Heart Association says in a new scientific statement.
“Cognitive impairment after stroke is very common, is associated with other post-stroke outcomes, and often has significant impact on the quality of life,” Nada El Husseini, MD, MHSc, chair of the scientific statement writing group, told this news organization.
“It is important to screen stroke survivors for cognitive impairment as well as for associated comorbidities such as mood and sleep disorders,” said Dr. El Husseini, associate professor of neurology at Duke University Medical Center in Durham, N.C.
The scientific statement was published online in Stroke. It’s the first to specifically focus on the cognitive impairment resulting from an overt stroke (ischemic or hemorrhagic).
‘Actionable’ considerations for care
The writing group performed a “scoping” review of the literature on the prevalence, diagnosis, and management of poststroke cognitive impairment (PSCI) to provide a framework for “actionable considerations” for clinical practice as well as to highlight gaps needing additional studies, Dr. El Husseini explained.
PSCI, ranging from mild to severe, occurs in up to 60% of stroke survivors in the first year after stroke; yet, it is often underreported and underdiagnosed, the writing group notes.
Up to 20% of stroke survivors who experience mild cognitive impairment fully recover cognitive function, and cognitive recovery is most likely within the first 6 months after a stroke.
However, improvement in cognitive impairment without return to prestroke levels is more frequent than is complete recovery. As many as one in three stroke survivors may develop dementia within 5 years of stroke.
The writing group also notes that PSCI is often associated with other conditions, including physical disability, sleep disorders, behavioral and personality changes, depression, and other neuropsychological changes – each of which may contribute to lower quality of life.
Currently, there is no “gold standard” for cognitive screening following stroke, but several brief cognitive screening tests, including the Mini–Mental State Examination and the Montreal Cognitive Assessment, are widely used to identify cognitive impairment after stroke.
The statement also highlights the importance of assessing cognitive changes over time after stroke. Stroke survivors who experience unexplained difficulties with cognitive-related activities of daily living, following care instructions, or providing a reliable health history may be candidates for additional cognitive screening.
Manage risk factors to prevent repeat stroke
“Anticipatory guidance regarding home and driving safety and, return to work (if applicable) along with interdisciplinary collaboration among different medical and ancillary specialists in the diagnosis and management of cognitive impairment is key for the holistic care of stroke survivors,” Dr. El Husseini told this news organization.
The multidisciplinary poststroke health care team could include neurologists, occupational therapists, speech therapists, nurses, neuropsychologists, gerontologists, and primary care providers.
“Because recurrent stroke is strongly associated with the development of cognitive impairment and dementia, prevention of recurrent strokes should be sought to decrease that risk,” Dr. El Husseini said. This includes addressing stroke risk factors, including high blood pressure, high cholesterol, type 2 diabetes, and atrial fibrillation.
The writing group says research is needed in the future to determine how cognitive impairment develops after stroke and the impact of nonbrain factors, including infection, frailty, and social factors.
Further research is also needed to determine best practices for cognitive screening after stroke, including the development and use of screening instruments that consider demographic, cultural, and linguistic factors in determining “normal” function.
“Perhaps the most pressing need, however, is the development of effective and culturally relevant treatments for poststroke cognitive impairment,” Dr. El Husseini said in a news release.
“We hope to see big enough clinical trials that assess various techniques, medications, and lifestyle changes in diverse groups of patients that may help improve cognitive function,” she added.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular Radiology and Intervention, the Council on Hypertension, and the Council on Lifestyle and Cardiometabolic Health.
U.S. incidence, prevalence of myasthenia gravis is rising
, an analysis of new claims data shows. Investigators speculate the rise of this rare disorder may be due to “increased diagnosis and more awareness of the disease over time, which has been shown in several studies,” study investigator Ema Rodrigues, DSc, MPH, with Alexion Pharmaceuticals, Boston.
Dr. Rodrigues presented her research at the 2023 annual meeting of the American Academy of Neurology.
Myasthenia gravis is a rare neuromuscular disease characterized by muscle weakness and fatigue caused by the binding of autoantibodies at the neuromuscular junction. It affects the voluntary muscles of the body, especially those that control the eyes, mouth, throat, and limbs.
In Europe, the incidence and prevalence of myasthenia gravis has increased for the past several decades. In the United States, increasing prevalence has also been observed, but recent estimates are lacking, making it tough to gauge the true burden of disease, Dr. Rodrigues explained.
Claims-based analysis
To investigate, Dr. Rodrigues and colleagues analyzed claims data (commercial, Medicare, and Medicaid) and electronic health records representing over 300 million patients in the United States from 2011 to present.
They calculated sex- and age-specific incidence and prevalence of myasthenia gravis for the year 2021 using U.S. Census data.
Prevalent patients were identified as having one or more myasthenia gravis records in 2021 and two or more myasthenia gravis records, at least 30 days apart, from 2016 to 2021. This cohort had 78,225 patients.
Incident patients were identified as those with a myasthenia gravis record in 2021 and no previous myasthenia gravis record from 2019 to 2020. This cohort had 4,214 patients.
For both the prevalent and incident cohort, the distribution of male and female patients was roughly 50/50, with a slightly higher proportion of females in the incident cohort, Dr. Rodrigues reported.
When looking at age groups, there were “very few pediatric patients,” she noted, with less than 1% of the patients under the age of 12. The highest proportion of patients were 65 years or older. The mean age was 67 in the prevalent cohort and 68 in the incident cohort.
In 2021, the overall incidence of myasthenia gravis was 3.2 per 100,000 with similar estimates for males and females (3.2 vs. 3.1 per 100,000, respectively).
Total prevalence was estimated to be 37.0 per 100,000 with sex-specific estimates being comparable at 37.3 and 36.7 per 100,000 for males and females, respectively.
The incidence and prevalence of myasthenia gravis increased with age, ranging from 0.3 and 0.4 per 100,000, respectively, in children younger than age 2 years, to 10.2 and 116.8 per 100,000, respectively, in people 65 and older.
These estimates are “significantly higher” than those from a prior U.S. analysis from 2003, Dr. Rodrigues told attendees, but they are quite similar to the estimates that were reported in Sweden in 2020.
A limitation of the analysis is that patients who do not seek care regularly may have not been identified due to inclusion criteria, potentially leading to underestimates. Also, no information was available on the myasthenia gravis subtype (ocular vs. generalized).
Underestimated burden
Reached for comment, Richard J. Nowak, MD, MS, director of the Yale Myasthenia Gravis Clinic, Yale School of Medicine, New Haven, Conn., noted that the new report, “albeit limited as a claims-based analysis, presents modern data on incidence and prevalence of myasthenia gravis in the United States.”
“It suggests that the current estimates of myasthenia gravis in the United States are too low and that the true impact/burden of myasthenia gravis is greater. While we are unable to verify the accuracy of the diagnosis, the total myasthenia gravis population is likely to be about 100,000, which is higher than prior estimates.”
“This, in fact, might be driven by greater disease awareness and increased diagnosis along with decreased mortality and longer life expectancy,” Dr. Nowak said.
“Anecdotally, we are most certainly seeing patients with new-onset myasthenia gravis in their 70s, 80s, and even 90s in recent years. The EXPLORE-MG registry published data from a tertiary center on age of onset breakdown showing myasthenia gravis can present at any age,” Dr. Nowak added.
Funding for the study was provided by Alexion, AstraZeneca Rare Disease. Dr. Rodrigues receives compensation and owns stock as an employee of Alexion, AstraZeneca Rare Diseases. Dr. Nowak has no relevant disclosures.
A version of this article originally appeared on Medscape.com.
, an analysis of new claims data shows. Investigators speculate the rise of this rare disorder may be due to “increased diagnosis and more awareness of the disease over time, which has been shown in several studies,” study investigator Ema Rodrigues, DSc, MPH, with Alexion Pharmaceuticals, Boston.
Dr. Rodrigues presented her research at the 2023 annual meeting of the American Academy of Neurology.
Myasthenia gravis is a rare neuromuscular disease characterized by muscle weakness and fatigue caused by the binding of autoantibodies at the neuromuscular junction. It affects the voluntary muscles of the body, especially those that control the eyes, mouth, throat, and limbs.
In Europe, the incidence and prevalence of myasthenia gravis has increased for the past several decades. In the United States, increasing prevalence has also been observed, but recent estimates are lacking, making it tough to gauge the true burden of disease, Dr. Rodrigues explained.
Claims-based analysis
To investigate, Dr. Rodrigues and colleagues analyzed claims data (commercial, Medicare, and Medicaid) and electronic health records representing over 300 million patients in the United States from 2011 to present.
They calculated sex- and age-specific incidence and prevalence of myasthenia gravis for the year 2021 using U.S. Census data.
Prevalent patients were identified as having one or more myasthenia gravis records in 2021 and two or more myasthenia gravis records, at least 30 days apart, from 2016 to 2021. This cohort had 78,225 patients.
Incident patients were identified as those with a myasthenia gravis record in 2021 and no previous myasthenia gravis record from 2019 to 2020. This cohort had 4,214 patients.
For both the prevalent and incident cohort, the distribution of male and female patients was roughly 50/50, with a slightly higher proportion of females in the incident cohort, Dr. Rodrigues reported.
When looking at age groups, there were “very few pediatric patients,” she noted, with less than 1% of the patients under the age of 12. The highest proportion of patients were 65 years or older. The mean age was 67 in the prevalent cohort and 68 in the incident cohort.
In 2021, the overall incidence of myasthenia gravis was 3.2 per 100,000 with similar estimates for males and females (3.2 vs. 3.1 per 100,000, respectively).
Total prevalence was estimated to be 37.0 per 100,000 with sex-specific estimates being comparable at 37.3 and 36.7 per 100,000 for males and females, respectively.
The incidence and prevalence of myasthenia gravis increased with age, ranging from 0.3 and 0.4 per 100,000, respectively, in children younger than age 2 years, to 10.2 and 116.8 per 100,000, respectively, in people 65 and older.
These estimates are “significantly higher” than those from a prior U.S. analysis from 2003, Dr. Rodrigues told attendees, but they are quite similar to the estimates that were reported in Sweden in 2020.
A limitation of the analysis is that patients who do not seek care regularly may have not been identified due to inclusion criteria, potentially leading to underestimates. Also, no information was available on the myasthenia gravis subtype (ocular vs. generalized).
Underestimated burden
Reached for comment, Richard J. Nowak, MD, MS, director of the Yale Myasthenia Gravis Clinic, Yale School of Medicine, New Haven, Conn., noted that the new report, “albeit limited as a claims-based analysis, presents modern data on incidence and prevalence of myasthenia gravis in the United States.”
“It suggests that the current estimates of myasthenia gravis in the United States are too low and that the true impact/burden of myasthenia gravis is greater. While we are unable to verify the accuracy of the diagnosis, the total myasthenia gravis population is likely to be about 100,000, which is higher than prior estimates.”
“This, in fact, might be driven by greater disease awareness and increased diagnosis along with decreased mortality and longer life expectancy,” Dr. Nowak said.
“Anecdotally, we are most certainly seeing patients with new-onset myasthenia gravis in their 70s, 80s, and even 90s in recent years. The EXPLORE-MG registry published data from a tertiary center on age of onset breakdown showing myasthenia gravis can present at any age,” Dr. Nowak added.
Funding for the study was provided by Alexion, AstraZeneca Rare Disease. Dr. Rodrigues receives compensation and owns stock as an employee of Alexion, AstraZeneca Rare Diseases. Dr. Nowak has no relevant disclosures.
A version of this article originally appeared on Medscape.com.
, an analysis of new claims data shows. Investigators speculate the rise of this rare disorder may be due to “increased diagnosis and more awareness of the disease over time, which has been shown in several studies,” study investigator Ema Rodrigues, DSc, MPH, with Alexion Pharmaceuticals, Boston.
Dr. Rodrigues presented her research at the 2023 annual meeting of the American Academy of Neurology.
Myasthenia gravis is a rare neuromuscular disease characterized by muscle weakness and fatigue caused by the binding of autoantibodies at the neuromuscular junction. It affects the voluntary muscles of the body, especially those that control the eyes, mouth, throat, and limbs.
In Europe, the incidence and prevalence of myasthenia gravis has increased for the past several decades. In the United States, increasing prevalence has also been observed, but recent estimates are lacking, making it tough to gauge the true burden of disease, Dr. Rodrigues explained.
Claims-based analysis
To investigate, Dr. Rodrigues and colleagues analyzed claims data (commercial, Medicare, and Medicaid) and electronic health records representing over 300 million patients in the United States from 2011 to present.
They calculated sex- and age-specific incidence and prevalence of myasthenia gravis for the year 2021 using U.S. Census data.
Prevalent patients were identified as having one or more myasthenia gravis records in 2021 and two or more myasthenia gravis records, at least 30 days apart, from 2016 to 2021. This cohort had 78,225 patients.
Incident patients were identified as those with a myasthenia gravis record in 2021 and no previous myasthenia gravis record from 2019 to 2020. This cohort had 4,214 patients.
For both the prevalent and incident cohort, the distribution of male and female patients was roughly 50/50, with a slightly higher proportion of females in the incident cohort, Dr. Rodrigues reported.
When looking at age groups, there were “very few pediatric patients,” she noted, with less than 1% of the patients under the age of 12. The highest proportion of patients were 65 years or older. The mean age was 67 in the prevalent cohort and 68 in the incident cohort.
In 2021, the overall incidence of myasthenia gravis was 3.2 per 100,000 with similar estimates for males and females (3.2 vs. 3.1 per 100,000, respectively).
Total prevalence was estimated to be 37.0 per 100,000 with sex-specific estimates being comparable at 37.3 and 36.7 per 100,000 for males and females, respectively.
The incidence and prevalence of myasthenia gravis increased with age, ranging from 0.3 and 0.4 per 100,000, respectively, in children younger than age 2 years, to 10.2 and 116.8 per 100,000, respectively, in people 65 and older.
These estimates are “significantly higher” than those from a prior U.S. analysis from 2003, Dr. Rodrigues told attendees, but they are quite similar to the estimates that were reported in Sweden in 2020.
A limitation of the analysis is that patients who do not seek care regularly may have not been identified due to inclusion criteria, potentially leading to underestimates. Also, no information was available on the myasthenia gravis subtype (ocular vs. generalized).
Underestimated burden
Reached for comment, Richard J. Nowak, MD, MS, director of the Yale Myasthenia Gravis Clinic, Yale School of Medicine, New Haven, Conn., noted that the new report, “albeit limited as a claims-based analysis, presents modern data on incidence and prevalence of myasthenia gravis in the United States.”
“It suggests that the current estimates of myasthenia gravis in the United States are too low and that the true impact/burden of myasthenia gravis is greater. While we are unable to verify the accuracy of the diagnosis, the total myasthenia gravis population is likely to be about 100,000, which is higher than prior estimates.”
“This, in fact, might be driven by greater disease awareness and increased diagnosis along with decreased mortality and longer life expectancy,” Dr. Nowak said.
“Anecdotally, we are most certainly seeing patients with new-onset myasthenia gravis in their 70s, 80s, and even 90s in recent years. The EXPLORE-MG registry published data from a tertiary center on age of onset breakdown showing myasthenia gravis can present at any age,” Dr. Nowak added.
Funding for the study was provided by Alexion, AstraZeneca Rare Disease. Dr. Rodrigues receives compensation and owns stock as an employee of Alexion, AstraZeneca Rare Diseases. Dr. Nowak has no relevant disclosures.
A version of this article originally appeared on Medscape.com.
From AAN 2023