Megan Brooks

TOPLINE:

While the prevalence of attention-deficit/hyperactivity disorder in U.S. children increased from the late 1990s to 2016, more recent data show rates remained steady at around 10% from 2017 to 2022.

METHODOLOGY:

• Based on prior data, the prevalence of ADHD in children rose from 6.1% in 1997-1998 to 10.2% in 2015-2016, with a 42.0% increase from 2003 to 2011. The new report provides updated prevalence data for 2017-2022.
• The cross-sectional analysis used data from the National Health Interview Survey (NHIS) from 2017 to 2022 for more than 37,609 U.S. children and adolescents 4-17 years old (52% male, 53% non-Hispanic White, 24% Hispanic, 11% non-Hispanic Black, and 12% non-Hispanic other race).
• Information on health care provider–diagnosed ADHD was reported by a parent or guardian.

TAKEAWAY:

• A total of 4,098 children and adolescents (10.9%) were reported to have an ADHD diagnosis during the study period.
• The weighted prevalence of ADHD ranged from 10.08% to 10.47% from 2017 to 2022, which is similar to the prevalence in 2015-2016 (10.20%).
• There was no significant change on an annual basis or in all subgroups evaluated. Notably, the estimated prevalence of ADHD among U.S. children and adolescents was higher than worldwide estimates (5.3%) in earlier years (1978-2005).
• The prevalence of ADHD in U.S. children differed significantly by age, sex, race/ethnicity, and family income, in line with previous findings, with higher rates in those 12-17 years (vs. 4-11 years), males, non-Hispanic populations, and those with higher family income.

IN PRACTICE:

The estimated ADHD prevalence remains “high” and “further investigation is warranted to assess potentially modifiable risk factors and provide adequate resources for treatment of individuals with ADHD in the future,” the authors write.

SOURCE:

The study, with first author Yanmei Li, Guangdong Pharmaceutical University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Information on ADHD relied on parent-reported diagnosis, which may lead to misreporting and recall bias. The NHIS underwent a major redesign in 2019, which may affect comparability with prior years, and the COVID-19 pandemic affected collection in 2020.

DISCLOSURES:

The study had no specific funding. The authors reported no relevant financial relationships.

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

TOPLINE:

While the prevalence of attention-deficit/hyperactivity disorder in U.S. children increased from the late 1990s to 2016, more recent data show rates remained steady at around 10% from 2017 to 2022.

METHODOLOGY:

• Based on prior data, the prevalence of ADHD in children rose from 6.1% in 1997-1998 to 10.2% in 2015-2016, with a 42.0% increase from 2003 to 2011. The new report provides updated prevalence data for 2017-2022.
• The cross-sectional analysis used data from the National Health Interview Survey (NHIS) from 2017 to 2022 for more than 37,609 U.S. children and adolescents 4-17 years old (52% male, 53% non-Hispanic White, 24% Hispanic, 11% non-Hispanic Black, and 12% non-Hispanic other race).
• Information on health care provider–diagnosed ADHD was reported by a parent or guardian.

TAKEAWAY:

• A total of 4,098 children and adolescents (10.9%) were reported to have an ADHD diagnosis during the study period.
• The weighted prevalence of ADHD ranged from 10.08% to 10.47% from 2017 to 2022, which is similar to the prevalence in 2015-2016 (10.20%).
• There was no significant change on an annual basis or in all subgroups evaluated. Notably, the estimated prevalence of ADHD among U.S. children and adolescents was higher than worldwide estimates (5.3%) in earlier years (1978-2005).
• The prevalence of ADHD in U.S. children differed significantly by age, sex, race/ethnicity, and family income, in line with previous findings, with higher rates in those 12-17 years (vs. 4-11 years), males, non-Hispanic populations, and those with higher family income.

IN PRACTICE:

The estimated ADHD prevalence remains “high” and “further investigation is warranted to assess potentially modifiable risk factors and provide adequate resources for treatment of individuals with ADHD in the future,” the authors write.

SOURCE:

The study, with first author Yanmei Li, Guangdong Pharmaceutical University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Information on ADHD relied on parent-reported diagnosis, which may lead to misreporting and recall bias. The NHIS underwent a major redesign in 2019, which may affect comparability with prior years, and the COVID-19 pandemic affected collection in 2020.

DISCLOSURES:

The study had no specific funding. The authors reported no relevant financial relationships.

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

TOPLINE:

While the prevalence of attention-deficit/hyperactivity disorder in U.S. children increased from the late 1990s to 2016, more recent data show rates remained steady at around 10% from 2017 to 2022.

METHODOLOGY:

• Based on prior data, the prevalence of ADHD in children rose from 6.1% in 1997-1998 to 10.2% in 2015-2016, with a 42.0% increase from 2003 to 2011. The new report provides updated prevalence data for 2017-2022.
• The cross-sectional analysis used data from the National Health Interview Survey (NHIS) from 2017 to 2022 for more than 37,609 U.S. children and adolescents 4-17 years old (52% male, 53% non-Hispanic White, 24% Hispanic, 11% non-Hispanic Black, and 12% non-Hispanic other race).
• Information on health care provider–diagnosed ADHD was reported by a parent or guardian.

TAKEAWAY:

• A total of 4,098 children and adolescents (10.9%) were reported to have an ADHD diagnosis during the study period.
• The weighted prevalence of ADHD ranged from 10.08% to 10.47% from 2017 to 2022, which is similar to the prevalence in 2015-2016 (10.20%).
• There was no significant change on an annual basis or in all subgroups evaluated. Notably, the estimated prevalence of ADHD among U.S. children and adolescents was higher than worldwide estimates (5.3%) in earlier years (1978-2005).
• The prevalence of ADHD in U.S. children differed significantly by age, sex, race/ethnicity, and family income, in line with previous findings, with higher rates in those 12-17 years (vs. 4-11 years), males, non-Hispanic populations, and those with higher family income.

IN PRACTICE:

The estimated ADHD prevalence remains “high” and “further investigation is warranted to assess potentially modifiable risk factors and provide adequate resources for treatment of individuals with ADHD in the future,” the authors write.

SOURCE:

The study, with first author Yanmei Li, Guangdong Pharmaceutical University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Information on ADHD relied on parent-reported diagnosis, which may lead to misreporting and recall bias. The NHIS underwent a major redesign in 2019, which may affect comparability with prior years, and the COVID-19 pandemic affected collection in 2020.

DISCLOSURES:

The study had no specific funding. The authors reported no relevant financial relationships.

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

The Food and Drug Administration has declined to approve the RNA interference (RNAi) therapeutic agent patisiran (Onpattro, Alnylam Pharmaceuticals) for treatment of transthyretin-mediated (ATTR) amyloidosis with cardiomyopathy, the company has announced.

ATTR amyloidosis is an underdiagnosed, rapidly progressive, debilitating, fatal disease caused by misfolded TTR proteins, which accumulate as amyloid deposits in various parts of the body, including the heart.

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

The Food and Drug Administration has declined to approve the RNA interference (RNAi) therapeutic agent patisiran (Onpattro, Alnylam Pharmaceuticals) for treatment of transthyretin-mediated (ATTR) amyloidosis with cardiomyopathy, the company has announced.

ATTR amyloidosis is an underdiagnosed, rapidly progressive, debilitating, fatal disease caused by misfolded TTR proteins, which accumulate as amyloid deposits in various parts of the body, including the heart.

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

The Food and Drug Administration has declined to approve the RNA interference (RNAi) therapeutic agent patisiran (Onpattro, Alnylam Pharmaceuticals) for treatment of transthyretin-mediated (ATTR) amyloidosis with cardiomyopathy, the company has announced.

ATTR amyloidosis is an underdiagnosed, rapidly progressive, debilitating, fatal disease caused by misfolded TTR proteins, which accumulate as amyloid deposits in various parts of the body, including the heart.

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

Citing the strong overlap between heart disease, kidney disease, type 2 diabetes, and obesity, the American Heart Association has for the first time formally defined what they are calling cardiovascular-kidney-metabolic (CKM) syndrome.

“This work was prompted by the fact that CKM syndrome leads to premature morbidity and mortality, primarily because of a higher burden of CVD,” writing committee chair Chiadi Ndumele, MD, PhD, said in an interview.

“While CKM syndrome is a public health emergency, there is also great potential for improving CKM health in the population, with an increasing number of therapies that favorably impact metabolic risk factors, risk for adverse kidney events, or both, which also protect against CVD,” added Dr. Ndumele, director of obesity and cardiometabolic research in the division of cardiology at Johns Hopkins University, Baltimore.

The AHA presidential advisory and accompanying scientific statement, which provides a synopsis of evidence for the science and clinical management of CKM, were published online in the journal Circulation.
 

CKM syndrome staging

According to the AHA, one in three U.S. adults have three or more risk factors that contribute to CVD, metabolic disorders, and/or kidney disease.

In addition to defining CKM syndrome, the advisory provides a “staging construct, to be used in both adults and youth, that reflects the progressive pathophysiology and risk within CKM syndrome, with therapeutic guidance tied to CKM stages,” Dr. Ndumele told this news organization.

The AHA outlines four stages of CKM syndrome:

Stage 0: At this stage, no CKM risk factors are present, and the goal is to prevent CKM syndrome (particularly unhealthy weight gain) by achieving and maintaining ideal health based on the AHA’s Life’s Essential 8 recommendations. Adults in this stage should be screened every 3-5 years to assess lipids, blood pressure, and blood sugar.

Stage 1: At this stage, excess weight, abdominal obesity, or dysfunctional adipose tissue (clinically manifest as impaired glucose tolerance or prediabetes) is present without other metabolic risk factors or CVD. Management includes providing support for healthy lifestyle changes (healthy eating and regular physical activity), with a goal of at least 5% weight loss and addressing glucose intolerance if needed. Screening adults with stage 1 CKM every 2-3 years is advised to assess blood pressure, triglycerides, cholesterol, and blood sugar.

Stage 2: At this stage, metabolic risk factors (hypertriglyceridemia, hypertension, metabolic syndrome, diabetes) and kidney disease are present. The goal is to address risk factors to prevent progression to CVD and kidney failure. Screening for stage 2 CKM syndrome aligns with AHA/ACC guidelines, which include yearly assessment of blood pressure, triglycerides, cholesterol, blood sugar, and kidney function. More frequent kidney screening is recommended for individuals with increased risk of kidney failure based on kidney function assessments.

Stage 3: This stage describes individuals with subclinical CVD with metabolic risk factors or kidney disease or those at high predicted risk for CVD. The goal is to intensify efforts to prevent progression to symptomatic CVD and kidney failure. This may involve increasing or changing medications, and additional focus on lifestyle changes. Coronary artery calcium (CAC) measurement in some adults is recommended to assess narrowing of the arteries when treatment decisions are unclear.

Stage 4: Individuals with stage 4 CKM syndrome have symptomatic CVD, excess body fat, metabolic risk factors, or kidney disease. Stage 4 CKM syndrome is divided into two subcategories: (4a) no kidney failure and (4b) kidney failure. In this stage, patients may have already had a myocardial infarction (MI) or stroke or may already have heart failure. They also may have additional CV conditions such as peripheral artery disease or atrial fibrillation. The goal of care is individualized treatment for CVD with consideration for CKM syndrome conditions.

The advisory also describes CKM syndrome regression, “an important concept and public health message in which people making healthy lifestyle changes and achieving weight loss may regress to lower CKM syndrome stages and a better state of health,” the AHA says in a news release.

They note that a “critical” next step is to update the pooled cohort equation (PCE) risk prediction algorithm to include measures of kidney function, type 2 diabetes control, and social determinants of health for a more comprehensive risk estimate.

The advisory also recommends risk calculator updates be expanded to assess risk in people as young as age 30 and to calculate both 10- and 30-year CVD risk.

“Clearly defining the patient with CKM syndrome, and providing new approaches for CKM syndrome staging and risk prediction, will help health care professionals to identify these individuals earlier and to provide timely, holistic, and patient-centered care,” Dr. Ndumele said.

This presidential advisory was prepared by the volunteer writing group on behalf of the AHA . The authors have reported no relevant financial relationships.

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

Citing the strong overlap between heart disease, kidney disease, type 2 diabetes, and obesity, the American Heart Association has for the first time formally defined what they are calling cardiovascular-kidney-metabolic (CKM) syndrome.

“This work was prompted by the fact that CKM syndrome leads to premature morbidity and mortality, primarily because of a higher burden of CVD,” writing committee chair Chiadi Ndumele, MD, PhD, said in an interview.

“While CKM syndrome is a public health emergency, there is also great potential for improving CKM health in the population, with an increasing number of therapies that favorably impact metabolic risk factors, risk for adverse kidney events, or both, which also protect against CVD,” added Dr. Ndumele, director of obesity and cardiometabolic research in the division of cardiology at Johns Hopkins University, Baltimore.

The AHA presidential advisory and accompanying scientific statement, which provides a synopsis of evidence for the science and clinical management of CKM, were published online in the journal Circulation.
 

CKM syndrome staging

According to the AHA, one in three U.S. adults have three or more risk factors that contribute to CVD, metabolic disorders, and/or kidney disease.

In addition to defining CKM syndrome, the advisory provides a “staging construct, to be used in both adults and youth, that reflects the progressive pathophysiology and risk within CKM syndrome, with therapeutic guidance tied to CKM stages,” Dr. Ndumele told this news organization.

The AHA outlines four stages of CKM syndrome:

Stage 0: At this stage, no CKM risk factors are present, and the goal is to prevent CKM syndrome (particularly unhealthy weight gain) by achieving and maintaining ideal health based on the AHA’s Life’s Essential 8 recommendations. Adults in this stage should be screened every 3-5 years to assess lipids, blood pressure, and blood sugar.

Stage 1: At this stage, excess weight, abdominal obesity, or dysfunctional adipose tissue (clinically manifest as impaired glucose tolerance or prediabetes) is present without other metabolic risk factors or CVD. Management includes providing support for healthy lifestyle changes (healthy eating and regular physical activity), with a goal of at least 5% weight loss and addressing glucose intolerance if needed. Screening adults with stage 1 CKM every 2-3 years is advised to assess blood pressure, triglycerides, cholesterol, and blood sugar.

Stage 2: At this stage, metabolic risk factors (hypertriglyceridemia, hypertension, metabolic syndrome, diabetes) and kidney disease are present. The goal is to address risk factors to prevent progression to CVD and kidney failure. Screening for stage 2 CKM syndrome aligns with AHA/ACC guidelines, which include yearly assessment of blood pressure, triglycerides, cholesterol, blood sugar, and kidney function. More frequent kidney screening is recommended for individuals with increased risk of kidney failure based on kidney function assessments.

Stage 3: This stage describes individuals with subclinical CVD with metabolic risk factors or kidney disease or those at high predicted risk for CVD. The goal is to intensify efforts to prevent progression to symptomatic CVD and kidney failure. This may involve increasing or changing medications, and additional focus on lifestyle changes. Coronary artery calcium (CAC) measurement in some adults is recommended to assess narrowing of the arteries when treatment decisions are unclear.

Stage 4: Individuals with stage 4 CKM syndrome have symptomatic CVD, excess body fat, metabolic risk factors, or kidney disease. Stage 4 CKM syndrome is divided into two subcategories: (4a) no kidney failure and (4b) kidney failure. In this stage, patients may have already had a myocardial infarction (MI) or stroke or may already have heart failure. They also may have additional CV conditions such as peripheral artery disease or atrial fibrillation. The goal of care is individualized treatment for CVD with consideration for CKM syndrome conditions.

The advisory also describes CKM syndrome regression, “an important concept and public health message in which people making healthy lifestyle changes and achieving weight loss may regress to lower CKM syndrome stages and a better state of health,” the AHA says in a news release.

They note that a “critical” next step is to update the pooled cohort equation (PCE) risk prediction algorithm to include measures of kidney function, type 2 diabetes control, and social determinants of health for a more comprehensive risk estimate.

The advisory also recommends risk calculator updates be expanded to assess risk in people as young as age 30 and to calculate both 10- and 30-year CVD risk.

“Clearly defining the patient with CKM syndrome, and providing new approaches for CKM syndrome staging and risk prediction, will help health care professionals to identify these individuals earlier and to provide timely, holistic, and patient-centered care,” Dr. Ndumele said.

This presidential advisory was prepared by the volunteer writing group on behalf of the AHA . The authors have reported no relevant financial relationships.

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

Citing the strong overlap between heart disease, kidney disease, type 2 diabetes, and obesity, the American Heart Association has for the first time formally defined what they are calling cardiovascular-kidney-metabolic (CKM) syndrome.

“This work was prompted by the fact that CKM syndrome leads to premature morbidity and mortality, primarily because of a higher burden of CVD,” writing committee chair Chiadi Ndumele, MD, PhD, said in an interview.

“While CKM syndrome is a public health emergency, there is also great potential for improving CKM health in the population, with an increasing number of therapies that favorably impact metabolic risk factors, risk for adverse kidney events, or both, which also protect against CVD,” added Dr. Ndumele, director of obesity and cardiometabolic research in the division of cardiology at Johns Hopkins University, Baltimore.

The AHA presidential advisory and accompanying scientific statement, which provides a synopsis of evidence for the science and clinical management of CKM, were published online in the journal Circulation.
 

CKM syndrome staging

According to the AHA, one in three U.S. adults have three or more risk factors that contribute to CVD, metabolic disorders, and/or kidney disease.

In addition to defining CKM syndrome, the advisory provides a “staging construct, to be used in both adults and youth, that reflects the progressive pathophysiology and risk within CKM syndrome, with therapeutic guidance tied to CKM stages,” Dr. Ndumele told this news organization.

The AHA outlines four stages of CKM syndrome:

Stage 0: At this stage, no CKM risk factors are present, and the goal is to prevent CKM syndrome (particularly unhealthy weight gain) by achieving and maintaining ideal health based on the AHA’s Life’s Essential 8 recommendations. Adults in this stage should be screened every 3-5 years to assess lipids, blood pressure, and blood sugar.

Stage 1: At this stage, excess weight, abdominal obesity, or dysfunctional adipose tissue (clinically manifest as impaired glucose tolerance or prediabetes) is present without other metabolic risk factors or CVD. Management includes providing support for healthy lifestyle changes (healthy eating and regular physical activity), with a goal of at least 5% weight loss and addressing glucose intolerance if needed. Screening adults with stage 1 CKM every 2-3 years is advised to assess blood pressure, triglycerides, cholesterol, and blood sugar.

Stage 2: At this stage, metabolic risk factors (hypertriglyceridemia, hypertension, metabolic syndrome, diabetes) and kidney disease are present. The goal is to address risk factors to prevent progression to CVD and kidney failure. Screening for stage 2 CKM syndrome aligns with AHA/ACC guidelines, which include yearly assessment of blood pressure, triglycerides, cholesterol, blood sugar, and kidney function. More frequent kidney screening is recommended for individuals with increased risk of kidney failure based on kidney function assessments.

Stage 3: This stage describes individuals with subclinical CVD with metabolic risk factors or kidney disease or those at high predicted risk for CVD. The goal is to intensify efforts to prevent progression to symptomatic CVD and kidney failure. This may involve increasing or changing medications, and additional focus on lifestyle changes. Coronary artery calcium (CAC) measurement in some adults is recommended to assess narrowing of the arteries when treatment decisions are unclear.

Stage 4: Individuals with stage 4 CKM syndrome have symptomatic CVD, excess body fat, metabolic risk factors, or kidney disease. Stage 4 CKM syndrome is divided into two subcategories: (4a) no kidney failure and (4b) kidney failure. In this stage, patients may have already had a myocardial infarction (MI) or stroke or may already have heart failure. They also may have additional CV conditions such as peripheral artery disease or atrial fibrillation. The goal of care is individualized treatment for CVD with consideration for CKM syndrome conditions.

The advisory also describes CKM syndrome regression, “an important concept and public health message in which people making healthy lifestyle changes and achieving weight loss may regress to lower CKM syndrome stages and a better state of health,” the AHA says in a news release.

They note that a “critical” next step is to update the pooled cohort equation (PCE) risk prediction algorithm to include measures of kidney function, type 2 diabetes control, and social determinants of health for a more comprehensive risk estimate.

The advisory also recommends risk calculator updates be expanded to assess risk in people as young as age 30 and to calculate both 10- and 30-year CVD risk.

“Clearly defining the patient with CKM syndrome, and providing new approaches for CKM syndrome staging and risk prediction, will help health care professionals to identify these individuals earlier and to provide timely, holistic, and patient-centered care,” Dr. Ndumele said.

This presidential advisory was prepared by the volunteer writing group on behalf of the AHA . The authors have reported no relevant financial relationships.

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

TOPLINE:

Metabolic dysfunction–associated steatotic liver disease (MASLD) significantly raises the risk for cardiovascular, metabolic, oncologic, and other outcomes, a new meta-analysis suggests.

METHODOLOGY:

• Researchers conducted a comprehensive meta-analysis of studies to investigate longitudinal clinical outcomes associated with MASLD, previously known as nonalcoholic fatty liver disease.
• They identified 129 original studies that evaluated the longitudinal risks for incident clinical outcomes in patients with MASLD vs those without the disease.
• Investigators calculated pooled risk estimates for clinical outcomes in patients with MASLD and those without MASLD, with MASLD being diagnosed by imaging, biopsy, blood tests, or ICD codes.

TAKEAWAY:

• MASLD was associated with a significant increased risk for cardiovascular disease outcomes (hazard ratio, 1.43), metabolic outcomes such as incident hypertension (HR, 1.75), prediabetes (HR, 1.69), diabetes (HR, 2.56), metabolic syndrome (HR, 2.57), chronic kidney disease (HR, 1.38), and various liver-related outcomes (HR, 3.92).
• Patients with advanced MASLD had a significantly greater risk (P = .02) of developing diabetes than did their peers with less severe MASLD (HR, 1.63), compared with persons without MASLD.
• MASLD was also associated with all cancers (HR, 1.54); the highest risk was seen for hepatocellular carcinoma (HR, 4.37).
• Subgroup analyses stratified by sex found no significant differences in the risks observed between men and women with MASLD.

IN PRACTICE:

“It is imperative to understand that MASLD is a complex and multifaceted condition that requires a comprehensive approach to recognition and treatment beyond that of the hepatologist alone,” the authors wrote. “The growing prevalence of MASLD will remain a major global health threat that requires effective disease management frameworks to be put in place.”

SOURCE:

The study, with co–first authors Kai En Chan and Elden Yen Hng Ong, National University of Singapore, was published online in Clinical Gastroenterology and Hepatology.

LIMITATIONS:

The results depend on the validity of the original studies, and residual confounding factors may have biased the reported results. The study is also limited in its inclusion of large population-based studies using ICD codes that may result in misclassification bias. There was no examination of longitudinal outcomes in patients with histologically confirmed MASLD.

DISCLOSURES:

The study had no funding. Some authors reported research support, consulting fees, or stock options from pharmaceutical companies.

A version of this article appeared on Medscape.com.

TOPLINE:

Metabolic dysfunction–associated steatotic liver disease (MASLD) significantly raises the risk for cardiovascular, metabolic, oncologic, and other outcomes, a new meta-analysis suggests.

METHODOLOGY:

• Researchers conducted a comprehensive meta-analysis of studies to investigate longitudinal clinical outcomes associated with MASLD, previously known as nonalcoholic fatty liver disease.
• They identified 129 original studies that evaluated the longitudinal risks for incident clinical outcomes in patients with MASLD vs those without the disease.
• Investigators calculated pooled risk estimates for clinical outcomes in patients with MASLD and those without MASLD, with MASLD being diagnosed by imaging, biopsy, blood tests, or ICD codes.

TAKEAWAY:

• MASLD was associated with a significant increased risk for cardiovascular disease outcomes (hazard ratio, 1.43), metabolic outcomes such as incident hypertension (HR, 1.75), prediabetes (HR, 1.69), diabetes (HR, 2.56), metabolic syndrome (HR, 2.57), chronic kidney disease (HR, 1.38), and various liver-related outcomes (HR, 3.92).
• Patients with advanced MASLD had a significantly greater risk (P = .02) of developing diabetes than did their peers with less severe MASLD (HR, 1.63), compared with persons without MASLD.
• MASLD was also associated with all cancers (HR, 1.54); the highest risk was seen for hepatocellular carcinoma (HR, 4.37).
• Subgroup analyses stratified by sex found no significant differences in the risks observed between men and women with MASLD.

IN PRACTICE:

“It is imperative to understand that MASLD is a complex and multifaceted condition that requires a comprehensive approach to recognition and treatment beyond that of the hepatologist alone,” the authors wrote. “The growing prevalence of MASLD will remain a major global health threat that requires effective disease management frameworks to be put in place.”

SOURCE:

The study, with co–first authors Kai En Chan and Elden Yen Hng Ong, National University of Singapore, was published online in Clinical Gastroenterology and Hepatology.

LIMITATIONS:

The results depend on the validity of the original studies, and residual confounding factors may have biased the reported results. The study is also limited in its inclusion of large population-based studies using ICD codes that may result in misclassification bias. There was no examination of longitudinal outcomes in patients with histologically confirmed MASLD.

DISCLOSURES:

The study had no funding. Some authors reported research support, consulting fees, or stock options from pharmaceutical companies.

A version of this article appeared on Medscape.com.

TOPLINE:

Metabolic dysfunction–associated steatotic liver disease (MASLD) significantly raises the risk for cardiovascular, metabolic, oncologic, and other outcomes, a new meta-analysis suggests.

METHODOLOGY:

• Researchers conducted a comprehensive meta-analysis of studies to investigate longitudinal clinical outcomes associated with MASLD, previously known as nonalcoholic fatty liver disease.
• They identified 129 original studies that evaluated the longitudinal risks for incident clinical outcomes in patients with MASLD vs those without the disease.
• Investigators calculated pooled risk estimates for clinical outcomes in patients with MASLD and those without MASLD, with MASLD being diagnosed by imaging, biopsy, blood tests, or ICD codes.

TAKEAWAY:

• MASLD was associated with a significant increased risk for cardiovascular disease outcomes (hazard ratio, 1.43), metabolic outcomes such as incident hypertension (HR, 1.75), prediabetes (HR, 1.69), diabetes (HR, 2.56), metabolic syndrome (HR, 2.57), chronic kidney disease (HR, 1.38), and various liver-related outcomes (HR, 3.92).
• Patients with advanced MASLD had a significantly greater risk (P = .02) of developing diabetes than did their peers with less severe MASLD (HR, 1.63), compared with persons without MASLD.
• MASLD was also associated with all cancers (HR, 1.54); the highest risk was seen for hepatocellular carcinoma (HR, 4.37).
• Subgroup analyses stratified by sex found no significant differences in the risks observed between men and women with MASLD.

IN PRACTICE:

“It is imperative to understand that MASLD is a complex and multifaceted condition that requires a comprehensive approach to recognition and treatment beyond that of the hepatologist alone,” the authors wrote. “The growing prevalence of MASLD will remain a major global health threat that requires effective disease management frameworks to be put in place.”

SOURCE:

The study, with co–first authors Kai En Chan and Elden Yen Hng Ong, National University of Singapore, was published online in Clinical Gastroenterology and Hepatology.

LIMITATIONS:

The results depend on the validity of the original studies, and residual confounding factors may have biased the reported results. The study is also limited in its inclusion of large population-based studies using ICD codes that may result in misclassification bias. There was no examination of longitudinal outcomes in patients with histologically confirmed MASLD.

DISCLOSURES:

The study had no funding. Some authors reported research support, consulting fees, or stock options from pharmaceutical companies.

A version of this article appeared on Medscape.com.

Damaged mitochondrial DNA (mtDNA) initiates and spreads Parkinson’s disease (PD) pathology, potentially opening new avenues for early diagnosis, disease monitoring, and drug development.

While defects in mitochondrial functions and in mitochondrial DNA have been implicated in PD in the past, the current study demonstrates “for the first time how damaged mitochondrial DNA can underlie the mechanisms of PD initiation and spread in brain,” lead investigator Shohreh Issazadeh-Navikas, PhD, with the University of Copenhagen, told this news organization.

“This has direct implication for clinical diagnosis” – if damaged mtDNA can be detected in blood, it could serve as an early biomarker for disease, she explained.

The study was published online in Molecular Psychiatry.
 

“Infectious-like” spread of PD pathology

In earlier work, the researchers identified dysregulated interferon-beta (IFN-beta) signaling as a “top candidate pathway” associated with sporadic PD and its progression to PD with dementia (PDD).

In mice PD models that were deficient in IFN-beta signaling, the investigators showed that neuronal IFN-beta is required to maintain mitochondrial homeostasis and metabolism.

Lack of neuronal IFN-beta or disruption of its downstream signaling causes the accumulation of damaged mitochondria with excessive oxidative stress and insufficient adenosine triphosphate production.

In the current study, using postmortem brain tissue samples from patients with sporadic PD, they confirmed that there were deletions of mtDNA in the medial frontal gyrus, a region implicated in cognitive impairments in PD, suggesting a potential role of damaged mtDNA in disease pathophysiology.

They also identified mtDNA deletions in a “hotspot” in complex I respiratory chain subunits that were associated with dysregulation of oxidative stress and DNA damage response pathways in cohorts with sporadic PD and PDD.

They confirmed the contribution of mtDNA damage to PD pathology in the PD mouse models. They showed that lack of neuronal IFN-beta signaling leads to oxidative damage and mutations in mtDNA in neurons, which are subsequently released outside the neurons.

Injecting damaged mtDNA into mouse brain induced PDD-like behavioral symptoms, including neuropsychiatric, motor, and cognitive impairments. It also caused neurodegeneration in brain regions distant from the injection site, suggesting that damaged mtDNA triggers spread of PDD characteristics in an “infectious-like” manner, the researchers report.

Further study revealed that the mechanism through which damaged mtDNA causes pathology in healthy neurons involves dual activation of Toll-like receptor (TLR) 9 and 4 pathways, leading to increased oxidative stress and neuronal cell death, respectively.

“Our proteomic analysis of extracellular vesicles containing damaged mtDNA identified the TLR4 activator, ribosomal protein S3, as a key protein involved in recognizing and extruding damaged mtDNA,” the investigators write.

In the future they plan to investigate how mtDNA damage can serve as a predictive marker for different disease stages and progression and to explore potential therapeutic strategies aimed at restoring normal mitochondrial function to rectify the mitochondrial dysfunctions implicated in PD.
 

Making a comeback?

Commenting on the research for this news organization, James Beck, PhD, chief scientific officer at the Parkinson’s Foundation, noted that the role of mitochondria in PD is “like a starlet that burst onto the scene in the 80s, faded into obscurity, and through diligence and continued research has moved beyond being a solid character actor and is reemerging as a force to reckon with.

“This paper only adds to the allure that mitochondria may have in contributing to PD by providing evidence of a novel process by which mitochondria may be not only contributing to PD and loss of dopamine neurons but may play a larger role in the subsequent effects that many people with PD experience – dementia,” Dr. Beck said.

He noted that the authors identified several proteins as facilitating the neurodegeneration that is wrought by damaged mitochondrial DNA.

“These could be potential targets for future drug development. In addition, this work implicates alterations in immune signaling and drugs in development to target inflammatory responses may also bring ancillary benefit,” Dr. Beck said.

However, he said, “while very interesting findings, this is really the first effort that demonstrates how damaged mitochondrial DNA may contribute to neurodegeneration in the context of PD and PD dementia. Further work needs to validate these findings as well as to elucidate mechanisms underlying the propagation of the mitochondrial DNA from cell to cell.”

Funding for this research was provided by the European Union’s Horizon 2020 Research and Innovation Program, the Lundbeck Foundation, and the Danish Council for Independent Research–Medicine. Dr. Issazadeh-Navikas and Dr. Beck have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Damaged mitochondrial DNA (mtDNA) initiates and spreads Parkinson’s disease (PD) pathology, potentially opening new avenues for early diagnosis, disease monitoring, and drug development.

While defects in mitochondrial functions and in mitochondrial DNA have been implicated in PD in the past, the current study demonstrates “for the first time how damaged mitochondrial DNA can underlie the mechanisms of PD initiation and spread in brain,” lead investigator Shohreh Issazadeh-Navikas, PhD, with the University of Copenhagen, told this news organization.

“This has direct implication for clinical diagnosis” – if damaged mtDNA can be detected in blood, it could serve as an early biomarker for disease, she explained.

The study was published online in Molecular Psychiatry.
 

“Infectious-like” spread of PD pathology

In earlier work, the researchers identified dysregulated interferon-beta (IFN-beta) signaling as a “top candidate pathway” associated with sporadic PD and its progression to PD with dementia (PDD).

In mice PD models that were deficient in IFN-beta signaling, the investigators showed that neuronal IFN-beta is required to maintain mitochondrial homeostasis and metabolism.

Lack of neuronal IFN-beta or disruption of its downstream signaling causes the accumulation of damaged mitochondria with excessive oxidative stress and insufficient adenosine triphosphate production.

In the current study, using postmortem brain tissue samples from patients with sporadic PD, they confirmed that there were deletions of mtDNA in the medial frontal gyrus, a region implicated in cognitive impairments in PD, suggesting a potential role of damaged mtDNA in disease pathophysiology.

They also identified mtDNA deletions in a “hotspot” in complex I respiratory chain subunits that were associated with dysregulation of oxidative stress and DNA damage response pathways in cohorts with sporadic PD and PDD.

They confirmed the contribution of mtDNA damage to PD pathology in the PD mouse models. They showed that lack of neuronal IFN-beta signaling leads to oxidative damage and mutations in mtDNA in neurons, which are subsequently released outside the neurons.

Injecting damaged mtDNA into mouse brain induced PDD-like behavioral symptoms, including neuropsychiatric, motor, and cognitive impairments. It also caused neurodegeneration in brain regions distant from the injection site, suggesting that damaged mtDNA triggers spread of PDD characteristics in an “infectious-like” manner, the researchers report.

Further study revealed that the mechanism through which damaged mtDNA causes pathology in healthy neurons involves dual activation of Toll-like receptor (TLR) 9 and 4 pathways, leading to increased oxidative stress and neuronal cell death, respectively.

“Our proteomic analysis of extracellular vesicles containing damaged mtDNA identified the TLR4 activator, ribosomal protein S3, as a key protein involved in recognizing and extruding damaged mtDNA,” the investigators write.

In the future they plan to investigate how mtDNA damage can serve as a predictive marker for different disease stages and progression and to explore potential therapeutic strategies aimed at restoring normal mitochondrial function to rectify the mitochondrial dysfunctions implicated in PD.
 

Making a comeback?

Commenting on the research for this news organization, James Beck, PhD, chief scientific officer at the Parkinson’s Foundation, noted that the role of mitochondria in PD is “like a starlet that burst onto the scene in the 80s, faded into obscurity, and through diligence and continued research has moved beyond being a solid character actor and is reemerging as a force to reckon with.

“This paper only adds to the allure that mitochondria may have in contributing to PD by providing evidence of a novel process by which mitochondria may be not only contributing to PD and loss of dopamine neurons but may play a larger role in the subsequent effects that many people with PD experience – dementia,” Dr. Beck said.

He noted that the authors identified several proteins as facilitating the neurodegeneration that is wrought by damaged mitochondrial DNA.

“These could be potential targets for future drug development. In addition, this work implicates alterations in immune signaling and drugs in development to target inflammatory responses may also bring ancillary benefit,” Dr. Beck said.

However, he said, “while very interesting findings, this is really the first effort that demonstrates how damaged mitochondrial DNA may contribute to neurodegeneration in the context of PD and PD dementia. Further work needs to validate these findings as well as to elucidate mechanisms underlying the propagation of the mitochondrial DNA from cell to cell.”

Funding for this research was provided by the European Union’s Horizon 2020 Research and Innovation Program, the Lundbeck Foundation, and the Danish Council for Independent Research–Medicine. Dr. Issazadeh-Navikas and Dr. Beck have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Damaged mitochondrial DNA (mtDNA) initiates and spreads Parkinson’s disease (PD) pathology, potentially opening new avenues for early diagnosis, disease monitoring, and drug development.

While defects in mitochondrial functions and in mitochondrial DNA have been implicated in PD in the past, the current study demonstrates “for the first time how damaged mitochondrial DNA can underlie the mechanisms of PD initiation and spread in brain,” lead investigator Shohreh Issazadeh-Navikas, PhD, with the University of Copenhagen, told this news organization.

“This has direct implication for clinical diagnosis” – if damaged mtDNA can be detected in blood, it could serve as an early biomarker for disease, she explained.

The study was published online in Molecular Psychiatry.
 

“Infectious-like” spread of PD pathology

In earlier work, the researchers identified dysregulated interferon-beta (IFN-beta) signaling as a “top candidate pathway” associated with sporadic PD and its progression to PD with dementia (PDD).

In mice PD models that were deficient in IFN-beta signaling, the investigators showed that neuronal IFN-beta is required to maintain mitochondrial homeostasis and metabolism.

Lack of neuronal IFN-beta or disruption of its downstream signaling causes the accumulation of damaged mitochondria with excessive oxidative stress and insufficient adenosine triphosphate production.

In the current study, using postmortem brain tissue samples from patients with sporadic PD, they confirmed that there were deletions of mtDNA in the medial frontal gyrus, a region implicated in cognitive impairments in PD, suggesting a potential role of damaged mtDNA in disease pathophysiology.

They also identified mtDNA deletions in a “hotspot” in complex I respiratory chain subunits that were associated with dysregulation of oxidative stress and DNA damage response pathways in cohorts with sporadic PD and PDD.

They confirmed the contribution of mtDNA damage to PD pathology in the PD mouse models. They showed that lack of neuronal IFN-beta signaling leads to oxidative damage and mutations in mtDNA in neurons, which are subsequently released outside the neurons.

Injecting damaged mtDNA into mouse brain induced PDD-like behavioral symptoms, including neuropsychiatric, motor, and cognitive impairments. It also caused neurodegeneration in brain regions distant from the injection site, suggesting that damaged mtDNA triggers spread of PDD characteristics in an “infectious-like” manner, the researchers report.

Further study revealed that the mechanism through which damaged mtDNA causes pathology in healthy neurons involves dual activation of Toll-like receptor (TLR) 9 and 4 pathways, leading to increased oxidative stress and neuronal cell death, respectively.

“Our proteomic analysis of extracellular vesicles containing damaged mtDNA identified the TLR4 activator, ribosomal protein S3, as a key protein involved in recognizing and extruding damaged mtDNA,” the investigators write.

In the future they plan to investigate how mtDNA damage can serve as a predictive marker for different disease stages and progression and to explore potential therapeutic strategies aimed at restoring normal mitochondrial function to rectify the mitochondrial dysfunctions implicated in PD.
 

Making a comeback?

Commenting on the research for this news organization, James Beck, PhD, chief scientific officer at the Parkinson’s Foundation, noted that the role of mitochondria in PD is “like a starlet that burst onto the scene in the 80s, faded into obscurity, and through diligence and continued research has moved beyond being a solid character actor and is reemerging as a force to reckon with.

“This paper only adds to the allure that mitochondria may have in contributing to PD by providing evidence of a novel process by which mitochondria may be not only contributing to PD and loss of dopamine neurons but may play a larger role in the subsequent effects that many people with PD experience – dementia,” Dr. Beck said.

He noted that the authors identified several proteins as facilitating the neurodegeneration that is wrought by damaged mitochondrial DNA.

“These could be potential targets for future drug development. In addition, this work implicates alterations in immune signaling and drugs in development to target inflammatory responses may also bring ancillary benefit,” Dr. Beck said.

However, he said, “while very interesting findings, this is really the first effort that demonstrates how damaged mitochondrial DNA may contribute to neurodegeneration in the context of PD and PD dementia. Further work needs to validate these findings as well as to elucidate mechanisms underlying the propagation of the mitochondrial DNA from cell to cell.”

Funding for this research was provided by the European Union’s Horizon 2020 Research and Innovation Program, the Lundbeck Foundation, and the Danish Council for Independent Research–Medicine. Dr. Issazadeh-Navikas and Dr. Beck have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

New research shows that adults who develop nonalcoholic fatty liver disease (NAFLD) before age 45 are at increased risk of developing cancer, particularly digestive system and lung cancer.

METHODOLOGY:

• Researchers conducted a prospective age- and sex-matched cohort study of 63,696 adults (mean age, 51 years; 83% men) in China. The patients were followed for a median of 10 years; 31,848 had NAFLD, and 31,848 were control participants.
• Participants were grouped on the basis of age at the time of diagnosis of new-onset NAFLD: younger than 45, 45-54, 55-64, and 65 and older.
• Multivariable Cox models were used to analyze cancer risk by age at NAFLD onset. Population-attributable fractions were calculated to quantify cancer risk associated with age at NAFLD onset.

TAKEAWAY:

• During follow-up, 2,415 participants were diagnosed with cancer.
• NAFLD onset before age 45 was associated with highest cancer risk in comparison with the risk among control persons (average hazard ratio [AHR], 1.52). Cancer risk decreased as age at NAFLD onset increased (AHR, 1.50 for the 45-54 cohort, 1.13 for the 55-64 cohort, and 0.75 for the 65-and-older cohort).
• Among adults younger than 45 at NAFLD onset, cancers were mainly digestive and lung cancers (AHR, 2.00 and 2.14, respectively).
• Close to 18% of the cancer risk among adults younger than 45 at NAFLD onset was attributed to their fatty liver disease.

IN PRACTICE:

“The increasing incidence of NAFLD among younger populations highlights the underestimation of harmful outcomes associated with this condition,” the authors wrote. “Our findings suggest that early control and intervention against NAFLD progression may be crucial to reduce the occurrence of NAFLD-related cancers and lessen the burden on public health.”

SOURCE:

The study, with first author Chenan Liu, MD, PhD, Beijing Shijitan Hospital, Capital Medical University, was published online in JAMA Network Open.

LIMITATIONS:

The study population was predominantly male, and NAFLD diagnosis relied on ultrasound rather than liver biopsy, potentially missing mild cases. The study lacked data on liver fibrosis elastography measurement and blood biomarkers. For some cancers, incidence rates were low.

DISCLOSURES:

The study was funded by a grant from the National Key Research and Development Program of China. The authors reported no conflicts of interest.

TOPLINE:

New research shows that adults who develop nonalcoholic fatty liver disease (NAFLD) before age 45 are at increased risk of developing cancer, particularly digestive system and lung cancer.

METHODOLOGY:

• Researchers conducted a prospective age- and sex-matched cohort study of 63,696 adults (mean age, 51 years; 83% men) in China. The patients were followed for a median of 10 years; 31,848 had NAFLD, and 31,848 were control participants.
• Participants were grouped on the basis of age at the time of diagnosis of new-onset NAFLD: younger than 45, 45-54, 55-64, and 65 and older.
• Multivariable Cox models were used to analyze cancer risk by age at NAFLD onset. Population-attributable fractions were calculated to quantify cancer risk associated with age at NAFLD onset.

TAKEAWAY:

• During follow-up, 2,415 participants were diagnosed with cancer.
• NAFLD onset before age 45 was associated with highest cancer risk in comparison with the risk among control persons (average hazard ratio [AHR], 1.52). Cancer risk decreased as age at NAFLD onset increased (AHR, 1.50 for the 45-54 cohort, 1.13 for the 55-64 cohort, and 0.75 for the 65-and-older cohort).
• Among adults younger than 45 at NAFLD onset, cancers were mainly digestive and lung cancers (AHR, 2.00 and 2.14, respectively).
• Close to 18% of the cancer risk among adults younger than 45 at NAFLD onset was attributed to their fatty liver disease.

IN PRACTICE:

“The increasing incidence of NAFLD among younger populations highlights the underestimation of harmful outcomes associated with this condition,” the authors wrote. “Our findings suggest that early control and intervention against NAFLD progression may be crucial to reduce the occurrence of NAFLD-related cancers and lessen the burden on public health.”

SOURCE:

The study, with first author Chenan Liu, MD, PhD, Beijing Shijitan Hospital, Capital Medical University, was published online in JAMA Network Open.

LIMITATIONS:

The study population was predominantly male, and NAFLD diagnosis relied on ultrasound rather than liver biopsy, potentially missing mild cases. The study lacked data on liver fibrosis elastography measurement and blood biomarkers. For some cancers, incidence rates were low.

DISCLOSURES:

The study was funded by a grant from the National Key Research and Development Program of China. The authors reported no conflicts of interest.

TOPLINE:

New research shows that adults who develop nonalcoholic fatty liver disease (NAFLD) before age 45 are at increased risk of developing cancer, particularly digestive system and lung cancer.

METHODOLOGY:

• Researchers conducted a prospective age- and sex-matched cohort study of 63,696 adults (mean age, 51 years; 83% men) in China. The patients were followed for a median of 10 years; 31,848 had NAFLD, and 31,848 were control participants.
• Participants were grouped on the basis of age at the time of diagnosis of new-onset NAFLD: younger than 45, 45-54, 55-64, and 65 and older.
• Multivariable Cox models were used to analyze cancer risk by age at NAFLD onset. Population-attributable fractions were calculated to quantify cancer risk associated with age at NAFLD onset.

TAKEAWAY:

• During follow-up, 2,415 participants were diagnosed with cancer.
• NAFLD onset before age 45 was associated with highest cancer risk in comparison with the risk among control persons (average hazard ratio [AHR], 1.52). Cancer risk decreased as age at NAFLD onset increased (AHR, 1.50 for the 45-54 cohort, 1.13 for the 55-64 cohort, and 0.75 for the 65-and-older cohort).
• Among adults younger than 45 at NAFLD onset, cancers were mainly digestive and lung cancers (AHR, 2.00 and 2.14, respectively).
• Close to 18% of the cancer risk among adults younger than 45 at NAFLD onset was attributed to their fatty liver disease.

IN PRACTICE:

“The increasing incidence of NAFLD among younger populations highlights the underestimation of harmful outcomes associated with this condition,” the authors wrote. “Our findings suggest that early control and intervention against NAFLD progression may be crucial to reduce the occurrence of NAFLD-related cancers and lessen the burden on public health.”

SOURCE:

The study, with first author Chenan Liu, MD, PhD, Beijing Shijitan Hospital, Capital Medical University, was published online in JAMA Network Open.

LIMITATIONS:

The study population was predominantly male, and NAFLD diagnosis relied on ultrasound rather than liver biopsy, potentially missing mild cases. The study lacked data on liver fibrosis elastography measurement and blood biomarkers. For some cancers, incidence rates were low.

DISCLOSURES:

The study was funded by a grant from the National Key Research and Development Program of China. The authors reported no conflicts of interest.

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

The updated draft recommendation from the U.S. Preventive Services Task Force that would lower the recommended start age for routine screening mammograms by a decade for all average-risk women is not justified, experts argue in a “dissenting view” published in the New England Journal of Medicine.

The proposed change would affect more than 20 million U.S. women, and it’s “hard to see any potential benefits associated with lowering the starting age,” coauthor Steven Woloshin, MD, with Dartmouth Cancer Center, Lebanon, N.H., said in an NEJM podcast.

Back in May, when USPSTF released the draft recommendation, task force member John Wong, MD, with Tufts Medical Center, Boston, said in an interview, “It is now clear that screening every other year starting at age 40 has the potential to save about 20% more lives among all women.”

But, according to Dr. Woloshin, there is no recent evidence that mortality from breast cancer is increasing in young women.

In fact, the United States has seen a steady decrease in breast cancer mortality, especially among younger women. Breast cancer mortality among women under 50 “has been cut in half over the past 30 years,” Dr. Woloshin and coauthors explained.

Another wrinkle: The task force did not base its recent recommendation on randomized trial data. In fact, there have been no new randomized trials of screening mammography for women in their 40s since 2016. Instead, the task force relied on statistical models to “estimate what might happen if the starting age were lowered,” Dr. Woloshin and colleagues said.

Relying on a statistical model, however, “is problematic because it has some very optimistic assumptions about the benefit of mammography,” Dr. Woloshin said in the podcast. For instance, the models assume that screening mammography reduces breast cancer mortality by about 25%.

That 25% reduction is “far greater than what’s reported in the meta-analyses of the available randomized trials,” Dr. Woloshin explained. The meta-analyses report about a 16% reduction for all the trials combined and an estimated 13% for trials at low risk of bias. But “even these meta-analyses are likely to overstate the effect of screening since the trials were done before the major advances in treatment.”

In their own calculations, Dr. Woloshin and colleagues found that lowering the screening age to 40 came with a small potential benefit and a substantial risk for harm.

Combing data from the National Cancer Institute, the team reported that the risk for death for women in their 40s from any cause over the next 10 years was about 3% whether or not they received their biennial mammogram.

The risk for death from breast cancer in that time was 0.23% with mammograms – about 2 in every 1,000 women – and 0.31% without. “That’s 1 less breast cancer death per 1,000 women screened for 10 years,” Dr. Woloshin said.

Put another way, with mammography screening, “the chance of not dying from breast cancer over the next 10 years increases from 99.7% to 99.8%,” Dr. Woloshin said.

The benefit is arguably small, while the harms appear quite significant, Dr. Woloshin said. About 36% of women who begin screening at age 40 would have at least one false alarm over 10 years, and almost 7% would have a false alarm requiring a biopsy in that time frame.
 

Ease or exacerbate racial disparity?

Another argument that the USPSTF highlighted for lowering the screening age: Research indicates that Black women get breast cancer at younger ages and are more likely to die of the disease, compared with White women.

Dr. Woloshin and coauthors, however, also took issue with the view that lowering the screening age could reduce disparities between Black and White women.

“There’s no question that there are substantial differences between Black and White women in terms of breast cancer mortality, but there’s actually very little disparity in breast cancer screening – about 60% of Black and White women in their 40s are screened regularly in the United States,” Dr. Woloshin explained in the podcast.

Therefore, it’s “really hard to imagine” how recommending the same intervention to both groups could possibly reduce the disparity, he said.

“The disparity is not a reflection of screening. It reflects differences in cancer biology,” he added. “Black women are at higher risk for more aggressive, fast-growing cancers that are less likely to be caught by screening and unfortunately are less likely to benefit from treatment.”

Earlier screening would also not address the problems facing poor women, who tend to be disproportionately Black, such as lower quality of available medical services, follow-up delays after abnormal scans, treatment delays, and less use of adjuvant therapy, Dr. Woloshin cautioned.

In Dr. Woloshin’s view, lowering the screening age, which broadens the eligible population, may actually “exacerbate problems contributing to disparity by diverting resources toward expanded screening rather than doing what we know works by ensuring that high-quality treatments are more readily accessible to poor women with breast cancer.”
 

Reconsider the change?

Because task force recommendations are so influential, Dr. Woloshin and colleagues worry that mammography screening for women in their 40s will probably become a performance measure.

“Our concern is that, rather than fostering informed decisions, clinicians and practices are going to be judged and rewarded and punished based on compliance with this quality metric,” Dr. Woloshin said.

That’s a problem, he noted, “because women should be able to make the decision for themselves rather than having this be a public health imperative, which is imposed by physicians and practices who are incentivized to meet a quality metric.”

The hope, said Dr. Woloshin, is that this prospective piece will help influence the task force to “reconsider the recommendation, because we think that the bottom line is that their models are insufficient to support a new imperative. The benefits are really limited, and there are really common and important harms for healthy women.”

The comment period for the draft recommendation is now closed, and a final decision from the task force is forthcoming.

The research had no funding. Dr. Woloshin has no relevant disclosures.

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

The updated draft recommendation from the U.S. Preventive Services Task Force that would lower the recommended start age for routine screening mammograms by a decade for all average-risk women is not justified, experts argue in a “dissenting view” published in the New England Journal of Medicine.

The proposed change would affect more than 20 million U.S. women, and it’s “hard to see any potential benefits associated with lowering the starting age,” coauthor Steven Woloshin, MD, with Dartmouth Cancer Center, Lebanon, N.H., said in an NEJM podcast.

Back in May, when USPSTF released the draft recommendation, task force member John Wong, MD, with Tufts Medical Center, Boston, said in an interview, “It is now clear that screening every other year starting at age 40 has the potential to save about 20% more lives among all women.”

But, according to Dr. Woloshin, there is no recent evidence that mortality from breast cancer is increasing in young women.

In fact, the United States has seen a steady decrease in breast cancer mortality, especially among younger women. Breast cancer mortality among women under 50 “has been cut in half over the past 30 years,” Dr. Woloshin and coauthors explained.

Another wrinkle: The task force did not base its recent recommendation on randomized trial data. In fact, there have been no new randomized trials of screening mammography for women in their 40s since 2016. Instead, the task force relied on statistical models to “estimate what might happen if the starting age were lowered,” Dr. Woloshin and colleagues said.

Relying on a statistical model, however, “is problematic because it has some very optimistic assumptions about the benefit of mammography,” Dr. Woloshin said in the podcast. For instance, the models assume that screening mammography reduces breast cancer mortality by about 25%.

That 25% reduction is “far greater than what’s reported in the meta-analyses of the available randomized trials,” Dr. Woloshin explained. The meta-analyses report about a 16% reduction for all the trials combined and an estimated 13% for trials at low risk of bias. But “even these meta-analyses are likely to overstate the effect of screening since the trials were done before the major advances in treatment.”

In their own calculations, Dr. Woloshin and colleagues found that lowering the screening age to 40 came with a small potential benefit and a substantial risk for harm.

Combing data from the National Cancer Institute, the team reported that the risk for death for women in their 40s from any cause over the next 10 years was about 3% whether or not they received their biennial mammogram.

The risk for death from breast cancer in that time was 0.23% with mammograms – about 2 in every 1,000 women – and 0.31% without. “That’s 1 less breast cancer death per 1,000 women screened for 10 years,” Dr. Woloshin said.

Put another way, with mammography screening, “the chance of not dying from breast cancer over the next 10 years increases from 99.7% to 99.8%,” Dr. Woloshin said.

The benefit is arguably small, while the harms appear quite significant, Dr. Woloshin said. About 36% of women who begin screening at age 40 would have at least one false alarm over 10 years, and almost 7% would have a false alarm requiring a biopsy in that time frame.
 

Ease or exacerbate racial disparity?

Another argument that the USPSTF highlighted for lowering the screening age: Research indicates that Black women get breast cancer at younger ages and are more likely to die of the disease, compared with White women.

Dr. Woloshin and coauthors, however, also took issue with the view that lowering the screening age could reduce disparities between Black and White women.

“There’s no question that there are substantial differences between Black and White women in terms of breast cancer mortality, but there’s actually very little disparity in breast cancer screening – about 60% of Black and White women in their 40s are screened regularly in the United States,” Dr. Woloshin explained in the podcast.

Therefore, it’s “really hard to imagine” how recommending the same intervention to both groups could possibly reduce the disparity, he said.

“The disparity is not a reflection of screening. It reflects differences in cancer biology,” he added. “Black women are at higher risk for more aggressive, fast-growing cancers that are less likely to be caught by screening and unfortunately are less likely to benefit from treatment.”

Earlier screening would also not address the problems facing poor women, who tend to be disproportionately Black, such as lower quality of available medical services, follow-up delays after abnormal scans, treatment delays, and less use of adjuvant therapy, Dr. Woloshin cautioned.

In Dr. Woloshin’s view, lowering the screening age, which broadens the eligible population, may actually “exacerbate problems contributing to disparity by diverting resources toward expanded screening rather than doing what we know works by ensuring that high-quality treatments are more readily accessible to poor women with breast cancer.”
 

Reconsider the change?

Because task force recommendations are so influential, Dr. Woloshin and colleagues worry that mammography screening for women in their 40s will probably become a performance measure.

“Our concern is that, rather than fostering informed decisions, clinicians and practices are going to be judged and rewarded and punished based on compliance with this quality metric,” Dr. Woloshin said.

That’s a problem, he noted, “because women should be able to make the decision for themselves rather than having this be a public health imperative, which is imposed by physicians and practices who are incentivized to meet a quality metric.”

The hope, said Dr. Woloshin, is that this prospective piece will help influence the task force to “reconsider the recommendation, because we think that the bottom line is that their models are insufficient to support a new imperative. The benefits are really limited, and there are really common and important harms for healthy women.”

The comment period for the draft recommendation is now closed, and a final decision from the task force is forthcoming.

The research had no funding. Dr. Woloshin has no relevant disclosures.

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

The updated draft recommendation from the U.S. Preventive Services Task Force that would lower the recommended start age for routine screening mammograms by a decade for all average-risk women is not justified, experts argue in a “dissenting view” published in the New England Journal of Medicine.

The proposed change would affect more than 20 million U.S. women, and it’s “hard to see any potential benefits associated with lowering the starting age,” coauthor Steven Woloshin, MD, with Dartmouth Cancer Center, Lebanon, N.H., said in an NEJM podcast.

Back in May, when USPSTF released the draft recommendation, task force member John Wong, MD, with Tufts Medical Center, Boston, said in an interview, “It is now clear that screening every other year starting at age 40 has the potential to save about 20% more lives among all women.”

But, according to Dr. Woloshin, there is no recent evidence that mortality from breast cancer is increasing in young women.

In fact, the United States has seen a steady decrease in breast cancer mortality, especially among younger women. Breast cancer mortality among women under 50 “has been cut in half over the past 30 years,” Dr. Woloshin and coauthors explained.

Another wrinkle: The task force did not base its recent recommendation on randomized trial data. In fact, there have been no new randomized trials of screening mammography for women in their 40s since 2016. Instead, the task force relied on statistical models to “estimate what might happen if the starting age were lowered,” Dr. Woloshin and colleagues said.

Relying on a statistical model, however, “is problematic because it has some very optimistic assumptions about the benefit of mammography,” Dr. Woloshin said in the podcast. For instance, the models assume that screening mammography reduces breast cancer mortality by about 25%.

That 25% reduction is “far greater than what’s reported in the meta-analyses of the available randomized trials,” Dr. Woloshin explained. The meta-analyses report about a 16% reduction for all the trials combined and an estimated 13% for trials at low risk of bias. But “even these meta-analyses are likely to overstate the effect of screening since the trials were done before the major advances in treatment.”

In their own calculations, Dr. Woloshin and colleagues found that lowering the screening age to 40 came with a small potential benefit and a substantial risk for harm.

Combing data from the National Cancer Institute, the team reported that the risk for death for women in their 40s from any cause over the next 10 years was about 3% whether or not they received their biennial mammogram.

The risk for death from breast cancer in that time was 0.23% with mammograms – about 2 in every 1,000 women – and 0.31% without. “That’s 1 less breast cancer death per 1,000 women screened for 10 years,” Dr. Woloshin said.

Put another way, with mammography screening, “the chance of not dying from breast cancer over the next 10 years increases from 99.7% to 99.8%,” Dr. Woloshin said.

The benefit is arguably small, while the harms appear quite significant, Dr. Woloshin said. About 36% of women who begin screening at age 40 would have at least one false alarm over 10 years, and almost 7% would have a false alarm requiring a biopsy in that time frame.
 

Ease or exacerbate racial disparity?

Another argument that the USPSTF highlighted for lowering the screening age: Research indicates that Black women get breast cancer at younger ages and are more likely to die of the disease, compared with White women.

Dr. Woloshin and coauthors, however, also took issue with the view that lowering the screening age could reduce disparities between Black and White women.

“There’s no question that there are substantial differences between Black and White women in terms of breast cancer mortality, but there’s actually very little disparity in breast cancer screening – about 60% of Black and White women in their 40s are screened regularly in the United States,” Dr. Woloshin explained in the podcast.

Therefore, it’s “really hard to imagine” how recommending the same intervention to both groups could possibly reduce the disparity, he said.

“The disparity is not a reflection of screening. It reflects differences in cancer biology,” he added. “Black women are at higher risk for more aggressive, fast-growing cancers that are less likely to be caught by screening and unfortunately are less likely to benefit from treatment.”

Earlier screening would also not address the problems facing poor women, who tend to be disproportionately Black, such as lower quality of available medical services, follow-up delays after abnormal scans, treatment delays, and less use of adjuvant therapy, Dr. Woloshin cautioned.

In Dr. Woloshin’s view, lowering the screening age, which broadens the eligible population, may actually “exacerbate problems contributing to disparity by diverting resources toward expanded screening rather than doing what we know works by ensuring that high-quality treatments are more readily accessible to poor women with breast cancer.”
 

Reconsider the change?

Because task force recommendations are so influential, Dr. Woloshin and colleagues worry that mammography screening for women in their 40s will probably become a performance measure.

“Our concern is that, rather than fostering informed decisions, clinicians and practices are going to be judged and rewarded and punished based on compliance with this quality metric,” Dr. Woloshin said.

That’s a problem, he noted, “because women should be able to make the decision for themselves rather than having this be a public health imperative, which is imposed by physicians and practices who are incentivized to meet a quality metric.”

The hope, said Dr. Woloshin, is that this prospective piece will help influence the task force to “reconsider the recommendation, because we think that the bottom line is that their models are insufficient to support a new imperative. The benefits are really limited, and there are really common and important harms for healthy women.”

The comment period for the draft recommendation is now closed, and a final decision from the task force is forthcoming.

The research had no funding. Dr. Woloshin has no relevant disclosures.

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

TOPLINE:

A meta-analysis finds that tea drinking may reduce the risk for colorectal cancer (CRC) by 24%, but the estimate is “uncertain,” and the actual effect on CRC risk can range from a reduction of 51% to an increase of 18%, researchers say.

METHODOLOGY:

• Researchers conducted a systematic review and meta-analysis of 15 studies (11 cohort, three case-control, and one randomized controlled trial) with nearly 2.7 million participants.
• The studies were conducted in Asia, North America, Europe, and Oceania between 1986 and 2015 and included black and green tea.
• Tea consumption was dichotomized as < 1 cup vs. ≥ 1 cups daily. A random effects model was used for data analysis.

TAKEAWAY:

• No statistically significant association was found between tea consumption and CRC risk (relative risk, 0.76).
• By geographic region, results of an American subgroup analysis suggested tea drinking might be protective against CRC (RR, 0.33), while data from the United Kingdom (RR, 1.45) and Italian (RR, 1.15) subgroups had opposite results.
• In subgroups by tea type, green tea was associated with a lower CRC risk (RR, 0.05).
• Sensitivity analysis revealed that the effect on CRC risk can range from a reduction of 51% (RR, 0.49) to an increase of 18% (RR, 1.18).

IN PRACTICE:

“Taken together, this meta-analysis suggests that tea consumption may not be linked to the development of CRC. These relationships still need to be confirmed by additional well-designed large prospective studies and randomized clinical trials,” the authors write.

SOURCE:

The study, with co–first authors Yu Huang and Qiang Chen, with the Third Hospital of Hebei Medical University, Shijiazhuang, China, was published online in BMC Gastroenterology.

LIMITATIONS:

There was a high level of heterogeneity in the original studies, as well as variations in the quantity and types of tea consumed and in the design and quality of the studies. Some studies did not account for potentially important variables, such as alcohol use and diet.

DISCLOSURES:

The study was supported by grants from the Hebei Provincial Natural Science Foundation and the Hebei Provincial Department of Science and Technology. The authors have disclosed no conflicts of interest.

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

TOPLINE:

A meta-analysis finds that tea drinking may reduce the risk for colorectal cancer (CRC) by 24%, but the estimate is “uncertain,” and the actual effect on CRC risk can range from a reduction of 51% to an increase of 18%, researchers say.

METHODOLOGY:

• Researchers conducted a systematic review and meta-analysis of 15 studies (11 cohort, three case-control, and one randomized controlled trial) with nearly 2.7 million participants.
• The studies were conducted in Asia, North America, Europe, and Oceania between 1986 and 2015 and included black and green tea.
• Tea consumption was dichotomized as < 1 cup vs. ≥ 1 cups daily. A random effects model was used for data analysis.

TAKEAWAY:

• No statistically significant association was found between tea consumption and CRC risk (relative risk, 0.76).
• By geographic region, results of an American subgroup analysis suggested tea drinking might be protective against CRC (RR, 0.33), while data from the United Kingdom (RR, 1.45) and Italian (RR, 1.15) subgroups had opposite results.
• In subgroups by tea type, green tea was associated with a lower CRC risk (RR, 0.05).
• Sensitivity analysis revealed that the effect on CRC risk can range from a reduction of 51% (RR, 0.49) to an increase of 18% (RR, 1.18).

IN PRACTICE:

“Taken together, this meta-analysis suggests that tea consumption may not be linked to the development of CRC. These relationships still need to be confirmed by additional well-designed large prospective studies and randomized clinical trials,” the authors write.

SOURCE:

The study, with co–first authors Yu Huang and Qiang Chen, with the Third Hospital of Hebei Medical University, Shijiazhuang, China, was published online in BMC Gastroenterology.

LIMITATIONS:

There was a high level of heterogeneity in the original studies, as well as variations in the quantity and types of tea consumed and in the design and quality of the studies. Some studies did not account for potentially important variables, such as alcohol use and diet.

DISCLOSURES:

The study was supported by grants from the Hebei Provincial Natural Science Foundation and the Hebei Provincial Department of Science and Technology. The authors have disclosed no conflicts of interest.

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

TOPLINE:

A meta-analysis finds that tea drinking may reduce the risk for colorectal cancer (CRC) by 24%, but the estimate is “uncertain,” and the actual effect on CRC risk can range from a reduction of 51% to an increase of 18%, researchers say.

METHODOLOGY:

• Researchers conducted a systematic review and meta-analysis of 15 studies (11 cohort, three case-control, and one randomized controlled trial) with nearly 2.7 million participants.
• The studies were conducted in Asia, North America, Europe, and Oceania between 1986 and 2015 and included black and green tea.
• Tea consumption was dichotomized as < 1 cup vs. ≥ 1 cups daily. A random effects model was used for data analysis.

TAKEAWAY:

• No statistically significant association was found between tea consumption and CRC risk (relative risk, 0.76).
• By geographic region, results of an American subgroup analysis suggested tea drinking might be protective against CRC (RR, 0.33), while data from the United Kingdom (RR, 1.45) and Italian (RR, 1.15) subgroups had opposite results.
• In subgroups by tea type, green tea was associated with a lower CRC risk (RR, 0.05).
• Sensitivity analysis revealed that the effect on CRC risk can range from a reduction of 51% (RR, 0.49) to an increase of 18% (RR, 1.18).

IN PRACTICE:

“Taken together, this meta-analysis suggests that tea consumption may not be linked to the development of CRC. These relationships still need to be confirmed by additional well-designed large prospective studies and randomized clinical trials,” the authors write.

SOURCE:

The study, with co–first authors Yu Huang and Qiang Chen, with the Third Hospital of Hebei Medical University, Shijiazhuang, China, was published online in BMC Gastroenterology.

LIMITATIONS:

There was a high level of heterogeneity in the original studies, as well as variations in the quantity and types of tea consumed and in the design and quality of the studies. Some studies did not account for potentially important variables, such as alcohol use and diet.

DISCLOSURES:

The study was supported by grants from the Hebei Provincial Natural Science Foundation and the Hebei Provincial Department of Science and Technology. The authors have disclosed no conflicts of interest.

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

TOPLINE:

Vegetarian diets may reduce the risk for gastric and colorectal cancers, according to the results of a meta-analysis.

METHODOLOGY:

• Researchers did a systematic review and meta-analysis of seven original studies (six cohorts and one case-control) involving 686,691 people.
• Pooled relative risk for gastric, colorectal, and upper gastrointestinal cancers were assessed with confidence intervals in multivariate analysis accounting for potential confounders.

TAKEAWAY:

• Compared with nonvegetarian diets, vegetarian diets were inversely associated with the risk for GI tumor development (relative risk, 0.77).
• In a subgroup analysis, vegetarian diets were negatively correlated with the risk for gastric cancer (RR, 0.41) and colorectal cancer (RR, 0.85) but not with upper GI cancer (excluding stomach; RR, 0.93).
• Vegetarian diets were negatively correlated with the risk for GI cancer in men (RR, 0.57) but not women (RR, 0.89).
• Vegetarian diets were negatively correlated with the risk for GI cancer in North American (RR, 0.76) and Asian populations (RR, 0.43) but not in European populations (RR, 0.83).

IN PRACTICE:

“The results of this systematic review indicate that adherence to vegetarian diets can reduce the risk of gastrointestinal cancers, compared with non-vegetarian diets. This study provides a reference for primary prevention strategies for gastrointestinal cancers,” the authors write.

SOURCE:

The study, with first author Tongtong Bai, of Nanjing University of Chinese Medicine, was published online on in the European Journal of Gastroenterology & Hepatology.

LIMITATIONS:

The effects of vegetarian diets on GI tumorigenesis may be influenced by gender and geographical region. The heterogeneity of effects of vegetarian diets on different GI cancers could be due to the small number of studies included and could represent chance variation. The results need to be confirmed by studies of populations in other regions. There was evidence of publication bias.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Vegetarian diets may reduce the risk for gastric and colorectal cancers, according to the results of a meta-analysis.

METHODOLOGY:

• Researchers did a systematic review and meta-analysis of seven original studies (six cohorts and one case-control) involving 686,691 people.
• Pooled relative risk for gastric, colorectal, and upper gastrointestinal cancers were assessed with confidence intervals in multivariate analysis accounting for potential confounders.

TAKEAWAY:

• Compared with nonvegetarian diets, vegetarian diets were inversely associated with the risk for GI tumor development (relative risk, 0.77).
• In a subgroup analysis, vegetarian diets were negatively correlated with the risk for gastric cancer (RR, 0.41) and colorectal cancer (RR, 0.85) but not with upper GI cancer (excluding stomach; RR, 0.93).
• Vegetarian diets were negatively correlated with the risk for GI cancer in men (RR, 0.57) but not women (RR, 0.89).
• Vegetarian diets were negatively correlated with the risk for GI cancer in North American (RR, 0.76) and Asian populations (RR, 0.43) but not in European populations (RR, 0.83).

IN PRACTICE:

“The results of this systematic review indicate that adherence to vegetarian diets can reduce the risk of gastrointestinal cancers, compared with non-vegetarian diets. This study provides a reference for primary prevention strategies for gastrointestinal cancers,” the authors write.

SOURCE:

The study, with first author Tongtong Bai, of Nanjing University of Chinese Medicine, was published online on in the European Journal of Gastroenterology & Hepatology.

LIMITATIONS:

The effects of vegetarian diets on GI tumorigenesis may be influenced by gender and geographical region. The heterogeneity of effects of vegetarian diets on different GI cancers could be due to the small number of studies included and could represent chance variation. The results need to be confirmed by studies of populations in other regions. There was evidence of publication bias.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Vegetarian diets may reduce the risk for gastric and colorectal cancers, according to the results of a meta-analysis.

METHODOLOGY:

• Researchers did a systematic review and meta-analysis of seven original studies (six cohorts and one case-control) involving 686,691 people.
• Pooled relative risk for gastric, colorectal, and upper gastrointestinal cancers were assessed with confidence intervals in multivariate analysis accounting for potential confounders.

TAKEAWAY:

• Compared with nonvegetarian diets, vegetarian diets were inversely associated with the risk for GI tumor development (relative risk, 0.77).
• In a subgroup analysis, vegetarian diets were negatively correlated with the risk for gastric cancer (RR, 0.41) and colorectal cancer (RR, 0.85) but not with upper GI cancer (excluding stomach; RR, 0.93).
• Vegetarian diets were negatively correlated with the risk for GI cancer in men (RR, 0.57) but not women (RR, 0.89).
• Vegetarian diets were negatively correlated with the risk for GI cancer in North American (RR, 0.76) and Asian populations (RR, 0.43) but not in European populations (RR, 0.83).

IN PRACTICE:

“The results of this systematic review indicate that adherence to vegetarian diets can reduce the risk of gastrointestinal cancers, compared with non-vegetarian diets. This study provides a reference for primary prevention strategies for gastrointestinal cancers,” the authors write.

SOURCE:

The study, with first author Tongtong Bai, of Nanjing University of Chinese Medicine, was published online on in the European Journal of Gastroenterology & Hepatology.

LIMITATIONS:

The effects of vegetarian diets on GI tumorigenesis may be influenced by gender and geographical region. The heterogeneity of effects of vegetarian diets on different GI cancers could be due to the small number of studies included and could represent chance variation. The results need to be confirmed by studies of populations in other regions. There was evidence of publication bias.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no conflicts of interest.

A version of this article appeared on Medscape.com.