Cardiology News

While the increased risk of cancer in patients with metabolic syndrome is well established by research, the authors of a new study delve deeper by examining metabolic syndrome trajectories.

The new research finds that adults with persistent metabolic syndrome that worsens over time are at increased risk for any type of cancer.

The conditions that make up metabolic syndrome (high blood pressure, high blood sugar, increased abdominal adiposity, and high cholesterol and triglycerides) have been associated with an increased risk of diseases, including heart disease, stroke, and type 2 diabetes, wrote Li Deng, PhD, of Capital Medical University, Beijing, and colleagues.

However, a single assessment of metabolic syndrome at one point in time is inadequate to show an association with cancer risk over time, they said. In the current study, the researchers used models to examine the association between trajectory patterns of metabolic syndrome over time and the risk of overall and specific cancer types. They also examined the impact of chronic inflammation concurrent with metabolic syndrome.
 

What We Know About Metabolic Syndrome and Cancer Risk

A systematic review and meta-analysis published in Diabetes Care in 2012 showed an association between the presence of metabolic syndrome and an increased risk of various cancers including liver, bladder, pancreatic, breast, and colorectal.

More recently, a 2020 study published in Diabetes showed evidence of increased risk for certain cancers (pancreatic, kidney, uterine, cervical) but no increased risk for cancer overall.

In addition, a 2022 study by some of the current study researchers of the same Chinese cohort focused on the role of inflammation in combination with metabolic syndrome on colorectal cancer specifically, and found an increased risk for cancer when both metabolic syndrome and inflammation were present.

However, the reasons for this association between metabolic syndrome and cancer remain unclear, and the effect of the fluctuating nature of metabolic syndrome over time on long-term cancer risk has not been explored, the researchers wrote.

“There is emerging evidence that even normal weight individuals who are metabolically unhealthy may be at an elevated cancer risk, and we need better metrics to define the underlying metabolic dysfunction in obesity,” Sheetal Hardikar, MBBS, PhD, MPH, an investigator at the Huntsman Cancer Institute, University of Utah, said in an interview.

Dr. Hardikar, who serves as assistant professor in the department of population health sciences at the University of Utah, was not involved in the current study. She and her colleagues published a research paper on data from the National Health and Nutrition Examination Survey in 2023 that showed an increased risk of obesity-related cancer.
 

What New Study Adds to Related Research

Previous studies have consistently reported an approximately 30% increased risk of cancer with metabolic syndrome, Dr. Hardikar said. “What is unique about this study is the examination of metabolic syndrome trajectories over four years, and not just the presence of metabolic syndrome at one point in time,” she said.

In the new study, published in Cancer on March 11 (doi: 10.1002/cncr.35235), 44,115 adults in China were separated into four trajectories based on metabolic syndrome scores for the period from 2006 to 2010. The scores were based on clinical evidence of metabolic syndrome, defined using the International Diabetes Federation criteria of central obesity and the presence of at least two other factors including increased triglycerides, decreased HDL cholesterol, high blood pressure (or treatment for previously diagnosed hypertension), and increased fasting plasma glucose (or previous diagnosis of type 2 diabetes).

The average age of the participants was 49 years; the mean body mass index ranged from approximately 22 kg/m² in the low-stable group to approximately 28 kg/m² in the elevated-increasing group.

The four trajectories of metabolic syndrome were low-stable (10.56% of participants), moderate-low (40.84%), moderate-high (41.46%), and elevated-increasing (7.14%), based on trends from the individuals’ initial physical exams on entering the study.

Over a median follow-up period of 9.4 years (from 2010 to 2021), 2,271 cancer diagnoses were reported in the study population. Those with an elevated-increasing metabolic syndrome trajectory had 1.3 times the risk of any cancer compared with those in the low-stable group. Risk for breast cancer, endometrial cancer, kidney cancer, colorectal cancer, and liver cancer in the highest trajectory group were 2.1, 3.3, 4.5, 2.5, and 1.6 times higher, respectively, compared to the lowest group. The increased risk in the elevated-trajectory group for all cancer types persisted when the low-stable, moderate-low, and moderate-high trajectory pattern groups were combined.

The researchers also examined the impact of chronic inflammation and found that individuals with persistently high metabolic syndrome scores and concurrent chronic inflammation had the highest risks of breast, endometrial, colon, and liver cancer. However, individuals with persistently high metabolic syndrome scores and no concurrent chronic inflammation had the highest risk of kidney cancer.
 

What Are the Limitations of This Research?

The researchers of the current study acknowledged the lack of information on other causes of cancer, including dietary habits, hepatitis C infection, and Helicobacter pylori infection. Other limitations include the focus only on individuals from a single community of mainly middle-aged men in China that may not generalize to other populations.

Also, the metabolic syndrome trajectories did not change much over time, which may be related to the short 4-year study period.

Using the International Diabetes Federation criteria was another limitation, because it prevented the assessment of cancer risk in normal weight individuals with metabolic dysfunction, Dr. Hardikar noted.
 

Does Metabolic Syndrome Cause Cancer?

“This research suggests that proactive and continuous management of metabolic syndrome may serve as an essential strategy in preventing cancer,” senior author Han-Ping Shi, MD, PhD, of Capital Medical University in Beijing, noted in a statement on the study.

More research is needed to assess the impact of these interventions on cancer risk. However, the data from the current study can guide future research that may lead to more targeted treatments and more effective preventive strategies, he continued.

“Current evidence based on this study and many other reports strongly suggests an increased risk for cancer associated with metabolic syndrome,” Dr. Hardikar said in an interview. The data serve as a reminder to clinicians to look beyond BMI as the only measure of obesity, and to consider metabolic factors together to identify individuals at increased risk for cancer, she said.

“We must continue to educate patients about obesity and all the chronic conditions it may lead to, but we cannot ignore this emerging phenotype of being of normal weight but metabolically unhealthy,” Dr. Hardikar emphasized.
 

What Additional Research is Needed?

Looking ahead, “we need well-designed interventions to test causality for metabolic syndrome and cancer risk, though the evidence from the observational studies is very strong,” Dr. Hardikar said.

In addition, a consensus is needed to better define metabolic dysfunction,and to explore cancer risk in normal weight but metabolically unhealthy individuals, she said.

The study was supported by the National Key Research and Development Program of China. The researchers and Dr. Hardikar had no financial conflicts to disclose.

While the increased risk of cancer in patients with metabolic syndrome is well established by research, the authors of a new study delve deeper by examining metabolic syndrome trajectories.

The new research finds that adults with persistent metabolic syndrome that worsens over time are at increased risk for any type of cancer.

The conditions that make up metabolic syndrome (high blood pressure, high blood sugar, increased abdominal adiposity, and high cholesterol and triglycerides) have been associated with an increased risk of diseases, including heart disease, stroke, and type 2 diabetes, wrote Li Deng, PhD, of Capital Medical University, Beijing, and colleagues.

However, a single assessment of metabolic syndrome at one point in time is inadequate to show an association with cancer risk over time, they said. In the current study, the researchers used models to examine the association between trajectory patterns of metabolic syndrome over time and the risk of overall and specific cancer types. They also examined the impact of chronic inflammation concurrent with metabolic syndrome.
 

What We Know About Metabolic Syndrome and Cancer Risk

A systematic review and meta-analysis published in Diabetes Care in 2012 showed an association between the presence of metabolic syndrome and an increased risk of various cancers including liver, bladder, pancreatic, breast, and colorectal.

More recently, a 2020 study published in Diabetes showed evidence of increased risk for certain cancers (pancreatic, kidney, uterine, cervical) but no increased risk for cancer overall.

In addition, a 2022 study by some of the current study researchers of the same Chinese cohort focused on the role of inflammation in combination with metabolic syndrome on colorectal cancer specifically, and found an increased risk for cancer when both metabolic syndrome and inflammation were present.

However, the reasons for this association between metabolic syndrome and cancer remain unclear, and the effect of the fluctuating nature of metabolic syndrome over time on long-term cancer risk has not been explored, the researchers wrote.

“There is emerging evidence that even normal weight individuals who are metabolically unhealthy may be at an elevated cancer risk, and we need better metrics to define the underlying metabolic dysfunction in obesity,” Sheetal Hardikar, MBBS, PhD, MPH, an investigator at the Huntsman Cancer Institute, University of Utah, said in an interview.

Dr. Hardikar, who serves as assistant professor in the department of population health sciences at the University of Utah, was not involved in the current study. She and her colleagues published a research paper on data from the National Health and Nutrition Examination Survey in 2023 that showed an increased risk of obesity-related cancer.
 

What New Study Adds to Related Research

Previous studies have consistently reported an approximately 30% increased risk of cancer with metabolic syndrome, Dr. Hardikar said. “What is unique about this study is the examination of metabolic syndrome trajectories over four years, and not just the presence of metabolic syndrome at one point in time,” she said.

In the new study, published in Cancer on March 11 (doi: 10.1002/cncr.35235), 44,115 adults in China were separated into four trajectories based on metabolic syndrome scores for the period from 2006 to 2010. The scores were based on clinical evidence of metabolic syndrome, defined using the International Diabetes Federation criteria of central obesity and the presence of at least two other factors including increased triglycerides, decreased HDL cholesterol, high blood pressure (or treatment for previously diagnosed hypertension), and increased fasting plasma glucose (or previous diagnosis of type 2 diabetes).

The average age of the participants was 49 years; the mean body mass index ranged from approximately 22 kg/m² in the low-stable group to approximately 28 kg/m² in the elevated-increasing group.

The four trajectories of metabolic syndrome were low-stable (10.56% of participants), moderate-low (40.84%), moderate-high (41.46%), and elevated-increasing (7.14%), based on trends from the individuals’ initial physical exams on entering the study.

Over a median follow-up period of 9.4 years (from 2010 to 2021), 2,271 cancer diagnoses were reported in the study population. Those with an elevated-increasing metabolic syndrome trajectory had 1.3 times the risk of any cancer compared with those in the low-stable group. Risk for breast cancer, endometrial cancer, kidney cancer, colorectal cancer, and liver cancer in the highest trajectory group were 2.1, 3.3, 4.5, 2.5, and 1.6 times higher, respectively, compared to the lowest group. The increased risk in the elevated-trajectory group for all cancer types persisted when the low-stable, moderate-low, and moderate-high trajectory pattern groups were combined.

The researchers also examined the impact of chronic inflammation and found that individuals with persistently high metabolic syndrome scores and concurrent chronic inflammation had the highest risks of breast, endometrial, colon, and liver cancer. However, individuals with persistently high metabolic syndrome scores and no concurrent chronic inflammation had the highest risk of kidney cancer.
 

What Are the Limitations of This Research?

The researchers of the current study acknowledged the lack of information on other causes of cancer, including dietary habits, hepatitis C infection, and Helicobacter pylori infection. Other limitations include the focus only on individuals from a single community of mainly middle-aged men in China that may not generalize to other populations.

Also, the metabolic syndrome trajectories did not change much over time, which may be related to the short 4-year study period.

Using the International Diabetes Federation criteria was another limitation, because it prevented the assessment of cancer risk in normal weight individuals with metabolic dysfunction, Dr. Hardikar noted.
 

Does Metabolic Syndrome Cause Cancer?

“This research suggests that proactive and continuous management of metabolic syndrome may serve as an essential strategy in preventing cancer,” senior author Han-Ping Shi, MD, PhD, of Capital Medical University in Beijing, noted in a statement on the study.

More research is needed to assess the impact of these interventions on cancer risk. However, the data from the current study can guide future research that may lead to more targeted treatments and more effective preventive strategies, he continued.

“Current evidence based on this study and many other reports strongly suggests an increased risk for cancer associated with metabolic syndrome,” Dr. Hardikar said in an interview. The data serve as a reminder to clinicians to look beyond BMI as the only measure of obesity, and to consider metabolic factors together to identify individuals at increased risk for cancer, she said.

“We must continue to educate patients about obesity and all the chronic conditions it may lead to, but we cannot ignore this emerging phenotype of being of normal weight but metabolically unhealthy,” Dr. Hardikar emphasized.
 

What Additional Research is Needed?

Looking ahead, “we need well-designed interventions to test causality for metabolic syndrome and cancer risk, though the evidence from the observational studies is very strong,” Dr. Hardikar said.

In addition, a consensus is needed to better define metabolic dysfunction,and to explore cancer risk in normal weight but metabolically unhealthy individuals, she said.

The study was supported by the National Key Research and Development Program of China. The researchers and Dr. Hardikar had no financial conflicts to disclose.

While the increased risk of cancer in patients with metabolic syndrome is well established by research, the authors of a new study delve deeper by examining metabolic syndrome trajectories.

The new research finds that adults with persistent metabolic syndrome that worsens over time are at increased risk for any type of cancer.

The conditions that make up metabolic syndrome (high blood pressure, high blood sugar, increased abdominal adiposity, and high cholesterol and triglycerides) have been associated with an increased risk of diseases, including heart disease, stroke, and type 2 diabetes, wrote Li Deng, PhD, of Capital Medical University, Beijing, and colleagues.

However, a single assessment of metabolic syndrome at one point in time is inadequate to show an association with cancer risk over time, they said. In the current study, the researchers used models to examine the association between trajectory patterns of metabolic syndrome over time and the risk of overall and specific cancer types. They also examined the impact of chronic inflammation concurrent with metabolic syndrome.
 

What We Know About Metabolic Syndrome and Cancer Risk

A systematic review and meta-analysis published in Diabetes Care in 2012 showed an association between the presence of metabolic syndrome and an increased risk of various cancers including liver, bladder, pancreatic, breast, and colorectal.

More recently, a 2020 study published in Diabetes showed evidence of increased risk for certain cancers (pancreatic, kidney, uterine, cervical) but no increased risk for cancer overall.

In addition, a 2022 study by some of the current study researchers of the same Chinese cohort focused on the role of inflammation in combination with metabolic syndrome on colorectal cancer specifically, and found an increased risk for cancer when both metabolic syndrome and inflammation were present.

However, the reasons for this association between metabolic syndrome and cancer remain unclear, and the effect of the fluctuating nature of metabolic syndrome over time on long-term cancer risk has not been explored, the researchers wrote.

“There is emerging evidence that even normal weight individuals who are metabolically unhealthy may be at an elevated cancer risk, and we need better metrics to define the underlying metabolic dysfunction in obesity,” Sheetal Hardikar, MBBS, PhD, MPH, an investigator at the Huntsman Cancer Institute, University of Utah, said in an interview.

Dr. Hardikar, who serves as assistant professor in the department of population health sciences at the University of Utah, was not involved in the current study. She and her colleagues published a research paper on data from the National Health and Nutrition Examination Survey in 2023 that showed an increased risk of obesity-related cancer.
 

What New Study Adds to Related Research

Previous studies have consistently reported an approximately 30% increased risk of cancer with metabolic syndrome, Dr. Hardikar said. “What is unique about this study is the examination of metabolic syndrome trajectories over four years, and not just the presence of metabolic syndrome at one point in time,” she said.

In the new study, published in Cancer on March 11 (doi: 10.1002/cncr.35235), 44,115 adults in China were separated into four trajectories based on metabolic syndrome scores for the period from 2006 to 2010. The scores were based on clinical evidence of metabolic syndrome, defined using the International Diabetes Federation criteria of central obesity and the presence of at least two other factors including increased triglycerides, decreased HDL cholesterol, high blood pressure (or treatment for previously diagnosed hypertension), and increased fasting plasma glucose (or previous diagnosis of type 2 diabetes).

The average age of the participants was 49 years; the mean body mass index ranged from approximately 22 kg/m² in the low-stable group to approximately 28 kg/m² in the elevated-increasing group.

The four trajectories of metabolic syndrome were low-stable (10.56% of participants), moderate-low (40.84%), moderate-high (41.46%), and elevated-increasing (7.14%), based on trends from the individuals’ initial physical exams on entering the study.

Over a median follow-up period of 9.4 years (from 2010 to 2021), 2,271 cancer diagnoses were reported in the study population. Those with an elevated-increasing metabolic syndrome trajectory had 1.3 times the risk of any cancer compared with those in the low-stable group. Risk for breast cancer, endometrial cancer, kidney cancer, colorectal cancer, and liver cancer in the highest trajectory group were 2.1, 3.3, 4.5, 2.5, and 1.6 times higher, respectively, compared to the lowest group. The increased risk in the elevated-trajectory group for all cancer types persisted when the low-stable, moderate-low, and moderate-high trajectory pattern groups were combined.

The researchers also examined the impact of chronic inflammation and found that individuals with persistently high metabolic syndrome scores and concurrent chronic inflammation had the highest risks of breast, endometrial, colon, and liver cancer. However, individuals with persistently high metabolic syndrome scores and no concurrent chronic inflammation had the highest risk of kidney cancer.
 

What Are the Limitations of This Research?

The researchers of the current study acknowledged the lack of information on other causes of cancer, including dietary habits, hepatitis C infection, and Helicobacter pylori infection. Other limitations include the focus only on individuals from a single community of mainly middle-aged men in China that may not generalize to other populations.

Also, the metabolic syndrome trajectories did not change much over time, which may be related to the short 4-year study period.

Using the International Diabetes Federation criteria was another limitation, because it prevented the assessment of cancer risk in normal weight individuals with metabolic dysfunction, Dr. Hardikar noted.
 

Does Metabolic Syndrome Cause Cancer?

“This research suggests that proactive and continuous management of metabolic syndrome may serve as an essential strategy in preventing cancer,” senior author Han-Ping Shi, MD, PhD, of Capital Medical University in Beijing, noted in a statement on the study.

More research is needed to assess the impact of these interventions on cancer risk. However, the data from the current study can guide future research that may lead to more targeted treatments and more effective preventive strategies, he continued.

“Current evidence based on this study and many other reports strongly suggests an increased risk for cancer associated with metabolic syndrome,” Dr. Hardikar said in an interview. The data serve as a reminder to clinicians to look beyond BMI as the only measure of obesity, and to consider metabolic factors together to identify individuals at increased risk for cancer, she said.

“We must continue to educate patients about obesity and all the chronic conditions it may lead to, but we cannot ignore this emerging phenotype of being of normal weight but metabolically unhealthy,” Dr. Hardikar emphasized.
 

What Additional Research is Needed?

Looking ahead, “we need well-designed interventions to test causality for metabolic syndrome and cancer risk, though the evidence from the observational studies is very strong,” Dr. Hardikar said.

In addition, a consensus is needed to better define metabolic dysfunction,and to explore cancer risk in normal weight but metabolically unhealthy individuals, she said.

The study was supported by the National Key Research and Development Program of China. The researchers and Dr. Hardikar had no financial conflicts to disclose.

TOPLINE:

A multicomponent strategy of nurse-led communication, home blood pressure monitoring, evidence-based treatment algorithms, and electronic health record tools improved systolic blood pressure (SBP) and non–high-density lipoprotein (non-HDL) cholesterol levels in people living with HIV.

METHODOLOGY:

• Investigators assessed if EXTRA-CVD, a nurse-led multicomponent intervention for preventing cardiovascular diseases (CVD), could effectively improve SBP and non-HDL cholesterol levels in people living with HIV whose viral replication has been controlled effectively using antiretroviral therapy.
• They recruited 297 individuals (median age, 59 years; 20.9% women) from three academic HIV clinics in the United States with an HIV-1 viral load < 200 copies/mL who were diagnosed with both hypertension and hypercholesterolemia.
• Participants were randomly assigned to either the EXTRA-CVD intervention group or a control group comprising individuals who received general prevention education.
• SBP (the primary outcome) was calculated as the mean of two SBP measurements obtained 1 minute apart, and non-HDL cholesterol (the secondary outcome) was calculated as total cholesterol minus HDL cholesterol.

TAKEAWAY:

• Participants in the intervention vs control group reported having significantly lower SBP as early as 4 months after the nurse-led strategy (mean difference, −6.4 mm Hg; P = .002), with the improvements sustaining until 12 months (mean difference, −4.2 mm Hg; P = .04).
• At 12 months, participants in the intervention group showed a 16.9-mg/dL (P < .001) reduction in non-HDL cholesterol levels compared with those in the control group.
• The nurse-led strategy led to a greater reduction in SBP in women with HIV vs men living with HIV (5.9 mm Hg greater SBP difference at 12 months), with the difference being clinically meaningful but not statistically significant.
• This nurse-led strategy did not increase the risk for adverse events in people living with HIV.

IN PRACTICE:

“Although the EXTRA-CVD intervention was limited to BP and cholesterol, nurse-led case management might be beneficial for a range of other primary care conditions in HIV clinics. If HIV clinics choose to implement EXTRA-CVD, they might consider adding staff trained in other chronic comorbidities and/or health promotion activities,” the authors noted.

SOURCE:

This study was led by Christopher T. Longenecker, MD, University of Washington School of Medicine, Seattle, and published online on March 5, 2024, in JAMA Network Open.

LIMITATIONS:

Because this trial was conducted at well-resourced, major academic HIV clinics, the results may not be applicable to other populations, such as smaller community-based clinics or HIV care outside the United States. The sensitivity analyses performed in this study may not have fully accounted for the bias introduced by the differential attrition in the intervention group.

DISCLOSURES:

This study was supported by grants from the National Institutes of Health (NIH). The authors declared receiving grants and personal fees from or having other ties with the NIH and other sources.

A version of this article appeared on Medscape.com.

TOPLINE:

A multicomponent strategy of nurse-led communication, home blood pressure monitoring, evidence-based treatment algorithms, and electronic health record tools improved systolic blood pressure (SBP) and non–high-density lipoprotein (non-HDL) cholesterol levels in people living with HIV.

METHODOLOGY:

• Investigators assessed if EXTRA-CVD, a nurse-led multicomponent intervention for preventing cardiovascular diseases (CVD), could effectively improve SBP and non-HDL cholesterol levels in people living with HIV whose viral replication has been controlled effectively using antiretroviral therapy.
• They recruited 297 individuals (median age, 59 years; 20.9% women) from three academic HIV clinics in the United States with an HIV-1 viral load < 200 copies/mL who were diagnosed with both hypertension and hypercholesterolemia.
• Participants were randomly assigned to either the EXTRA-CVD intervention group or a control group comprising individuals who received general prevention education.
• SBP (the primary outcome) was calculated as the mean of two SBP measurements obtained 1 minute apart, and non-HDL cholesterol (the secondary outcome) was calculated as total cholesterol minus HDL cholesterol.

TAKEAWAY:

• Participants in the intervention vs control group reported having significantly lower SBP as early as 4 months after the nurse-led strategy (mean difference, −6.4 mm Hg; P = .002), with the improvements sustaining until 12 months (mean difference, −4.2 mm Hg; P = .04).
• At 12 months, participants in the intervention group showed a 16.9-mg/dL (P < .001) reduction in non-HDL cholesterol levels compared with those in the control group.
• The nurse-led strategy led to a greater reduction in SBP in women with HIV vs men living with HIV (5.9 mm Hg greater SBP difference at 12 months), with the difference being clinically meaningful but not statistically significant.
• This nurse-led strategy did not increase the risk for adverse events in people living with HIV.

IN PRACTICE:

“Although the EXTRA-CVD intervention was limited to BP and cholesterol, nurse-led case management might be beneficial for a range of other primary care conditions in HIV clinics. If HIV clinics choose to implement EXTRA-CVD, they might consider adding staff trained in other chronic comorbidities and/or health promotion activities,” the authors noted.

SOURCE:

This study was led by Christopher T. Longenecker, MD, University of Washington School of Medicine, Seattle, and published online on March 5, 2024, in JAMA Network Open.

LIMITATIONS:

Because this trial was conducted at well-resourced, major academic HIV clinics, the results may not be applicable to other populations, such as smaller community-based clinics or HIV care outside the United States. The sensitivity analyses performed in this study may not have fully accounted for the bias introduced by the differential attrition in the intervention group.

DISCLOSURES:

This study was supported by grants from the National Institutes of Health (NIH). The authors declared receiving grants and personal fees from or having other ties with the NIH and other sources.

A version of this article appeared on Medscape.com.

TOPLINE:

A multicomponent strategy of nurse-led communication, home blood pressure monitoring, evidence-based treatment algorithms, and electronic health record tools improved systolic blood pressure (SBP) and non–high-density lipoprotein (non-HDL) cholesterol levels in people living with HIV.

METHODOLOGY:

• Investigators assessed if EXTRA-CVD, a nurse-led multicomponent intervention for preventing cardiovascular diseases (CVD), could effectively improve SBP and non-HDL cholesterol levels in people living with HIV whose viral replication has been controlled effectively using antiretroviral therapy.
• They recruited 297 individuals (median age, 59 years; 20.9% women) from three academic HIV clinics in the United States with an HIV-1 viral load < 200 copies/mL who were diagnosed with both hypertension and hypercholesterolemia.
• Participants were randomly assigned to either the EXTRA-CVD intervention group or a control group comprising individuals who received general prevention education.
• SBP (the primary outcome) was calculated as the mean of two SBP measurements obtained 1 minute apart, and non-HDL cholesterol (the secondary outcome) was calculated as total cholesterol minus HDL cholesterol.

TAKEAWAY:

• Participants in the intervention vs control group reported having significantly lower SBP as early as 4 months after the nurse-led strategy (mean difference, −6.4 mm Hg; P = .002), with the improvements sustaining until 12 months (mean difference, −4.2 mm Hg; P = .04).
• At 12 months, participants in the intervention group showed a 16.9-mg/dL (P < .001) reduction in non-HDL cholesterol levels compared with those in the control group.
• The nurse-led strategy led to a greater reduction in SBP in women with HIV vs men living with HIV (5.9 mm Hg greater SBP difference at 12 months), with the difference being clinically meaningful but not statistically significant.
• This nurse-led strategy did not increase the risk for adverse events in people living with HIV.

IN PRACTICE:

“Although the EXTRA-CVD intervention was limited to BP and cholesterol, nurse-led case management might be beneficial for a range of other primary care conditions in HIV clinics. If HIV clinics choose to implement EXTRA-CVD, they might consider adding staff trained in other chronic comorbidities and/or health promotion activities,” the authors noted.

SOURCE:

This study was led by Christopher T. Longenecker, MD, University of Washington School of Medicine, Seattle, and published online on March 5, 2024, in JAMA Network Open.

LIMITATIONS:

Because this trial was conducted at well-resourced, major academic HIV clinics, the results may not be applicable to other populations, such as smaller community-based clinics or HIV care outside the United States. The sensitivity analyses performed in this study may not have fully accounted for the bias introduced by the differential attrition in the intervention group.

DISCLOSURES:

This study was supported by grants from the National Institutes of Health (NIH). The authors declared receiving grants and personal fees from or having other ties with the NIH and other sources.

A version of this article appeared on Medscape.com.

TOPLINE:

Higher dietary niacin intake is associated with a lower risk for all-cause mortality among people with metabolic dysfunction-associated steatotic liver disease (MASLD), but there is no connection between niacin consumption and cardiovascular disease (CVD) mortality, a recent study suggested.

METHODOLOGY:

• Researchers analyzed data from the National Health and Nutrition Examination Survey (2003-2018) for 4315 adults with MASLD (mean age, 52.5 years; 55%, men; 67%, non-Hispanic White).
• Dietary niacin intake levels were based on two 24-hour dietary recall interviews to report the types and quantities of foods that participants consumed in the 24 hours prior to the interviews.
• Participants were categorized by tertile of dietary niacin intake: Tertile 1 (n = 1440), < 18.4 mg; tertile 2 (n = 1441), 18.5-26.6 mg; and tertile 3 (n = 1434), > 26.7 mg.

TAKEAWAY:

• During a median follow-up of 8.8 years, 566 deaths occurred, of which 197 were attributed to CVD.
• Compared with participants with a niacin intake of 18.4 mg or lower (the lowest tertile), the multivariable-adjusted hazard ratios (HRs) for participants with a niacin intake of 26.7 mg or higher (the highest tertile) were 0.70 for all-cause mortality and 0.65 for CVD mortality.
• For the subgroup with diabetes compared with the reference group (the first tertile), the HR of all-cause mortality in the third tertile was 0.82.
• When the subgroup without diabetes was compared with the reference group, the HR of all-cause mortality in the third tertile was 0.58, suggesting a significant interaction between niacin and diabetes with the risk of all-cause mortality.
• An inverse association between dietary niacin intake and all-cause mortality was seen in sensitivity analyses, when excluding a participant who died within 2 years of follow-up.

IN PRACTICE:

“Higher dietary niacin intake was associated with a lower risk of all-cause mortality,” but not CVD, among individuals with MASLD, and “the dose-response association…needs to be further investigated to determine optimal intake level,” the authors wrote.

SOURCE:

The study, led by Jie Pan, MD, Sun Yat-sen University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Physical activity data were missing and could not be adjusted for. The National Death Index used by the researchers has only “modest” ability to accurately classify CVD mortality, and the dietary data were subject to recall bias.

DISCLOSURES:

One author was supported by a grant from the National Nature Science Foundation of China. No other conflicts of interest were reported.

A version of this article appeared on Medscape.com.

TOPLINE:

Higher dietary niacin intake is associated with a lower risk for all-cause mortality among people with metabolic dysfunction-associated steatotic liver disease (MASLD), but there is no connection between niacin consumption and cardiovascular disease (CVD) mortality, a recent study suggested.

METHODOLOGY:

• Researchers analyzed data from the National Health and Nutrition Examination Survey (2003-2018) for 4315 adults with MASLD (mean age, 52.5 years; 55%, men; 67%, non-Hispanic White).
• Dietary niacin intake levels were based on two 24-hour dietary recall interviews to report the types and quantities of foods that participants consumed in the 24 hours prior to the interviews.
• Participants were categorized by tertile of dietary niacin intake: Tertile 1 (n = 1440), < 18.4 mg; tertile 2 (n = 1441), 18.5-26.6 mg; and tertile 3 (n = 1434), > 26.7 mg.

TAKEAWAY:

• During a median follow-up of 8.8 years, 566 deaths occurred, of which 197 were attributed to CVD.
• Compared with participants with a niacin intake of 18.4 mg or lower (the lowest tertile), the multivariable-adjusted hazard ratios (HRs) for participants with a niacin intake of 26.7 mg or higher (the highest tertile) were 0.70 for all-cause mortality and 0.65 for CVD mortality.
• For the subgroup with diabetes compared with the reference group (the first tertile), the HR of all-cause mortality in the third tertile was 0.82.
• When the subgroup without diabetes was compared with the reference group, the HR of all-cause mortality in the third tertile was 0.58, suggesting a significant interaction between niacin and diabetes with the risk of all-cause mortality.
• An inverse association between dietary niacin intake and all-cause mortality was seen in sensitivity analyses, when excluding a participant who died within 2 years of follow-up.

IN PRACTICE:

“Higher dietary niacin intake was associated with a lower risk of all-cause mortality,” but not CVD, among individuals with MASLD, and “the dose-response association…needs to be further investigated to determine optimal intake level,” the authors wrote.

SOURCE:

The study, led by Jie Pan, MD, Sun Yat-sen University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Physical activity data were missing and could not be adjusted for. The National Death Index used by the researchers has only “modest” ability to accurately classify CVD mortality, and the dietary data were subject to recall bias.

DISCLOSURES:

One author was supported by a grant from the National Nature Science Foundation of China. No other conflicts of interest were reported.

A version of this article appeared on Medscape.com.

TOPLINE:

Higher dietary niacin intake is associated with a lower risk for all-cause mortality among people with metabolic dysfunction-associated steatotic liver disease (MASLD), but there is no connection between niacin consumption and cardiovascular disease (CVD) mortality, a recent study suggested.

METHODOLOGY:

• Researchers analyzed data from the National Health and Nutrition Examination Survey (2003-2018) for 4315 adults with MASLD (mean age, 52.5 years; 55%, men; 67%, non-Hispanic White).
• Dietary niacin intake levels were based on two 24-hour dietary recall interviews to report the types and quantities of foods that participants consumed in the 24 hours prior to the interviews.
• Participants were categorized by tertile of dietary niacin intake: Tertile 1 (n = 1440), < 18.4 mg; tertile 2 (n = 1441), 18.5-26.6 mg; and tertile 3 (n = 1434), > 26.7 mg.

TAKEAWAY:

• During a median follow-up of 8.8 years, 566 deaths occurred, of which 197 were attributed to CVD.
• Compared with participants with a niacin intake of 18.4 mg or lower (the lowest tertile), the multivariable-adjusted hazard ratios (HRs) for participants with a niacin intake of 26.7 mg or higher (the highest tertile) were 0.70 for all-cause mortality and 0.65 for CVD mortality.
• For the subgroup with diabetes compared with the reference group (the first tertile), the HR of all-cause mortality in the third tertile was 0.82.
• When the subgroup without diabetes was compared with the reference group, the HR of all-cause mortality in the third tertile was 0.58, suggesting a significant interaction between niacin and diabetes with the risk of all-cause mortality.
• An inverse association between dietary niacin intake and all-cause mortality was seen in sensitivity analyses, when excluding a participant who died within 2 years of follow-up.

IN PRACTICE:

“Higher dietary niacin intake was associated with a lower risk of all-cause mortality,” but not CVD, among individuals with MASLD, and “the dose-response association…needs to be further investigated to determine optimal intake level,” the authors wrote.

SOURCE:

The study, led by Jie Pan, MD, Sun Yat-sen University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Physical activity data were missing and could not be adjusted for. The National Death Index used by the researchers has only “modest” ability to accurately classify CVD mortality, and the dietary data were subject to recall bias.

DISCLOSURES:

One author was supported by a grant from the National Nature Science Foundation of China. No other conflicts of interest were reported.

A version of this article appeared on Medscape.com.

TOPLINE:

Hypertension prevalence remained stable in the United States at 30% after guidelines updated in 2017 lowered the threshold for the condition, while antihypertensive medication use rose about 3%, new research from the Centers for Disease Control and Prevention (CDC) shows.

METHODOLOGY:

• Researchers analyzed data from the Behavioral Risk Factor Surveillance System, a telephone survey of US adults aged 18 years and older.
• Self-reported diagnosed hypertension was defined as an affirmative response to the question, “Have you ever been told by a doctor, nurse, or other health professional that you have high blood pressure?”
• To determine treatment, respondents who answered the first question affirmatively were then asked, “Are you currently taking medicine for your high blood pressure?”
• Hypertension and treatment were assessed by age group (18-44, 45-64, and > 65 years), sex, race, ethnicity, level of education, and state of residence.

TAKEAWAY:

• The final analytic samples for 2017, 2019, and 2021 included 425,417, 392,100, and 410,318 participants, respectively.
• From 2017 to 2021, the overall age-standardized prevalence of hypertension did not change, remaining at almost exactly 30%.
• The age-standardized prevalence of antihypertensive medication use among individuals with hypertension increased by 3.1 percentage points, from 59.8% to 62.9%.
• Increases in medication use were seen in most sociodemographic groups; for example, in 2021, the prevalence was higher among women than among men (68.5% vs 59.4%), among adults aged ≥ 65 years than among those aged 18-44 years (92.5% vs 42.5%), and among Black patients than among White patients (71.3% vs 62%).
• Increases in medication use were also seen by state; use increased in 11 states, ranging from 52.2% in Utah to 72.8% in Mississippi in 2021, and did not decrease significantly in any state.

IN PRACTICE:

“These findings can be used to increase awareness of hypertension and promote lifestyle modifications and antihypertensive medication use to optimize blood pressure control and reduce disparities in prevalence and control,” the authors wrote.

SOURCE:

The study was led by Ahlia Sekkarie, PhD, of CDC’s Division for Heart Disease and Stroke Prevention, and published online in Morbidity and Mortality Weekly Report.

LIMITATIONS:

The study had several limitations. The findings were based on self-report. Median response rates of less than 50% could lead to under- or overestimates of prevalence. Parts of the population, such as those in long-term care facilities or without a telephone, were not included in the analysis. Some demographic categories had small sample sizes; therefore, prevalence changes might not be detectable.

DISCLOSURES:

No specific funding was reported. The authors reported no potential conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Hypertension prevalence remained stable in the United States at 30% after guidelines updated in 2017 lowered the threshold for the condition, while antihypertensive medication use rose about 3%, new research from the Centers for Disease Control and Prevention (CDC) shows.

METHODOLOGY:

• Researchers analyzed data from the Behavioral Risk Factor Surveillance System, a telephone survey of US adults aged 18 years and older.
• Self-reported diagnosed hypertension was defined as an affirmative response to the question, “Have you ever been told by a doctor, nurse, or other health professional that you have high blood pressure?”
• To determine treatment, respondents who answered the first question affirmatively were then asked, “Are you currently taking medicine for your high blood pressure?”
• Hypertension and treatment were assessed by age group (18-44, 45-64, and > 65 years), sex, race, ethnicity, level of education, and state of residence.

TAKEAWAY:

• The final analytic samples for 2017, 2019, and 2021 included 425,417, 392,100, and 410,318 participants, respectively.
• From 2017 to 2021, the overall age-standardized prevalence of hypertension did not change, remaining at almost exactly 30%.
• The age-standardized prevalence of antihypertensive medication use among individuals with hypertension increased by 3.1 percentage points, from 59.8% to 62.9%.
• Increases in medication use were seen in most sociodemographic groups; for example, in 2021, the prevalence was higher among women than among men (68.5% vs 59.4%), among adults aged ≥ 65 years than among those aged 18-44 years (92.5% vs 42.5%), and among Black patients than among White patients (71.3% vs 62%).
• Increases in medication use were also seen by state; use increased in 11 states, ranging from 52.2% in Utah to 72.8% in Mississippi in 2021, and did not decrease significantly in any state.

IN PRACTICE:

“These findings can be used to increase awareness of hypertension and promote lifestyle modifications and antihypertensive medication use to optimize blood pressure control and reduce disparities in prevalence and control,” the authors wrote.

SOURCE:

The study was led by Ahlia Sekkarie, PhD, of CDC’s Division for Heart Disease and Stroke Prevention, and published online in Morbidity and Mortality Weekly Report.

LIMITATIONS:

The study had several limitations. The findings were based on self-report. Median response rates of less than 50% could lead to under- or overestimates of prevalence. Parts of the population, such as those in long-term care facilities or without a telephone, were not included in the analysis. Some demographic categories had small sample sizes; therefore, prevalence changes might not be detectable.

DISCLOSURES:

No specific funding was reported. The authors reported no potential conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Hypertension prevalence remained stable in the United States at 30% after guidelines updated in 2017 lowered the threshold for the condition, while antihypertensive medication use rose about 3%, new research from the Centers for Disease Control and Prevention (CDC) shows.

METHODOLOGY:

• Researchers analyzed data from the Behavioral Risk Factor Surveillance System, a telephone survey of US adults aged 18 years and older.
• Self-reported diagnosed hypertension was defined as an affirmative response to the question, “Have you ever been told by a doctor, nurse, or other health professional that you have high blood pressure?”
• To determine treatment, respondents who answered the first question affirmatively were then asked, “Are you currently taking medicine for your high blood pressure?”
• Hypertension and treatment were assessed by age group (18-44, 45-64, and > 65 years), sex, race, ethnicity, level of education, and state of residence.

TAKEAWAY:

• The final analytic samples for 2017, 2019, and 2021 included 425,417, 392,100, and 410,318 participants, respectively.
• From 2017 to 2021, the overall age-standardized prevalence of hypertension did not change, remaining at almost exactly 30%.
• The age-standardized prevalence of antihypertensive medication use among individuals with hypertension increased by 3.1 percentage points, from 59.8% to 62.9%.
• Increases in medication use were seen in most sociodemographic groups; for example, in 2021, the prevalence was higher among women than among men (68.5% vs 59.4%), among adults aged ≥ 65 years than among those aged 18-44 years (92.5% vs 42.5%), and among Black patients than among White patients (71.3% vs 62%).
• Increases in medication use were also seen by state; use increased in 11 states, ranging from 52.2% in Utah to 72.8% in Mississippi in 2021, and did not decrease significantly in any state.

IN PRACTICE:

“These findings can be used to increase awareness of hypertension and promote lifestyle modifications and antihypertensive medication use to optimize blood pressure control and reduce disparities in prevalence and control,” the authors wrote.

SOURCE:

The study was led by Ahlia Sekkarie, PhD, of CDC’s Division for Heart Disease and Stroke Prevention, and published online in Morbidity and Mortality Weekly Report.

LIMITATIONS:

The study had several limitations. The findings were based on self-report. Median response rates of less than 50% could lead to under- or overestimates of prevalence. Parts of the population, such as those in long-term care facilities or without a telephone, were not included in the analysis. Some demographic categories had small sample sizes; therefore, prevalence changes might not be detectable.

DISCLOSURES:

No specific funding was reported. The authors reported no potential conflicts of interest.

A version of this article appeared on Medscape.com.

Chronic smoking remains a major cause of premature mortality on a global scale. Despite intensified efforts to combat this scourge, a quarter of deaths among middle-aged adults in Europe and North America are attributed to it. However, over the past decades, antismoking campaigns have borne fruit, and many smokers have quit before the age of 40 years, enabling some case-control studies.

Among those abstainers who made the right choice, the excess mortality attributable to smoking over a lifetime would be reduced by 90% compared with controls who continued smoking. The estimated benefit is clear, but the analysis lacks nuance. Is smoking cessation beneficial even at older ages? If so, is the effect measurable in terms of magnitude and speed of the effect? An article published online in The New England Journal of Medicine Evidence provided some answers to these questions.
 

Four-Cohort Meta-Analysis

The study was a meta-analysis of individual data collected within four national cohort studies that were linked to each country’s death registry. Two of these studies were nationally representative. The National Health Interview Survey involved a sample of US citizens living in the community, aged 20-79 years, who were included annually in the cohort between 1997 and 2018. The second, the Canadian Community Health Survey, included subjects in the same age group, with samples analyzed between 2000 and 2014.

In Norway, three cohort studies conducted between 1974 and 2003, in which participants aged 25-79 years were included, were combined to form the Norwegian Health Screening Survey. These were the Counties Study (1974-1988), the 40 Years Study (1985-1999), and the Cohort of Norway (1994-2003), respectively. The fourth cohort was established through recruitment via the UK Biobank, with adults aged 40-73 years invited to participate in the survey. The data analysis ultimately covered a relatively heterogeneous total population of 1.48 million adults, all from high-income countries and followed for 15 years. It relied on the Cox proportional hazards model applied to each study, considering smoker vs nonsmoker status, as well as the time elapsed since smoking cessation (less than 3 years, between 3 and 9 years, or at least 10 years). Statistical adjustments made in the context of multivariate Cox analysis considered age, education, alcohol consumption, and obesity.
 

Excess Mortality Confirmed

At the end of follow-up, 122,697 deaths were recorded. The comparison of smokers and nonsmokers confirmed smoking-related excess mortality, with adjusted hazard ratios (HRs) estimated at 2.80 for women and 2.70 for men. Smoking shortened life expectancy in the 40- to 79-year-age group by 12 years for women and 13 years for men, in terms of overall mortality. In terms of smoking-attributable specific mortality, the corresponding figures reached 24 and 26 years, respectively. Respiratory diseases ranked highest in both sexes (HR, 7.6 for women and 6.3 for men), followed by cardiovascular diseases (HR, 3.1 for women and 2.9 for men) and cancers (HR, 2.8 for women and 3.1 for men).
 

The Earlier, the Better

Smoking cessation halves overall excess mortality. Above all, quitting before age 40 years brings overall mortality back to the level of nonsmokers as early as the third year after quitting. The excess mortality decreases even more as the cessation period is prolonged, even after age 40 years. Thus, cessation ≥ 10 years in smokers aged 40-49 years almost cancels out overall excess mortality (-99% in women, -96% in men). The trend is almost as favorable in the older age group (50-59 years), with corresponding figures of -95% and -92%, respectively.

Long-term survival increases in the early years after cessation, especially if it occurs at a younger age, but the benefit remains tangible even in older smokers. Thus, cessation of less than 3 years, effective in patients aged 50-59 years, reduces overall excess mortality by 63% in women and 54% in men. In patients aged 60-79 years, the figures are -40% and -33%, respectively.

Naturally, the earlier the cessation, the greater the number of years gained. It is 12 years for cessation before age 40 years, reduced to 6 years for cessation between 40 and 49 years, and 2.5 years when it is even later (50-59 years). These quantitative results are approximate, given the methodology (a meta-analysis) and some heterogeneity in the studies, as well as the multitude of potential confounding factors that have not all been considered. Nevertheless, the results probably contain a kernel of truth, and their optimistic implications should be highlighted to encourage smokers to abstain, even older ones. Better late than never, even if the benefit of cessation is maximal when it occurs as early as possible, knowing that a minimum of 3 years of cessation would be sufficient to gain years of life.

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

Chronic smoking remains a major cause of premature mortality on a global scale. Despite intensified efforts to combat this scourge, a quarter of deaths among middle-aged adults in Europe and North America are attributed to it. However, over the past decades, antismoking campaigns have borne fruit, and many smokers have quit before the age of 40 years, enabling some case-control studies.

Among those abstainers who made the right choice, the excess mortality attributable to smoking over a lifetime would be reduced by 90% compared with controls who continued smoking. The estimated benefit is clear, but the analysis lacks nuance. Is smoking cessation beneficial even at older ages? If so, is the effect measurable in terms of magnitude and speed of the effect? An article published online in The New England Journal of Medicine Evidence provided some answers to these questions.
 

Four-Cohort Meta-Analysis

The study was a meta-analysis of individual data collected within four national cohort studies that were linked to each country’s death registry. Two of these studies were nationally representative. The National Health Interview Survey involved a sample of US citizens living in the community, aged 20-79 years, who were included annually in the cohort between 1997 and 2018. The second, the Canadian Community Health Survey, included subjects in the same age group, with samples analyzed between 2000 and 2014.

In Norway, three cohort studies conducted between 1974 and 2003, in which participants aged 25-79 years were included, were combined to form the Norwegian Health Screening Survey. These were the Counties Study (1974-1988), the 40 Years Study (1985-1999), and the Cohort of Norway (1994-2003), respectively. The fourth cohort was established through recruitment via the UK Biobank, with adults aged 40-73 years invited to participate in the survey. The data analysis ultimately covered a relatively heterogeneous total population of 1.48 million adults, all from high-income countries and followed for 15 years. It relied on the Cox proportional hazards model applied to each study, considering smoker vs nonsmoker status, as well as the time elapsed since smoking cessation (less than 3 years, between 3 and 9 years, or at least 10 years). Statistical adjustments made in the context of multivariate Cox analysis considered age, education, alcohol consumption, and obesity.
 

Excess Mortality Confirmed

At the end of follow-up, 122,697 deaths were recorded. The comparison of smokers and nonsmokers confirmed smoking-related excess mortality, with adjusted hazard ratios (HRs) estimated at 2.80 for women and 2.70 for men. Smoking shortened life expectancy in the 40- to 79-year-age group by 12 years for women and 13 years for men, in terms of overall mortality. In terms of smoking-attributable specific mortality, the corresponding figures reached 24 and 26 years, respectively. Respiratory diseases ranked highest in both sexes (HR, 7.6 for women and 6.3 for men), followed by cardiovascular diseases (HR, 3.1 for women and 2.9 for men) and cancers (HR, 2.8 for women and 3.1 for men).
 

The Earlier, the Better

Smoking cessation halves overall excess mortality. Above all, quitting before age 40 years brings overall mortality back to the level of nonsmokers as early as the third year after quitting. The excess mortality decreases even more as the cessation period is prolonged, even after age 40 years. Thus, cessation ≥ 10 years in smokers aged 40-49 years almost cancels out overall excess mortality (-99% in women, -96% in men). The trend is almost as favorable in the older age group (50-59 years), with corresponding figures of -95% and -92%, respectively.

Long-term survival increases in the early years after cessation, especially if it occurs at a younger age, but the benefit remains tangible even in older smokers. Thus, cessation of less than 3 years, effective in patients aged 50-59 years, reduces overall excess mortality by 63% in women and 54% in men. In patients aged 60-79 years, the figures are -40% and -33%, respectively.

Naturally, the earlier the cessation, the greater the number of years gained. It is 12 years for cessation before age 40 years, reduced to 6 years for cessation between 40 and 49 years, and 2.5 years when it is even later (50-59 years). These quantitative results are approximate, given the methodology (a meta-analysis) and some heterogeneity in the studies, as well as the multitude of potential confounding factors that have not all been considered. Nevertheless, the results probably contain a kernel of truth, and their optimistic implications should be highlighted to encourage smokers to abstain, even older ones. Better late than never, even if the benefit of cessation is maximal when it occurs as early as possible, knowing that a minimum of 3 years of cessation would be sufficient to gain years of life.

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

Chronic smoking remains a major cause of premature mortality on a global scale. Despite intensified efforts to combat this scourge, a quarter of deaths among middle-aged adults in Europe and North America are attributed to it. However, over the past decades, antismoking campaigns have borne fruit, and many smokers have quit before the age of 40 years, enabling some case-control studies.

Among those abstainers who made the right choice, the excess mortality attributable to smoking over a lifetime would be reduced by 90% compared with controls who continued smoking. The estimated benefit is clear, but the analysis lacks nuance. Is smoking cessation beneficial even at older ages? If so, is the effect measurable in terms of magnitude and speed of the effect? An article published online in The New England Journal of Medicine Evidence provided some answers to these questions.
 

Four-Cohort Meta-Analysis

The study was a meta-analysis of individual data collected within four national cohort studies that were linked to each country’s death registry. Two of these studies were nationally representative. The National Health Interview Survey involved a sample of US citizens living in the community, aged 20-79 years, who were included annually in the cohort between 1997 and 2018. The second, the Canadian Community Health Survey, included subjects in the same age group, with samples analyzed between 2000 and 2014.

In Norway, three cohort studies conducted between 1974 and 2003, in which participants aged 25-79 years were included, were combined to form the Norwegian Health Screening Survey. These were the Counties Study (1974-1988), the 40 Years Study (1985-1999), and the Cohort of Norway (1994-2003), respectively. The fourth cohort was established through recruitment via the UK Biobank, with adults aged 40-73 years invited to participate in the survey. The data analysis ultimately covered a relatively heterogeneous total population of 1.48 million adults, all from high-income countries and followed for 15 years. It relied on the Cox proportional hazards model applied to each study, considering smoker vs nonsmoker status, as well as the time elapsed since smoking cessation (less than 3 years, between 3 and 9 years, or at least 10 years). Statistical adjustments made in the context of multivariate Cox analysis considered age, education, alcohol consumption, and obesity.
 

Excess Mortality Confirmed

At the end of follow-up, 122,697 deaths were recorded. The comparison of smokers and nonsmokers confirmed smoking-related excess mortality, with adjusted hazard ratios (HRs) estimated at 2.80 for women and 2.70 for men. Smoking shortened life expectancy in the 40- to 79-year-age group by 12 years for women and 13 years for men, in terms of overall mortality. In terms of smoking-attributable specific mortality, the corresponding figures reached 24 and 26 years, respectively. Respiratory diseases ranked highest in both sexes (HR, 7.6 for women and 6.3 for men), followed by cardiovascular diseases (HR, 3.1 for women and 2.9 for men) and cancers (HR, 2.8 for women and 3.1 for men).
 

The Earlier, the Better

Smoking cessation halves overall excess mortality. Above all, quitting before age 40 years brings overall mortality back to the level of nonsmokers as early as the third year after quitting. The excess mortality decreases even more as the cessation period is prolonged, even after age 40 years. Thus, cessation ≥ 10 years in smokers aged 40-49 years almost cancels out overall excess mortality (-99% in women, -96% in men). The trend is almost as favorable in the older age group (50-59 years), with corresponding figures of -95% and -92%, respectively.

Long-term survival increases in the early years after cessation, especially if it occurs at a younger age, but the benefit remains tangible even in older smokers. Thus, cessation of less than 3 years, effective in patients aged 50-59 years, reduces overall excess mortality by 63% in women and 54% in men. In patients aged 60-79 years, the figures are -40% and -33%, respectively.

Naturally, the earlier the cessation, the greater the number of years gained. It is 12 years for cessation before age 40 years, reduced to 6 years for cessation between 40 and 49 years, and 2.5 years when it is even later (50-59 years). These quantitative results are approximate, given the methodology (a meta-analysis) and some heterogeneity in the studies, as well as the multitude of potential confounding factors that have not all been considered. Nevertheless, the results probably contain a kernel of truth, and their optimistic implications should be highlighted to encourage smokers to abstain, even older ones. Better late than never, even if the benefit of cessation is maximal when it occurs as early as possible, knowing that a minimum of 3 years of cessation would be sufficient to gain years of life.

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

Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.

Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.

Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
 

CV Effects

OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.

Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
 

Snoring and Hypertension

A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m²) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:

An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.

The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.

Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.

Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
 

Implications for Practice

This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.

Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.

Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.

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

Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.

Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.

Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
 

CV Effects

OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.

Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
 

Snoring and Hypertension

A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m²) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:

An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.

The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.

Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.

Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
 

Implications for Practice

This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.

Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.

Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.

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

Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.

Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.

Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
 

CV Effects

OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.

Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
 

Snoring and Hypertension

A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m²) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:

An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.

The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.

Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.

Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
 

Implications for Practice

This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.

Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.

Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.

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

Adults with persistent metabolic syndrome that worsens over time are at increased risk for any type of cancer, according to a new study of more than 44,000 individuals.

The conditions that comprise metabolic syndrome (high blood pressure, high blood sugar, increased abdominal adiposity, and high cholesterol and triglycerides) have been associated with an increased risk of diseases, including heart disease, stroke, and type 2 diabetes, wrote Li Deng, PhD, of Capital Medical University, Beijing, China, and colleagues.

A systematic review and meta-analysis published in Diabetes Care in 2012 showed an association between the presence of metabolic syndrome and an increased risk of various cancers including liver, bladder, pancreatic, breast, and colorectal.

More recently, a 2019 study published in Diabetes showed evidence of increased risk for certain cancers (pancreatic, kidney, uterine, cervical) but no increased risk for cancer overall.

However, the reasons for this association between metabolic syndrome and cancer remain unclear, and the effect of the fluctuating nature of metabolic syndrome over time on long-term cancer risk has not been explored, the researchers wrote.
 

What Does New Study Add to Other Research on Metabolic Syndrome and Cancer Risk?

In the new study, published in Cancer on March 11 (doi: 10.1002/cncr.35235), 44,115 adults in China were separated into four trajectories based on metabolic syndrome scores for the period from 2006 to 2010. The scores were based on clinical evidence of metabolic syndrome, defined using the International Diabetes Federation criteria of central obesity and the presence of at least two other factors including increased triglycerides, decreased HDL cholesterol, high blood pressure (or treatment for previously diagnosed hypertension), and increased fasting plasma glucose (or previous diagnosis of type 2 diabetes).

The average age of the participants was 49 years. The four trajectories of metabolic syndrome were low-stable (10.56% of participants), moderate-low (40.84%), moderate-high (41.46%), and elevated-increasing (7.14%), based on trends from the individuals’ initial physical exams on entering the study.

Over a median follow-up period of 9.4 years (from 2010 to 2021), 2,271 cancer diagnoses were reported in the study population. Those with an elevated-increasing metabolic syndrome trajectory had 1.3 times the risk of any cancer compared with those in the low-stable group. Risk for breast cancer, endometrial cancer, kidney cancer, colorectal cancer, and liver cancer in the highest trajectory group were 2.1, 3.3, 4.5, 2.5, and 1.6 times higher, respectively, compared to the lowest group. The increased risk in the elevated-trajectory group for all cancer types persisted when the low-stable, moderate-low, and moderate-high trajectory pattern groups were combined.

The researchers also examined the impact of chronic inflammation and found that individuals with persistently high metabolic syndrome scores and concurrent chronic inflammation had the highest risks of breast, endometrial, colon, and liver cancer. However, individuals with persistently high metabolic syndrome scores and no concurrent chronic inflammation had the highest risk of kidney cancer.
 

 What Are the Limitations of This Research?

The researchers of the current study acknowledged the lack of information on other causes of cancer, including dietary habits, hepatitis C infection, and Helicobacter pylori infection. Other limitations include the focus only on individuals from a single community of mainly middle-aged men in China that may not generalize to other populations.

Also, the metabolic syndrome trajectories did not change much over time, which may be related to the short 4-year study period.
 

What Is the Takeaway Message for Clinical Practice?

The results suggest that monitoring and managing metabolic syndrome could help reduce cancer risk, the researchers concluded. 

“This research suggests that proactive and continuous management of metabolic syndrome may serve as an essential strategy in preventing cancer,” senior author Han-Ping Shi, MD, PhD, of Capital Medical University in Beijing, said in a press release accompanying the study.

More research is needed to assess the impact of these interventions on cancer risk, he noted. However, the data from the current study can guide future research that may lead to more targeted treatments and more effective preventive strategies, he said in a statement.

The study was supported by the National Key Research and Development Program of China. The researchers had no financial conflicts to disclose.

Adults with persistent metabolic syndrome that worsens over time are at increased risk for any type of cancer, according to a new study of more than 44,000 individuals.

The conditions that comprise metabolic syndrome (high blood pressure, high blood sugar, increased abdominal adiposity, and high cholesterol and triglycerides) have been associated with an increased risk of diseases, including heart disease, stroke, and type 2 diabetes, wrote Li Deng, PhD, of Capital Medical University, Beijing, China, and colleagues.

A systematic review and meta-analysis published in Diabetes Care in 2012 showed an association between the presence of metabolic syndrome and an increased risk of various cancers including liver, bladder, pancreatic, breast, and colorectal.

More recently, a 2019 study published in Diabetes showed evidence of increased risk for certain cancers (pancreatic, kidney, uterine, cervical) but no increased risk for cancer overall.

However, the reasons for this association between metabolic syndrome and cancer remain unclear, and the effect of the fluctuating nature of metabolic syndrome over time on long-term cancer risk has not been explored, the researchers wrote.
 

What Does New Study Add to Other Research on Metabolic Syndrome and Cancer Risk?

In the new study, published in Cancer on March 11 (doi: 10.1002/cncr.35235), 44,115 adults in China were separated into four trajectories based on metabolic syndrome scores for the period from 2006 to 2010. The scores were based on clinical evidence of metabolic syndrome, defined using the International Diabetes Federation criteria of central obesity and the presence of at least two other factors including increased triglycerides, decreased HDL cholesterol, high blood pressure (or treatment for previously diagnosed hypertension), and increased fasting plasma glucose (or previous diagnosis of type 2 diabetes).

The average age of the participants was 49 years. The four trajectories of metabolic syndrome were low-stable (10.56% of participants), moderate-low (40.84%), moderate-high (41.46%), and elevated-increasing (7.14%), based on trends from the individuals’ initial physical exams on entering the study.

Over a median follow-up period of 9.4 years (from 2010 to 2021), 2,271 cancer diagnoses were reported in the study population. Those with an elevated-increasing metabolic syndrome trajectory had 1.3 times the risk of any cancer compared with those in the low-stable group. Risk for breast cancer, endometrial cancer, kidney cancer, colorectal cancer, and liver cancer in the highest trajectory group were 2.1, 3.3, 4.5, 2.5, and 1.6 times higher, respectively, compared to the lowest group. The increased risk in the elevated-trajectory group for all cancer types persisted when the low-stable, moderate-low, and moderate-high trajectory pattern groups were combined.

The researchers also examined the impact of chronic inflammation and found that individuals with persistently high metabolic syndrome scores and concurrent chronic inflammation had the highest risks of breast, endometrial, colon, and liver cancer. However, individuals with persistently high metabolic syndrome scores and no concurrent chronic inflammation had the highest risk of kidney cancer.
 

 What Are the Limitations of This Research?

The researchers of the current study acknowledged the lack of information on other causes of cancer, including dietary habits, hepatitis C infection, and Helicobacter pylori infection. Other limitations include the focus only on individuals from a single community of mainly middle-aged men in China that may not generalize to other populations.

Also, the metabolic syndrome trajectories did not change much over time, which may be related to the short 4-year study period.
 

What Is the Takeaway Message for Clinical Practice?

The results suggest that monitoring and managing metabolic syndrome could help reduce cancer risk, the researchers concluded. 

“This research suggests that proactive and continuous management of metabolic syndrome may serve as an essential strategy in preventing cancer,” senior author Han-Ping Shi, MD, PhD, of Capital Medical University in Beijing, said in a press release accompanying the study.

More research is needed to assess the impact of these interventions on cancer risk, he noted. However, the data from the current study can guide future research that may lead to more targeted treatments and more effective preventive strategies, he said in a statement.

The study was supported by the National Key Research and Development Program of China. The researchers had no financial conflicts to disclose.

Adults with persistent metabolic syndrome that worsens over time are at increased risk for any type of cancer, according to a new study of more than 44,000 individuals.

The conditions that comprise metabolic syndrome (high blood pressure, high blood sugar, increased abdominal adiposity, and high cholesterol and triglycerides) have been associated with an increased risk of diseases, including heart disease, stroke, and type 2 diabetes, wrote Li Deng, PhD, of Capital Medical University, Beijing, China, and colleagues.

A systematic review and meta-analysis published in Diabetes Care in 2012 showed an association between the presence of metabolic syndrome and an increased risk of various cancers including liver, bladder, pancreatic, breast, and colorectal.

More recently, a 2019 study published in Diabetes showed evidence of increased risk for certain cancers (pancreatic, kidney, uterine, cervical) but no increased risk for cancer overall.

However, the reasons for this association between metabolic syndrome and cancer remain unclear, and the effect of the fluctuating nature of metabolic syndrome over time on long-term cancer risk has not been explored, the researchers wrote.
 

What Does New Study Add to Other Research on Metabolic Syndrome and Cancer Risk?

In the new study, published in Cancer on March 11 (doi: 10.1002/cncr.35235), 44,115 adults in China were separated into four trajectories based on metabolic syndrome scores for the period from 2006 to 2010. The scores were based on clinical evidence of metabolic syndrome, defined using the International Diabetes Federation criteria of central obesity and the presence of at least two other factors including increased triglycerides, decreased HDL cholesterol, high blood pressure (or treatment for previously diagnosed hypertension), and increased fasting plasma glucose (or previous diagnosis of type 2 diabetes).

The average age of the participants was 49 years. The four trajectories of metabolic syndrome were low-stable (10.56% of participants), moderate-low (40.84%), moderate-high (41.46%), and elevated-increasing (7.14%), based on trends from the individuals’ initial physical exams on entering the study.

Over a median follow-up period of 9.4 years (from 2010 to 2021), 2,271 cancer diagnoses were reported in the study population. Those with an elevated-increasing metabolic syndrome trajectory had 1.3 times the risk of any cancer compared with those in the low-stable group. Risk for breast cancer, endometrial cancer, kidney cancer, colorectal cancer, and liver cancer in the highest trajectory group were 2.1, 3.3, 4.5, 2.5, and 1.6 times higher, respectively, compared to the lowest group. The increased risk in the elevated-trajectory group for all cancer types persisted when the low-stable, moderate-low, and moderate-high trajectory pattern groups were combined.

The researchers also examined the impact of chronic inflammation and found that individuals with persistently high metabolic syndrome scores and concurrent chronic inflammation had the highest risks of breast, endometrial, colon, and liver cancer. However, individuals with persistently high metabolic syndrome scores and no concurrent chronic inflammation had the highest risk of kidney cancer.
 

 What Are the Limitations of This Research?

The researchers of the current study acknowledged the lack of information on other causes of cancer, including dietary habits, hepatitis C infection, and Helicobacter pylori infection. Other limitations include the focus only on individuals from a single community of mainly middle-aged men in China that may not generalize to other populations.

Also, the metabolic syndrome trajectories did not change much over time, which may be related to the short 4-year study period.
 

What Is the Takeaway Message for Clinical Practice?

The results suggest that monitoring and managing metabolic syndrome could help reduce cancer risk, the researchers concluded. 

“This research suggests that proactive and continuous management of metabolic syndrome may serve as an essential strategy in preventing cancer,” senior author Han-Ping Shi, MD, PhD, of Capital Medical University in Beijing, said in a press release accompanying the study.

More research is needed to assess the impact of these interventions on cancer risk, he noted. However, the data from the current study can guide future research that may lead to more targeted treatments and more effective preventive strategies, he said in a statement.

The study was supported by the National Key Research and Development Program of China. The researchers had no financial conflicts to disclose.

According to a new study, patients found to have microplastics and nanoplastics in their carotid artery plaque had a higher risk for death or major cardiovascular events compared with patients who had plaques where particles were not found.

This is the first study to show plastic particles are present in atheroma plaques, but the most important finding is that this was related to a four times higher risk for cardiovascular events, study coauthor Antonio Ceriello, MD, IRCCS MultiMedica, Milan, told this news organization. 

“I believe we have demonstrated that plastics are a new risk factor for cardiovascular disease,” he added. And while plastics may have made our lives easier in many respects, it appears that the price we are paying for that is a shortening of our lives. That is not a good balance.”

The trial involved 304 patients undergoing carotid endarterectomy for asymptomatic carotid artery disease, whose excised plaque specimens were analyzed for the presence of microplastics and nanoplastics, ultimately found in almost 60% of patients. 

After a mean follow-up of 34 months, patients in whom microplastics and nanoplastics were detected within the atheroma had a 4.5 times higher risk for the composite endpoint of all cause death, myocardial infarction, or stroke than those in whom these substances were not detected (hazard ratio, 4.53; 95% CI, 2.00-10.27; P < .001).

The study, led by Raffaele Marfella, MD, University of Campania Luigi Vanvitelli, Naples, Italy, was published in The New England Journal of Medicine on March 7, 2024.

The researchers say the study does not prove causality, and many other unmeasured confounding factors could have contributed to the findings. 

However, Dr. Ceriello noted that many important risk factors such as diabetes, hypertension, and dyslipidemia, were controlled for. 

“In this study, all the patients involved were at high risk of cardiovascular events and they were well treated with statins and antithrombotics, so the relationship between the presence of plastic particles in plaque and cardiovascular events is seen on top of good preventive therapy,” he said. 

“While we cannot say for sure that we have shown a causal relationship, we found a large effect and there is a great deal of literature than supports this. We know that plastic particles can penetrate cells and act at the mitochondrial level to increase free radical production and produce chronic inflammation which is the basis for atherosclerosis,” Dr. Ceriello added. 

He believes there is only one approach to addressing this issue, and that is to reduce the amount of plastic in the environment. 

“Plastic is everywhere — in water pipes, in the ocean. We are hoping that this study will increase the push for government to act on this. This is even more important for the long-term health of our children, who will be exposed to high levels of plastics for the whole of their lives,” he said. 
 

‘Strongly Suggestive of a Causal Relationship’

Commenting for this news organization, Philip J. Landrigan, MD, author of an editorial accompanying publication of the study in the NEJM, described the link as “strongly suggestive.”

“Because this was just a single observational study, it doesn’t prove cause and effect, but I think this is strongly suggestive of a causal relationship,” he said. “While there may be some other confounding factors at play, it is hard for me to imagine that these could account for a hazard ratio of 4.5 — that is a large and alarming increase in just 3 years.”

Dr. Landrigan, who is director of the Program for Global Public Health and the Common Good, Boston College, points out that although it is not known what other exposures may have contributed to the adverse outcomes in patients in this study, the finding of microplastics and nanoplastics in plaque tissue is itself a breakthrough discovery that raises a series of urgent questions. These include: “Should exposure to microplastics and nanoplastics be considered a cardiovascular risk factor? What organs in addition to the heart may be at risk? How can we reduce exposure?”

Dr. Landrigan said he was not surprised that plastic particles had been found in carotid plaques. “Previous studies have found microplastics in other tissues including the lungs, colon and placenta. Now they have turned up in the vessel wall,” he said. “But what is really striking about this study is that it suggests the presence of these plastic particles is causing serious harm.”

He says this should be a wake-up call. “It is telling us that we need to worry about the amount of plastic in our environment. And it is not something that’s going to be a problem down the line — it is affecting us now.” 

Dr. Landrigan explained that plastic particles are taken into the body predominantly by ingestion, which could include drinking from plastic bottles or eating food wrapped in plastic. He said it is particularly damaging to use plastic containers to heat food in the microwave, as heating plastic up drives particles into the food. “That will really increase exposure.” 

He noted that plastics are often already in the food itself, especially seafood. 

“Plastics are dumped in the ocean, they break down and get picked up by the fish. Especially if you eat fish at the top of the food chain like tuna, or if you eat oysters or mussels that are filter feeders, you are more likely to ingest microplastics.” 

Dr. Landrigan said he would not advise against eating fish in general, however. “Maybe tuna or other predatory fish may be an issue, but fish in general are good for us, and fish like salmon which have a mainly vegetarian diet are probably safer in this regard.”

The other route is inhalation, with these small plastic particles being widely present in the air, from sources such as vehicle tires becoming abraded from running along the highway.

While it is impossible to avoid taking in plastic completely, Dr. Landrigan says individuals can make efforts to reduce their exposure. 

“People can make intelligent choices in their homes about what they purchase for themselves and their families, and they can act in their local environments and workplace to try and reduce plastics.”

He noted that 40% of all plastic currently being made is single use plastic, and that percentage is growing, with global production of plastic on track to double by 2040 and triple by 2060, and most of this rapid growth being single use plastic. 

“We are all members of the broader society, and we need to become educated about the plastic situation and lobby our elected officials to come up with a good strong legally binding treaty that will place a cap on plastic production,” Dr. Landrigan said. 
 

A version of this article appeared on Medscape.com.

According to a new study, patients found to have microplastics and nanoplastics in their carotid artery plaque had a higher risk for death or major cardiovascular events compared with patients who had plaques where particles were not found.

This is the first study to show plastic particles are present in atheroma plaques, but the most important finding is that this was related to a four times higher risk for cardiovascular events, study coauthor Antonio Ceriello, MD, IRCCS MultiMedica, Milan, told this news organization. 

“I believe we have demonstrated that plastics are a new risk factor for cardiovascular disease,” he added. And while plastics may have made our lives easier in many respects, it appears that the price we are paying for that is a shortening of our lives. That is not a good balance.”

The trial involved 304 patients undergoing carotid endarterectomy for asymptomatic carotid artery disease, whose excised plaque specimens were analyzed for the presence of microplastics and nanoplastics, ultimately found in almost 60% of patients. 

After a mean follow-up of 34 months, patients in whom microplastics and nanoplastics were detected within the atheroma had a 4.5 times higher risk for the composite endpoint of all cause death, myocardial infarction, or stroke than those in whom these substances were not detected (hazard ratio, 4.53; 95% CI, 2.00-10.27; P < .001).

The study, led by Raffaele Marfella, MD, University of Campania Luigi Vanvitelli, Naples, Italy, was published in The New England Journal of Medicine on March 7, 2024.

The researchers say the study does not prove causality, and many other unmeasured confounding factors could have contributed to the findings. 

However, Dr. Ceriello noted that many important risk factors such as diabetes, hypertension, and dyslipidemia, were controlled for. 

“In this study, all the patients involved were at high risk of cardiovascular events and they were well treated with statins and antithrombotics, so the relationship between the presence of plastic particles in plaque and cardiovascular events is seen on top of good preventive therapy,” he said. 

“While we cannot say for sure that we have shown a causal relationship, we found a large effect and there is a great deal of literature than supports this. We know that plastic particles can penetrate cells and act at the mitochondrial level to increase free radical production and produce chronic inflammation which is the basis for atherosclerosis,” Dr. Ceriello added. 

He believes there is only one approach to addressing this issue, and that is to reduce the amount of plastic in the environment. 

“Plastic is everywhere — in water pipes, in the ocean. We are hoping that this study will increase the push for government to act on this. This is even more important for the long-term health of our children, who will be exposed to high levels of plastics for the whole of their lives,” he said. 
 

‘Strongly Suggestive of a Causal Relationship’

Commenting for this news organization, Philip J. Landrigan, MD, author of an editorial accompanying publication of the study in the NEJM, described the link as “strongly suggestive.”

“Because this was just a single observational study, it doesn’t prove cause and effect, but I think this is strongly suggestive of a causal relationship,” he said. “While there may be some other confounding factors at play, it is hard for me to imagine that these could account for a hazard ratio of 4.5 — that is a large and alarming increase in just 3 years.”

Dr. Landrigan, who is director of the Program for Global Public Health and the Common Good, Boston College, points out that although it is not known what other exposures may have contributed to the adverse outcomes in patients in this study, the finding of microplastics and nanoplastics in plaque tissue is itself a breakthrough discovery that raises a series of urgent questions. These include: “Should exposure to microplastics and nanoplastics be considered a cardiovascular risk factor? What organs in addition to the heart may be at risk? How can we reduce exposure?”

Dr. Landrigan said he was not surprised that plastic particles had been found in carotid plaques. “Previous studies have found microplastics in other tissues including the lungs, colon and placenta. Now they have turned up in the vessel wall,” he said. “But what is really striking about this study is that it suggests the presence of these plastic particles is causing serious harm.”

He says this should be a wake-up call. “It is telling us that we need to worry about the amount of plastic in our environment. And it is not something that’s going to be a problem down the line — it is affecting us now.” 

Dr. Landrigan explained that plastic particles are taken into the body predominantly by ingestion, which could include drinking from plastic bottles or eating food wrapped in plastic. He said it is particularly damaging to use plastic containers to heat food in the microwave, as heating plastic up drives particles into the food. “That will really increase exposure.” 

He noted that plastics are often already in the food itself, especially seafood. 

“Plastics are dumped in the ocean, they break down and get picked up by the fish. Especially if you eat fish at the top of the food chain like tuna, or if you eat oysters or mussels that are filter feeders, you are more likely to ingest microplastics.” 

Dr. Landrigan said he would not advise against eating fish in general, however. “Maybe tuna or other predatory fish may be an issue, but fish in general are good for us, and fish like salmon which have a mainly vegetarian diet are probably safer in this regard.”

The other route is inhalation, with these small plastic particles being widely present in the air, from sources such as vehicle tires becoming abraded from running along the highway.

While it is impossible to avoid taking in plastic completely, Dr. Landrigan says individuals can make efforts to reduce their exposure. 

“People can make intelligent choices in their homes about what they purchase for themselves and their families, and they can act in their local environments and workplace to try and reduce plastics.”

He noted that 40% of all plastic currently being made is single use plastic, and that percentage is growing, with global production of plastic on track to double by 2040 and triple by 2060, and most of this rapid growth being single use plastic. 

“We are all members of the broader society, and we need to become educated about the plastic situation and lobby our elected officials to come up with a good strong legally binding treaty that will place a cap on plastic production,” Dr. Landrigan said. 
 

A version of this article appeared on Medscape.com.

According to a new study, patients found to have microplastics and nanoplastics in their carotid artery plaque had a higher risk for death or major cardiovascular events compared with patients who had plaques where particles were not found.

This is the first study to show plastic particles are present in atheroma plaques, but the most important finding is that this was related to a four times higher risk for cardiovascular events, study coauthor Antonio Ceriello, MD, IRCCS MultiMedica, Milan, told this news organization. 

“I believe we have demonstrated that plastics are a new risk factor for cardiovascular disease,” he added. And while plastics may have made our lives easier in many respects, it appears that the price we are paying for that is a shortening of our lives. That is not a good balance.”

The trial involved 304 patients undergoing carotid endarterectomy for asymptomatic carotid artery disease, whose excised plaque specimens were analyzed for the presence of microplastics and nanoplastics, ultimately found in almost 60% of patients. 

After a mean follow-up of 34 months, patients in whom microplastics and nanoplastics were detected within the atheroma had a 4.5 times higher risk for the composite endpoint of all cause death, myocardial infarction, or stroke than those in whom these substances were not detected (hazard ratio, 4.53; 95% CI, 2.00-10.27; P < .001).

The study, led by Raffaele Marfella, MD, University of Campania Luigi Vanvitelli, Naples, Italy, was published in The New England Journal of Medicine on March 7, 2024.

The researchers say the study does not prove causality, and many other unmeasured confounding factors could have contributed to the findings. 

However, Dr. Ceriello noted that many important risk factors such as diabetes, hypertension, and dyslipidemia, were controlled for. 

“In this study, all the patients involved were at high risk of cardiovascular events and they were well treated with statins and antithrombotics, so the relationship between the presence of plastic particles in plaque and cardiovascular events is seen on top of good preventive therapy,” he said. 

“While we cannot say for sure that we have shown a causal relationship, we found a large effect and there is a great deal of literature than supports this. We know that plastic particles can penetrate cells and act at the mitochondrial level to increase free radical production and produce chronic inflammation which is the basis for atherosclerosis,” Dr. Ceriello added. 

He believes there is only one approach to addressing this issue, and that is to reduce the amount of plastic in the environment. 

“Plastic is everywhere — in water pipes, in the ocean. We are hoping that this study will increase the push for government to act on this. This is even more important for the long-term health of our children, who will be exposed to high levels of plastics for the whole of their lives,” he said. 
 

‘Strongly Suggestive of a Causal Relationship’

Commenting for this news organization, Philip J. Landrigan, MD, author of an editorial accompanying publication of the study in the NEJM, described the link as “strongly suggestive.”

“Because this was just a single observational study, it doesn’t prove cause and effect, but I think this is strongly suggestive of a causal relationship,” he said. “While there may be some other confounding factors at play, it is hard for me to imagine that these could account for a hazard ratio of 4.5 — that is a large and alarming increase in just 3 years.”

Dr. Landrigan, who is director of the Program for Global Public Health and the Common Good, Boston College, points out that although it is not known what other exposures may have contributed to the adverse outcomes in patients in this study, the finding of microplastics and nanoplastics in plaque tissue is itself a breakthrough discovery that raises a series of urgent questions. These include: “Should exposure to microplastics and nanoplastics be considered a cardiovascular risk factor? What organs in addition to the heart may be at risk? How can we reduce exposure?”

Dr. Landrigan said he was not surprised that plastic particles had been found in carotid plaques. “Previous studies have found microplastics in other tissues including the lungs, colon and placenta. Now they have turned up in the vessel wall,” he said. “But what is really striking about this study is that it suggests the presence of these plastic particles is causing serious harm.”

He says this should be a wake-up call. “It is telling us that we need to worry about the amount of plastic in our environment. And it is not something that’s going to be a problem down the line — it is affecting us now.” 

Dr. Landrigan explained that plastic particles are taken into the body predominantly by ingestion, which could include drinking from plastic bottles or eating food wrapped in plastic. He said it is particularly damaging to use plastic containers to heat food in the microwave, as heating plastic up drives particles into the food. “That will really increase exposure.” 

He noted that plastics are often already in the food itself, especially seafood. 

“Plastics are dumped in the ocean, they break down and get picked up by the fish. Especially if you eat fish at the top of the food chain like tuna, or if you eat oysters or mussels that are filter feeders, you are more likely to ingest microplastics.” 

Dr. Landrigan said he would not advise against eating fish in general, however. “Maybe tuna or other predatory fish may be an issue, but fish in general are good for us, and fish like salmon which have a mainly vegetarian diet are probably safer in this regard.”

The other route is inhalation, with these small plastic particles being widely present in the air, from sources such as vehicle tires becoming abraded from running along the highway.

While it is impossible to avoid taking in plastic completely, Dr. Landrigan says individuals can make efforts to reduce their exposure. 

“People can make intelligent choices in their homes about what they purchase for themselves and their families, and they can act in their local environments and workplace to try and reduce plastics.”

He noted that 40% of all plastic currently being made is single use plastic, and that percentage is growing, with global production of plastic on track to double by 2040 and triple by 2060, and most of this rapid growth being single use plastic. 

“We are all members of the broader society, and we need to become educated about the plastic situation and lobby our elected officials to come up with a good strong legally binding treaty that will place a cap on plastic production,” Dr. Landrigan said. 
 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Hospital administrators and some department heads have been vocal about the potential for unions to affect both the attending-resident relationship and the ability for residents to directly discuss concerns and educational plans.

Critics feel that having a third party at the table, such as a union representative who isn’t as knowledgeable about the nuances of medical education, could complicate the decision-making process.

Sometimes, there are institution-specific issues as well. One example was at Loma Linda. They argued that unionization would go against their religious principles. They filed a lawsuit. That didn’t go through, and the residents won a few months later.

I know there’s always that one senior, older doctor who says, “Back in our day, we just worked, and we never complained.”

Look at the current situation that residents are facing now, with housing and rent prices and increasing costs of childcare. Sprinkle in some inflation, poor hospital staffing, increasing workload, and add in the fact that the average first-year resident salary in 2023 was around $64,000.

Now, if you look back to 2012, the average salary was around $55,000. If you adjust that for inflation, it would be around $75,000 today, which is more than what the average resident is getting paid.

Then, there are hospital administrators who say that the hospital does not have the money to meet these demands; meanwhile, hospital graduate medical education (GME) offices receive about $150,000 of Medicare funds per resident.

Obviously, there are additional costs when it comes to training and supporting residents. In general, unionizing freaks out the people handling all the cash.

There’s also the threat of a strike, which no hospital wants on their public record. A recent highly publicized event happened at New York’s Elmhurst Hospital, when 160 residents went on strike for 3 days until a deal was made.

Critics of unionizing also cite a particular study in JAMA, which included a survey of 5700 general surgery residents at 285 programs. It found that while unions helped with vacation time and housing stipends, the unions were not associated with improved burnout rates, suicidality, job satisfaction, duty hour violations, mistreatment, educational environment, or salary.

Now, granted, this isn’t the strongest study. It only sampled one group of residents, so I wouldn’t generalize these findings, but it’s still commonly cited by anti-union advocates.

Another potential downside, which is purely anecdotal because I can’t find any data to support this, is potential retaliation against residents or harm to the attending-resident relationship.

I’m an attending. I don’t really understand this one. I don’t exactly own stock in my hospital, nor am I making millions of dollars by siphoning GME money. I’m just trying to focus on educating and supporting my residents the best I can.

Dr. Patel is Clinical Instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons; Pediatric Hospitalist, Morgan Stanley Children’s Hospital of NewYork–Presbyterian, and Benioff Children’s Hospital, University of California San Francisco. He disclosed ties with Medumo Inc.

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

This transcript has been edited for clarity.

Hospital administrators and some department heads have been vocal about the potential for unions to affect both the attending-resident relationship and the ability for residents to directly discuss concerns and educational plans.

Critics feel that having a third party at the table, such as a union representative who isn’t as knowledgeable about the nuances of medical education, could complicate the decision-making process.

Sometimes, there are institution-specific issues as well. One example was at Loma Linda. They argued that unionization would go against their religious principles. They filed a lawsuit. That didn’t go through, and the residents won a few months later.

I know there’s always that one senior, older doctor who says, “Back in our day, we just worked, and we never complained.”

Look at the current situation that residents are facing now, with housing and rent prices and increasing costs of childcare. Sprinkle in some inflation, poor hospital staffing, increasing workload, and add in the fact that the average first-year resident salary in 2023 was around $64,000.

Now, if you look back to 2012, the average salary was around $55,000. If you adjust that for inflation, it would be around $75,000 today, which is more than what the average resident is getting paid.

Then, there are hospital administrators who say that the hospital does not have the money to meet these demands; meanwhile, hospital graduate medical education (GME) offices receive about $150,000 of Medicare funds per resident.

Obviously, there are additional costs when it comes to training and supporting residents. In general, unionizing freaks out the people handling all the cash.

There’s also the threat of a strike, which no hospital wants on their public record. A recent highly publicized event happened at New York’s Elmhurst Hospital, when 160 residents went on strike for 3 days until a deal was made.

Critics of unionizing also cite a particular study in JAMA, which included a survey of 5700 general surgery residents at 285 programs. It found that while unions helped with vacation time and housing stipends, the unions were not associated with improved burnout rates, suicidality, job satisfaction, duty hour violations, mistreatment, educational environment, or salary.

Now, granted, this isn’t the strongest study. It only sampled one group of residents, so I wouldn’t generalize these findings, but it’s still commonly cited by anti-union advocates.

Another potential downside, which is purely anecdotal because I can’t find any data to support this, is potential retaliation against residents or harm to the attending-resident relationship.

I’m an attending. I don’t really understand this one. I don’t exactly own stock in my hospital, nor am I making millions of dollars by siphoning GME money. I’m just trying to focus on educating and supporting my residents the best I can.

Dr. Patel is Clinical Instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons; Pediatric Hospitalist, Morgan Stanley Children’s Hospital of NewYork–Presbyterian, and Benioff Children’s Hospital, University of California San Francisco. He disclosed ties with Medumo Inc.

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

This transcript has been edited for clarity.

Hospital administrators and some department heads have been vocal about the potential for unions to affect both the attending-resident relationship and the ability for residents to directly discuss concerns and educational plans.

Critics feel that having a third party at the table, such as a union representative who isn’t as knowledgeable about the nuances of medical education, could complicate the decision-making process.

Sometimes, there are institution-specific issues as well. One example was at Loma Linda. They argued that unionization would go against their religious principles. They filed a lawsuit. That didn’t go through, and the residents won a few months later.

I know there’s always that one senior, older doctor who says, “Back in our day, we just worked, and we never complained.”

Look at the current situation that residents are facing now, with housing and rent prices and increasing costs of childcare. Sprinkle in some inflation, poor hospital staffing, increasing workload, and add in the fact that the average first-year resident salary in 2023 was around $64,000.

Now, if you look back to 2012, the average salary was around $55,000. If you adjust that for inflation, it would be around $75,000 today, which is more than what the average resident is getting paid.

Then, there are hospital administrators who say that the hospital does not have the money to meet these demands; meanwhile, hospital graduate medical education (GME) offices receive about $150,000 of Medicare funds per resident.

Obviously, there are additional costs when it comes to training and supporting residents. In general, unionizing freaks out the people handling all the cash.

There’s also the threat of a strike, which no hospital wants on their public record. A recent highly publicized event happened at New York’s Elmhurst Hospital, when 160 residents went on strike for 3 days until a deal was made.

Critics of unionizing also cite a particular study in JAMA, which included a survey of 5700 general surgery residents at 285 programs. It found that while unions helped with vacation time and housing stipends, the unions were not associated with improved burnout rates, suicidality, job satisfaction, duty hour violations, mistreatment, educational environment, or salary.

Now, granted, this isn’t the strongest study. It only sampled one group of residents, so I wouldn’t generalize these findings, but it’s still commonly cited by anti-union advocates.

Another potential downside, which is purely anecdotal because I can’t find any data to support this, is potential retaliation against residents or harm to the attending-resident relationship.

I’m an attending. I don’t really understand this one. I don’t exactly own stock in my hospital, nor am I making millions of dollars by siphoning GME money. I’m just trying to focus on educating and supporting my residents the best I can.

Dr. Patel is Clinical Instructor, Department of Pediatrics, Columbia University College of Physicians and Surgeons; Pediatric Hospitalist, Morgan Stanley Children’s Hospital of NewYork–Presbyterian, and Benioff Children’s Hospital, University of California San Francisco. He disclosed ties with Medumo Inc.

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

TOPLINE:

Women with daily exposure to spironolactone for dermatologic conditions showed no higher risk of developing breast or gynecologic cancer than that of unexposed women.

METHODOLOGY:

• Spironolactone, used off-label for several skin conditions in women, carries a warning about an increased tumor risk associated with high doses in rat models, and its antiandrogen properties have prompted hypotheses about a possible increased risk for breast or gynecologic cancers.
• The researchers reviewed data on 420 women with a history of spironolactone use for acne, hair loss, and hirsutism and 3272 women with no spironolactone use at the authors› institution. Their mean age ranged from 42 to 63 years; the majority were White, and 38% were non-White.
• Median spironolactone doses ranged from 25 mg to 225 mg; chart reviews included 5-year follow-up data from the first spironolactone exposure to allow time for tumor development.

TAKEAWAY:

• A total of 37 of the 420 women exposed to spironolactone developed any tumors, as did 546 of the 3272 with no spironolactone exposure.
• After the researchers controlled for age and race, women exposed to spironolactone were no more likely to develop a malignant tumor than a benign tumor, compared with unexposed women (odds ratio [OR], 0.48, P = .2).
• The risk for breast or uterine cancer was not significantly different in the spironolactone and non-spironolactone groups (OR, 0.95, P > .9).

IN PRACTICE:

“Women taking spironolactone for acne, hair loss, and hirsutism and who are at low risk of breast or gynecologic cancers may be counseled to have regular gynecology follow-up, but no more frequently than the general population,” but more studies are needed to evaluate risk over longer periods of time, the researchers wrote.

SOURCE:

The lead author of the study was Rachel C. Hill, BS, a student at Weill Cornell Medical College, New York City, and Shari R. Lipner, MD, PhD, of the department of dermatology at Weill Cornell Medical College, was the corresponding author. The study was published online in The Journal of the American Academy of Dermatology.

LIMITATIONS:

The findings were limited by the retrospective design, as well as the small number of spironolactone patients analyzed, the short follow-up period, the lack of information about spironolactone courses, and the inability to control for family history of malignancy.

DISCLOSURES:

The study was supported by the National Center for Advancing Translational Sciences and a grant from the Clinical and Translational Science Center at Weill Cornell Medical College awarded to Ms. Hill. None of the authors had relevant disclosures; Dr. Lipner disclosed serving as a consultant for Ortho-Dermatologics, Eli Lilly, Moberg Pharmaceuticals, and BelleTorus Corporation.

A version of this article appeared on Medscape.com.

TOPLINE:

Women with daily exposure to spironolactone for dermatologic conditions showed no higher risk of developing breast or gynecologic cancer than that of unexposed women.

METHODOLOGY:

• Spironolactone, used off-label for several skin conditions in women, carries a warning about an increased tumor risk associated with high doses in rat models, and its antiandrogen properties have prompted hypotheses about a possible increased risk for breast or gynecologic cancers.
• The researchers reviewed data on 420 women with a history of spironolactone use for acne, hair loss, and hirsutism and 3272 women with no spironolactone use at the authors› institution. Their mean age ranged from 42 to 63 years; the majority were White, and 38% were non-White.
• Median spironolactone doses ranged from 25 mg to 225 mg; chart reviews included 5-year follow-up data from the first spironolactone exposure to allow time for tumor development.

TAKEAWAY:

• A total of 37 of the 420 women exposed to spironolactone developed any tumors, as did 546 of the 3272 with no spironolactone exposure.
• After the researchers controlled for age and race, women exposed to spironolactone were no more likely to develop a malignant tumor than a benign tumor, compared with unexposed women (odds ratio [OR], 0.48, P = .2).
• The risk for breast or uterine cancer was not significantly different in the spironolactone and non-spironolactone groups (OR, 0.95, P > .9).

IN PRACTICE:

“Women taking spironolactone for acne, hair loss, and hirsutism and who are at low risk of breast or gynecologic cancers may be counseled to have regular gynecology follow-up, but no more frequently than the general population,” but more studies are needed to evaluate risk over longer periods of time, the researchers wrote.

SOURCE:

The lead author of the study was Rachel C. Hill, BS, a student at Weill Cornell Medical College, New York City, and Shari R. Lipner, MD, PhD, of the department of dermatology at Weill Cornell Medical College, was the corresponding author. The study was published online in The Journal of the American Academy of Dermatology.

LIMITATIONS:

The findings were limited by the retrospective design, as well as the small number of spironolactone patients analyzed, the short follow-up period, the lack of information about spironolactone courses, and the inability to control for family history of malignancy.

DISCLOSURES:

The study was supported by the National Center for Advancing Translational Sciences and a grant from the Clinical and Translational Science Center at Weill Cornell Medical College awarded to Ms. Hill. None of the authors had relevant disclosures; Dr. Lipner disclosed serving as a consultant for Ortho-Dermatologics, Eli Lilly, Moberg Pharmaceuticals, and BelleTorus Corporation.

A version of this article appeared on Medscape.com.

TOPLINE:

Women with daily exposure to spironolactone for dermatologic conditions showed no higher risk of developing breast or gynecologic cancer than that of unexposed women.

METHODOLOGY:

• Spironolactone, used off-label for several skin conditions in women, carries a warning about an increased tumor risk associated with high doses in rat models, and its antiandrogen properties have prompted hypotheses about a possible increased risk for breast or gynecologic cancers.
• The researchers reviewed data on 420 women with a history of spironolactone use for acne, hair loss, and hirsutism and 3272 women with no spironolactone use at the authors› institution. Their mean age ranged from 42 to 63 years; the majority were White, and 38% were non-White.
• Median spironolactone doses ranged from 25 mg to 225 mg; chart reviews included 5-year follow-up data from the first spironolactone exposure to allow time for tumor development.

TAKEAWAY:

• A total of 37 of the 420 women exposed to spironolactone developed any tumors, as did 546 of the 3272 with no spironolactone exposure.
• After the researchers controlled for age and race, women exposed to spironolactone were no more likely to develop a malignant tumor than a benign tumor, compared with unexposed women (odds ratio [OR], 0.48, P = .2).
• The risk for breast or uterine cancer was not significantly different in the spironolactone and non-spironolactone groups (OR, 0.95, P > .9).

IN PRACTICE:

“Women taking spironolactone for acne, hair loss, and hirsutism and who are at low risk of breast or gynecologic cancers may be counseled to have regular gynecology follow-up, but no more frequently than the general population,” but more studies are needed to evaluate risk over longer periods of time, the researchers wrote.

SOURCE:

The lead author of the study was Rachel C. Hill, BS, a student at Weill Cornell Medical College, New York City, and Shari R. Lipner, MD, PhD, of the department of dermatology at Weill Cornell Medical College, was the corresponding author. The study was published online in The Journal of the American Academy of Dermatology.

LIMITATIONS:

The findings were limited by the retrospective design, as well as the small number of spironolactone patients analyzed, the short follow-up period, the lack of information about spironolactone courses, and the inability to control for family history of malignancy.

DISCLOSURES:

The study was supported by the National Center for Advancing Translational Sciences and a grant from the Clinical and Translational Science Center at Weill Cornell Medical College awarded to Ms. Hill. None of the authors had relevant disclosures; Dr. Lipner disclosed serving as a consultant for Ortho-Dermatologics, Eli Lilly, Moberg Pharmaceuticals, and BelleTorus Corporation.

A version of this article appeared on Medscape.com.