Clinician Reviews

TOPLINE:

Changes in plasma growth hormone mediators such as growth hormone receptor (GHR) and insulin-like growth factor-binding protein 1 (IGFBP-1) were associated with glycemic failure in youth-onset type 2 diabetes (T2D), an analysis of the TODAY trial showed.

METHODOLOGY:

• In youth, T2D often occurs during or after puberty, hinting at hormonal influences in the development and/or progression of the disease.
• This secondary analysis assessed the role of growth hormone mediators including insulin-like growth factor-1 (IGF-1), GHR, and IGFBP-1 in glycemic failure in a subset of 398 youths, aged 10-17 years, with a T2D duration of less than 2 years (62% girls; 21% White).
• The participants were followed up for a mean of 3.9 years.
• The primary outcomes included glycemic failure, defined as an A1c level of 8% or more for 6 months, or acute metabolic decompensation requiring insulin.
• Other assessments included baseline and 36-month measures of glycemia, insulin sensitivity, high molecular weight adiponectin, and beta cell function.

TAKEAWAY:

• Of 398 participants, 182 (46%) experienced glycemic failure, while 216 (54%) retained glycemic control.
• At 36 months, youths with glycemic failure had lower IGF-1 levels (P < .001) and higher log₂ GHR (P = .03) and log₂ IGFBP-1 (P = .009) levels than those who maintained glycemic control.
• A greater increase in IGF-1 level at 36 months was associated with lower odds of glycemic failure (odds ratio [OR], 0.995; P < .001).
• Increased levels of log₂ GHR and log₂ IGFBP-1 were associated with higher odds of glycemic failure (OR, 1.75; P = .04 and OR, 1.37; P = .007, respectively). Results were adjusted for body mass index (BMI), suggesting that associations between GHR level and glycemic outcomes exist independent of BMI.
• Interhormonal correlations suggested an association between glucose metabolism and growth hormone signaling or a shared process leading to changes in both processes.

IN PRACTICE:

“Our study has identified GHR level as a novel biomarker of decrease in glycemic control in youths with T2D,” the study authors wrote. Future research is needed, with an emphasis on assessing alterations in growth hormone mediators which may contribute to diabetes complications in youth.

SOURCE:

The study, published online in JAMA Network Open, was led by Chang Lu, MD, Division of Endocrinology, Boston Children’s Hospital, and Joslin Diabetes Center at Harvard Medical School, Boston, Massachusetts.

LIMITATIONS:

The study did not include a control group (individuals without diabetes). The cohort largely included youth in late puberty or after puberty, affecting subgroup analysis. Moreover, only circulating growth hormone mediators were measured, limiting the identity of the source tissue of the hormone and the target organs.

DISCLOSURES:

Some authors reported receiving grants from the National Institutes of Health and National Institute of Diabetes and Digestive and Kidney Diseases while conducting the study. Also, certain authors reported receiving grants and personal fees from various trusts as well as pharmaceutical, healthcare, and medical technology companies outside the submitted work.

TOPLINE:

Changes in plasma growth hormone mediators such as growth hormone receptor (GHR) and insulin-like growth factor-binding protein 1 (IGFBP-1) were associated with glycemic failure in youth-onset type 2 diabetes (T2D), an analysis of the TODAY trial showed.

METHODOLOGY:

• In youth, T2D often occurs during or after puberty, hinting at hormonal influences in the development and/or progression of the disease.
• This secondary analysis assessed the role of growth hormone mediators including insulin-like growth factor-1 (IGF-1), GHR, and IGFBP-1 in glycemic failure in a subset of 398 youths, aged 10-17 years, with a T2D duration of less than 2 years (62% girls; 21% White).
• The participants were followed up for a mean of 3.9 years.
• The primary outcomes included glycemic failure, defined as an A1c level of 8% or more for 6 months, or acute metabolic decompensation requiring insulin.
• Other assessments included baseline and 36-month measures of glycemia, insulin sensitivity, high molecular weight adiponectin, and beta cell function.

TAKEAWAY:

• Of 398 participants, 182 (46%) experienced glycemic failure, while 216 (54%) retained glycemic control.
• At 36 months, youths with glycemic failure had lower IGF-1 levels (P < .001) and higher log₂ GHR (P = .03) and log₂ IGFBP-1 (P = .009) levels than those who maintained glycemic control.
• A greater increase in IGF-1 level at 36 months was associated with lower odds of glycemic failure (odds ratio [OR], 0.995; P < .001).
• Increased levels of log₂ GHR and log₂ IGFBP-1 were associated with higher odds of glycemic failure (OR, 1.75; P = .04 and OR, 1.37; P = .007, respectively). Results were adjusted for body mass index (BMI), suggesting that associations between GHR level and glycemic outcomes exist independent of BMI.
• Interhormonal correlations suggested an association between glucose metabolism and growth hormone signaling or a shared process leading to changes in both processes.

IN PRACTICE:

“Our study has identified GHR level as a novel biomarker of decrease in glycemic control in youths with T2D,” the study authors wrote. Future research is needed, with an emphasis on assessing alterations in growth hormone mediators which may contribute to diabetes complications in youth.

SOURCE:

The study, published online in JAMA Network Open, was led by Chang Lu, MD, Division of Endocrinology, Boston Children’s Hospital, and Joslin Diabetes Center at Harvard Medical School, Boston, Massachusetts.

LIMITATIONS:

The study did not include a control group (individuals without diabetes). The cohort largely included youth in late puberty or after puberty, affecting subgroup analysis. Moreover, only circulating growth hormone mediators were measured, limiting the identity of the source tissue of the hormone and the target organs.

DISCLOSURES:

Some authors reported receiving grants from the National Institutes of Health and National Institute of Diabetes and Digestive and Kidney Diseases while conducting the study. Also, certain authors reported receiving grants and personal fees from various trusts as well as pharmaceutical, healthcare, and medical technology companies outside the submitted work.

TOPLINE:

Changes in plasma growth hormone mediators such as growth hormone receptor (GHR) and insulin-like growth factor-binding protein 1 (IGFBP-1) were associated with glycemic failure in youth-onset type 2 diabetes (T2D), an analysis of the TODAY trial showed.

METHODOLOGY:

• In youth, T2D often occurs during or after puberty, hinting at hormonal influences in the development and/or progression of the disease.
• This secondary analysis assessed the role of growth hormone mediators including insulin-like growth factor-1 (IGF-1), GHR, and IGFBP-1 in glycemic failure in a subset of 398 youths, aged 10-17 years, with a T2D duration of less than 2 years (62% girls; 21% White).
• The participants were followed up for a mean of 3.9 years.
• The primary outcomes included glycemic failure, defined as an A1c level of 8% or more for 6 months, or acute metabolic decompensation requiring insulin.
• Other assessments included baseline and 36-month measures of glycemia, insulin sensitivity, high molecular weight adiponectin, and beta cell function.

TAKEAWAY:

• Of 398 participants, 182 (46%) experienced glycemic failure, while 216 (54%) retained glycemic control.
• At 36 months, youths with glycemic failure had lower IGF-1 levels (P < .001) and higher log₂ GHR (P = .03) and log₂ IGFBP-1 (P = .009) levels than those who maintained glycemic control.
• A greater increase in IGF-1 level at 36 months was associated with lower odds of glycemic failure (odds ratio [OR], 0.995; P < .001).
• Increased levels of log₂ GHR and log₂ IGFBP-1 were associated with higher odds of glycemic failure (OR, 1.75; P = .04 and OR, 1.37; P = .007, respectively). Results were adjusted for body mass index (BMI), suggesting that associations between GHR level and glycemic outcomes exist independent of BMI.
• Interhormonal correlations suggested an association between glucose metabolism and growth hormone signaling or a shared process leading to changes in both processes.

IN PRACTICE:

“Our study has identified GHR level as a novel biomarker of decrease in glycemic control in youths with T2D,” the study authors wrote. Future research is needed, with an emphasis on assessing alterations in growth hormone mediators which may contribute to diabetes complications in youth.

SOURCE:

The study, published online in JAMA Network Open, was led by Chang Lu, MD, Division of Endocrinology, Boston Children’s Hospital, and Joslin Diabetes Center at Harvard Medical School, Boston, Massachusetts.

LIMITATIONS:

The study did not include a control group (individuals without diabetes). The cohort largely included youth in late puberty or after puberty, affecting subgroup analysis. Moreover, only circulating growth hormone mediators were measured, limiting the identity of the source tissue of the hormone and the target organs.

DISCLOSURES:

Some authors reported receiving grants from the National Institutes of Health and National Institute of Diabetes and Digestive and Kidney Diseases while conducting the study. Also, certain authors reported receiving grants and personal fees from various trusts as well as pharmaceutical, healthcare, and medical technology companies outside the submitted work.

TOPLINE:

The remission period of type 1 diabetes (T1D) can be prolonged with high-dose ergocalciferol (a vitamin D analog), by preserving the function of insulin-producing beta cells in newly diagnosed patients.

METHODOLOGY:

• Beta cells may retain approximately 30%-50% function at the time of T1D diagnosis and continue producing insulin for months or years. Preserving beta-cell function early on can extend this remission period and improve long-term glycemic control.
• Researchers conducted a secondary post hoc analysis of a randomized clinical trial looking at residual beta function and vitamin D supplementation in 36 youths (age, 10-21 years; mean age, 13.5 years; 33.3% women) with recently diagnosed T1D.
• Participants were randomly assigned to receive vitamin D (50,000 international units) or placebo every week for 2 months and then biweekly for 10 months.
• Mixed-meal tolerance tests were performed after overnight fasting at 0, 3, 6, 9, and 12 months, and blood draws were obtained 30 minutes and 90 minutes for post-meal C-peptide and glucose estimations.
• The fasting proinsulin to C-peptide ratio (PI:C) and the percentage change in the area under the curve of C-peptide from baseline (%ΔAUC) were calculated to test the effect of vitamin D on beta-cell function.

TAKEAWAY: 

• Vitamin D supplementation improved the insulin secretion capacity of beta cells, as observed by the decrease in the mean fasting PI:C ratio compared with placebo (−0.0009 vs 0.0011; P =.01).
• The reduction in %ΔAUC of C-peptide was notably slower with vitamin D than placebo (−2.8% vs −4.7%; P =.03), indicating a longer delay in the loss of C-peptide.

IN PRACTICE:

“It is exciting to know that vitamin D could protect the beta cells of the pancreas and increase the natural production of good and functional insulin in these patients. This, in turn, prolongs the honeymoon phase of type 1 diabetes and leads to reduced long-term complications of this disease,” Benjamin Udoka Nwosu, MD, Northwell Health, Division of Endocrinology, Department of Pediatrics, Cohen Children’s Medical Center, New Hyde Park, New York, the principal author, said in a press release.

SOURCE:

The study was published online in JAMA Network Open.

LIMITATIONS:

It was a single-center study.

DISCLOSURES:

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The authors did not report any conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

The remission period of type 1 diabetes (T1D) can be prolonged with high-dose ergocalciferol (a vitamin D analog), by preserving the function of insulin-producing beta cells in newly diagnosed patients.

METHODOLOGY:

• Beta cells may retain approximately 30%-50% function at the time of T1D diagnosis and continue producing insulin for months or years. Preserving beta-cell function early on can extend this remission period and improve long-term glycemic control.
• Researchers conducted a secondary post hoc analysis of a randomized clinical trial looking at residual beta function and vitamin D supplementation in 36 youths (age, 10-21 years; mean age, 13.5 years; 33.3% women) with recently diagnosed T1D.
• Participants were randomly assigned to receive vitamin D (50,000 international units) or placebo every week for 2 months and then biweekly for 10 months.
• Mixed-meal tolerance tests were performed after overnight fasting at 0, 3, 6, 9, and 12 months, and blood draws were obtained 30 minutes and 90 minutes for post-meal C-peptide and glucose estimations.
• The fasting proinsulin to C-peptide ratio (PI:C) and the percentage change in the area under the curve of C-peptide from baseline (%ΔAUC) were calculated to test the effect of vitamin D on beta-cell function.

TAKEAWAY: 

• Vitamin D supplementation improved the insulin secretion capacity of beta cells, as observed by the decrease in the mean fasting PI:C ratio compared with placebo (−0.0009 vs 0.0011; P =.01).
• The reduction in %ΔAUC of C-peptide was notably slower with vitamin D than placebo (−2.8% vs −4.7%; P =.03), indicating a longer delay in the loss of C-peptide.

IN PRACTICE:

“It is exciting to know that vitamin D could protect the beta cells of the pancreas and increase the natural production of good and functional insulin in these patients. This, in turn, prolongs the honeymoon phase of type 1 diabetes and leads to reduced long-term complications of this disease,” Benjamin Udoka Nwosu, MD, Northwell Health, Division of Endocrinology, Department of Pediatrics, Cohen Children’s Medical Center, New Hyde Park, New York, the principal author, said in a press release.

SOURCE:

The study was published online in JAMA Network Open.

LIMITATIONS:

It was a single-center study.

DISCLOSURES:

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The authors did not report any conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

The remission period of type 1 diabetes (T1D) can be prolonged with high-dose ergocalciferol (a vitamin D analog), by preserving the function of insulin-producing beta cells in newly diagnosed patients.

METHODOLOGY:

• Beta cells may retain approximately 30%-50% function at the time of T1D diagnosis and continue producing insulin for months or years. Preserving beta-cell function early on can extend this remission period and improve long-term glycemic control.
• Researchers conducted a secondary post hoc analysis of a randomized clinical trial looking at residual beta function and vitamin D supplementation in 36 youths (age, 10-21 years; mean age, 13.5 years; 33.3% women) with recently diagnosed T1D.
• Participants were randomly assigned to receive vitamin D (50,000 international units) or placebo every week for 2 months and then biweekly for 10 months.
• Mixed-meal tolerance tests were performed after overnight fasting at 0, 3, 6, 9, and 12 months, and blood draws were obtained 30 minutes and 90 minutes for post-meal C-peptide and glucose estimations.
• The fasting proinsulin to C-peptide ratio (PI:C) and the percentage change in the area under the curve of C-peptide from baseline (%ΔAUC) were calculated to test the effect of vitamin D on beta-cell function.

TAKEAWAY: 

• Vitamin D supplementation improved the insulin secretion capacity of beta cells, as observed by the decrease in the mean fasting PI:C ratio compared with placebo (−0.0009 vs 0.0011; P =.01).
• The reduction in %ΔAUC of C-peptide was notably slower with vitamin D than placebo (−2.8% vs −4.7%; P =.03), indicating a longer delay in the loss of C-peptide.

IN PRACTICE:

“It is exciting to know that vitamin D could protect the beta cells of the pancreas and increase the natural production of good and functional insulin in these patients. This, in turn, prolongs the honeymoon phase of type 1 diabetes and leads to reduced long-term complications of this disease,” Benjamin Udoka Nwosu, MD, Northwell Health, Division of Endocrinology, Department of Pediatrics, Cohen Children’s Medical Center, New Hyde Park, New York, the principal author, said in a press release.

SOURCE:

The study was published online in JAMA Network Open.

LIMITATIONS:

It was a single-center study.

DISCLOSURES:

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The authors did not report any conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

A version of this article appeared on Medscape.com.

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

A version of this article appeared on Medscape.com.

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

A version of this article appeared on Medscape.com.

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

A version of this article appeared on Medscape.com.

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

A version of this article appeared on Medscape.com.

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

A version of this article appeared on Medscape.com.

A new position statement from the International Diabetes Federation advises using a 1-hour 75-g oral glucose tolerance test (OGTT) to improve identification of people at risk of developing type 2 diabetes.

“There are many, many people who may appear ‘normal’ if you use A1c or fasting glucose, but if you do a glucose tolerance test, they may have an abnormality after a glucose load. …The 1-hour plasma glucose has been found to be a more sensitive biomarker for the earlier identification of these high-risk individuals,” lead author Michael Bergman, MD, professor of medicine and population health at New York University Grossman School of Medicine, New York City, told this news organization in an interview.

Dr. Bergman presented the document, written by a 22-member international expert panel, on March 6, 2024, at the annual Advanced Technologies & Treatments for Diabetes meeting. It was simultaneously published in Diabetes Research and Clinical Practice.

This is the International Diabetes Federation’s (IDF’s) proposed screening algorithm for “intermediate hyperglycemia” and type 2 diabetes:

• At-risk high-risk individuals are first screened with a validated questionnaire such as the FINDRISK or the American Diabetes Association’s (ADA’s) risk screening tool.
• People identified as high risk should undergo laboratory screening with a 1-hour 75-g OGTT (although a 2-hour OGTT, fasting glucose, or A1c, as currently recommended by several organizations, is still considered acceptable).
• People with a 1-hour plasma glucose value at or above 155 mg (8.6 mmol/L) are considered to have intermediate hyperglycemia and should be prescribed lifestyle intervention and referred to a diabetes prevention program.
• Those with a 1-hour value greater than or equal to 209 mg/dL (11.6 mmol/L) are considered to have type 2 diabetes and should have a repeat test to confirm the diagnosis, with referral for further evaluation and treatment.

The new guidance is based on increasing evidence that the 1-hour test is a better predictor than other tests, including the 2-hour OGTT, of progression to type 2 diabetes and its associated complications, in a variety of populations. The document cites data showing that a plasma glucose of 155 mg/dl or greater on the 1-hour post-75-g test can identify people with undiagnosed type 2 diabetes or who are at increased risk but who have “normal” glucose tolerance as defined by an A1c < 5.7% (38.8 mmol/mol), a fasting plasma glucose < 100 mg/dL (5.6 mmol/L), or a 2-hour value below 140 mg/dL (7.8 mmol/L).

However, even though a 1-hour test may be more convenient than the traditional 2-hour test, incorporating OGTT into busy clinical practice may still pose logistical problems and may not improve ultimate outcomes, Elizabeth Selvin, PhD, MPH, of the Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, told this news organization. “I worry that emphasizing a burdensome test is not going to improve diabetes screening or diabetes prevention. Doing more 1-hour glucose screening is not going to get more people into diabetes prevention programs.”

When an audience member raised the logistics concern during the session Q&A, Dr. Bergman replied, “It’s no different than recommending colonoscopy or a mammogram. … I tell patients that we want to learn more about what is going on before we make a firm diagnosis. … I’ve done more than a hundred 1-hour glucose tolerance tests and have not seen one patient who refused because of inconvenience. Everything depends on the way we discuss things with patients.”
 

Recommendation Based on Emerging Evidence

“Intermediate hyperglycemia” is the World Health Organization’s term to refer to either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). These conditions are often called “prediabetes,” especially in the United States, but that term has been controversial because not everyone with IFG and IGT will go on to develop type 2 diabetes, said Dr. Bergman, who is also director of the NYU Langone Diabetes Prevention Program.

“With ‘prediabetes’ you’re labeling someone with a disease they may not develop. It’s not normal, but it’s not diabetes, so it’s an intermediate state,” he explained.

The statement provides a detailed summary of the data from 19 studies supporting use of a 1-hour plasma glucose of ≥ 155 mg/dL (8.6 mmol/L) to diagnose intermediate hyperglycemia and type 2 diabetes, including links between that level of glycemia and worsened metabolic and atherogenic profiles, risk for microvascular and macrovascular complications and mortality, and identification of risks for obstructive sleep apnea, cystic fibrosis-related diabetes mellitus, fatty liver disease, and premature mortality.

One major problem with current testing, Dr. Bergman said, is that “there is a huge disconnect between A1c and glucose values. … Only about 30% of individuals with an abnormal A1c will have an abnormal fasting glucose, and the inverse is also true. There’s a big mismatch between the two.”

Current guidelines suggest using both A1c and fasting glucose, but Dr. Bergman said that even then “you’re still missing about 20-30% who have IGT. … Part of the problem is that the criteria we use for defining abnormal fasting and 2-hour levels are too high. … 140 [mg/dL] for the 2-hour is too high and 100 [mg/dL] fasting is too high. … And that’s one of the reasons why many people progress to type 2 diabetes, because we’re using screening thresholds that are nonphysiologic.”

But Dr. Selvin disagrees, pointing to her own work showing that “using a combination of fasting glucose and A1c for screening does an excellent job at identifying high-risk individuals.”

She’s also unconvinced by other data cited in the paper. “I am deeply skeptical about 1-hour glucose being more prognostic than all other glycemic tests. … Associations of glucose tests with incident diabetes are inherently a circular analysis since diabetes is defined by elevations in those same tests. It is helpful to look at progression of diabetes, but these analyses are not simple and doing them well, especially with head-to-head comparisons against different glycemic tests, is hard,” she said.

In her view, “lifestyle interventions and weight loss should be recommended in at-risk individuals, including those with overweight and obesity, hypertension, metabolic syndrome, etc., regardless of 1-hour glucose test results.”

She added, “If we want to prevent diabetes, we need to focus on preventing weight gain and obesity and managing cardiometabolic risk factors. Lifestyle interventions are not effective unless they are intensive and patients are highly adherent. We need to make lifestyle interventions available and affordable for patients. That is the big barrier. I don’t think more screening with 1-hour glucose is going to help.”

Dr. Bergman pointed out that the International Diabetes Federation represents more than 100 countries, including many that are middle- and low-income. “They need a simple, cost-effective tool for screening effectively. A1c is more expensive, and fasting glucose alone will underestimate disease prevalence. So, the IDF felt, after doing a fairly comprehensive due diligence, that the data warranted recommendation of the 1-hour glucose.”

He’s hoping other organizations like the ADA and the World Health Organization will sign on to bring this guidance into the primary care arena. This news organization reached out to ADA for comment, but their representative hadn’t responded by press time.

Dr. Bergman had no disclosures. Dr. Selvin was supported by the National Institutes of Health.

A version of this article appeared on Medscape.com.

A new position statement from the International Diabetes Federation advises using a 1-hour 75-g oral glucose tolerance test (OGTT) to improve identification of people at risk of developing type 2 diabetes.

“There are many, many people who may appear ‘normal’ if you use A1c or fasting glucose, but if you do a glucose tolerance test, they may have an abnormality after a glucose load. …The 1-hour plasma glucose has been found to be a more sensitive biomarker for the earlier identification of these high-risk individuals,” lead author Michael Bergman, MD, professor of medicine and population health at New York University Grossman School of Medicine, New York City, told this news organization in an interview.

Dr. Bergman presented the document, written by a 22-member international expert panel, on March 6, 2024, at the annual Advanced Technologies & Treatments for Diabetes meeting. It was simultaneously published in Diabetes Research and Clinical Practice.

This is the International Diabetes Federation’s (IDF’s) proposed screening algorithm for “intermediate hyperglycemia” and type 2 diabetes:

• At-risk high-risk individuals are first screened with a validated questionnaire such as the FINDRISK or the American Diabetes Association’s (ADA’s) risk screening tool.
• People identified as high risk should undergo laboratory screening with a 1-hour 75-g OGTT (although a 2-hour OGTT, fasting glucose, or A1c, as currently recommended by several organizations, is still considered acceptable).
• People with a 1-hour plasma glucose value at or above 155 mg (8.6 mmol/L) are considered to have intermediate hyperglycemia and should be prescribed lifestyle intervention and referred to a diabetes prevention program.
• Those with a 1-hour value greater than or equal to 209 mg/dL (11.6 mmol/L) are considered to have type 2 diabetes and should have a repeat test to confirm the diagnosis, with referral for further evaluation and treatment.

The new guidance is based on increasing evidence that the 1-hour test is a better predictor than other tests, including the 2-hour OGTT, of progression to type 2 diabetes and its associated complications, in a variety of populations. The document cites data showing that a plasma glucose of 155 mg/dl or greater on the 1-hour post-75-g test can identify people with undiagnosed type 2 diabetes or who are at increased risk but who have “normal” glucose tolerance as defined by an A1c < 5.7% (38.8 mmol/mol), a fasting plasma glucose < 100 mg/dL (5.6 mmol/L), or a 2-hour value below 140 mg/dL (7.8 mmol/L).

However, even though a 1-hour test may be more convenient than the traditional 2-hour test, incorporating OGTT into busy clinical practice may still pose logistical problems and may not improve ultimate outcomes, Elizabeth Selvin, PhD, MPH, of the Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, told this news organization. “I worry that emphasizing a burdensome test is not going to improve diabetes screening or diabetes prevention. Doing more 1-hour glucose screening is not going to get more people into diabetes prevention programs.”

When an audience member raised the logistics concern during the session Q&A, Dr. Bergman replied, “It’s no different than recommending colonoscopy or a mammogram. … I tell patients that we want to learn more about what is going on before we make a firm diagnosis. … I’ve done more than a hundred 1-hour glucose tolerance tests and have not seen one patient who refused because of inconvenience. Everything depends on the way we discuss things with patients.”
 

Recommendation Based on Emerging Evidence

“Intermediate hyperglycemia” is the World Health Organization’s term to refer to either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). These conditions are often called “prediabetes,” especially in the United States, but that term has been controversial because not everyone with IFG and IGT will go on to develop type 2 diabetes, said Dr. Bergman, who is also director of the NYU Langone Diabetes Prevention Program.

“With ‘prediabetes’ you’re labeling someone with a disease they may not develop. It’s not normal, but it’s not diabetes, so it’s an intermediate state,” he explained.

The statement provides a detailed summary of the data from 19 studies supporting use of a 1-hour plasma glucose of ≥ 155 mg/dL (8.6 mmol/L) to diagnose intermediate hyperglycemia and type 2 diabetes, including links between that level of glycemia and worsened metabolic and atherogenic profiles, risk for microvascular and macrovascular complications and mortality, and identification of risks for obstructive sleep apnea, cystic fibrosis-related diabetes mellitus, fatty liver disease, and premature mortality.

One major problem with current testing, Dr. Bergman said, is that “there is a huge disconnect between A1c and glucose values. … Only about 30% of individuals with an abnormal A1c will have an abnormal fasting glucose, and the inverse is also true. There’s a big mismatch between the two.”

Current guidelines suggest using both A1c and fasting glucose, but Dr. Bergman said that even then “you’re still missing about 20-30% who have IGT. … Part of the problem is that the criteria we use for defining abnormal fasting and 2-hour levels are too high. … 140 [mg/dL] for the 2-hour is too high and 100 [mg/dL] fasting is too high. … And that’s one of the reasons why many people progress to type 2 diabetes, because we’re using screening thresholds that are nonphysiologic.”

But Dr. Selvin disagrees, pointing to her own work showing that “using a combination of fasting glucose and A1c for screening does an excellent job at identifying high-risk individuals.”

She’s also unconvinced by other data cited in the paper. “I am deeply skeptical about 1-hour glucose being more prognostic than all other glycemic tests. … Associations of glucose tests with incident diabetes are inherently a circular analysis since diabetes is defined by elevations in those same tests. It is helpful to look at progression of diabetes, but these analyses are not simple and doing them well, especially with head-to-head comparisons against different glycemic tests, is hard,” she said.

In her view, “lifestyle interventions and weight loss should be recommended in at-risk individuals, including those with overweight and obesity, hypertension, metabolic syndrome, etc., regardless of 1-hour glucose test results.”

She added, “If we want to prevent diabetes, we need to focus on preventing weight gain and obesity and managing cardiometabolic risk factors. Lifestyle interventions are not effective unless they are intensive and patients are highly adherent. We need to make lifestyle interventions available and affordable for patients. That is the big barrier. I don’t think more screening with 1-hour glucose is going to help.”

Dr. Bergman pointed out that the International Diabetes Federation represents more than 100 countries, including many that are middle- and low-income. “They need a simple, cost-effective tool for screening effectively. A1c is more expensive, and fasting glucose alone will underestimate disease prevalence. So, the IDF felt, after doing a fairly comprehensive due diligence, that the data warranted recommendation of the 1-hour glucose.”

He’s hoping other organizations like the ADA and the World Health Organization will sign on to bring this guidance into the primary care arena. This news organization reached out to ADA for comment, but their representative hadn’t responded by press time.

Dr. Bergman had no disclosures. Dr. Selvin was supported by the National Institutes of Health.

A version of this article appeared on Medscape.com.

A new position statement from the International Diabetes Federation advises using a 1-hour 75-g oral glucose tolerance test (OGTT) to improve identification of people at risk of developing type 2 diabetes.

“There are many, many people who may appear ‘normal’ if you use A1c or fasting glucose, but if you do a glucose tolerance test, they may have an abnormality after a glucose load. …The 1-hour plasma glucose has been found to be a more sensitive biomarker for the earlier identification of these high-risk individuals,” lead author Michael Bergman, MD, professor of medicine and population health at New York University Grossman School of Medicine, New York City, told this news organization in an interview.

Dr. Bergman presented the document, written by a 22-member international expert panel, on March 6, 2024, at the annual Advanced Technologies & Treatments for Diabetes meeting. It was simultaneously published in Diabetes Research and Clinical Practice.

This is the International Diabetes Federation’s (IDF’s) proposed screening algorithm for “intermediate hyperglycemia” and type 2 diabetes:

• At-risk high-risk individuals are first screened with a validated questionnaire such as the FINDRISK or the American Diabetes Association’s (ADA’s) risk screening tool.
• People identified as high risk should undergo laboratory screening with a 1-hour 75-g OGTT (although a 2-hour OGTT, fasting glucose, or A1c, as currently recommended by several organizations, is still considered acceptable).
• People with a 1-hour plasma glucose value at or above 155 mg (8.6 mmol/L) are considered to have intermediate hyperglycemia and should be prescribed lifestyle intervention and referred to a diabetes prevention program.
• Those with a 1-hour value greater than or equal to 209 mg/dL (11.6 mmol/L) are considered to have type 2 diabetes and should have a repeat test to confirm the diagnosis, with referral for further evaluation and treatment.

The new guidance is based on increasing evidence that the 1-hour test is a better predictor than other tests, including the 2-hour OGTT, of progression to type 2 diabetes and its associated complications, in a variety of populations. The document cites data showing that a plasma glucose of 155 mg/dl or greater on the 1-hour post-75-g test can identify people with undiagnosed type 2 diabetes or who are at increased risk but who have “normal” glucose tolerance as defined by an A1c < 5.7% (38.8 mmol/mol), a fasting plasma glucose < 100 mg/dL (5.6 mmol/L), or a 2-hour value below 140 mg/dL (7.8 mmol/L).

However, even though a 1-hour test may be more convenient than the traditional 2-hour test, incorporating OGTT into busy clinical practice may still pose logistical problems and may not improve ultimate outcomes, Elizabeth Selvin, PhD, MPH, of the Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, told this news organization. “I worry that emphasizing a burdensome test is not going to improve diabetes screening or diabetes prevention. Doing more 1-hour glucose screening is not going to get more people into diabetes prevention programs.”

When an audience member raised the logistics concern during the session Q&A, Dr. Bergman replied, “It’s no different than recommending colonoscopy or a mammogram. … I tell patients that we want to learn more about what is going on before we make a firm diagnosis. … I’ve done more than a hundred 1-hour glucose tolerance tests and have not seen one patient who refused because of inconvenience. Everything depends on the way we discuss things with patients.”
 

Recommendation Based on Emerging Evidence

“Intermediate hyperglycemia” is the World Health Organization’s term to refer to either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). These conditions are often called “prediabetes,” especially in the United States, but that term has been controversial because not everyone with IFG and IGT will go on to develop type 2 diabetes, said Dr. Bergman, who is also director of the NYU Langone Diabetes Prevention Program.

“With ‘prediabetes’ you’re labeling someone with a disease they may not develop. It’s not normal, but it’s not diabetes, so it’s an intermediate state,” he explained.

The statement provides a detailed summary of the data from 19 studies supporting use of a 1-hour plasma glucose of ≥ 155 mg/dL (8.6 mmol/L) to diagnose intermediate hyperglycemia and type 2 diabetes, including links between that level of glycemia and worsened metabolic and atherogenic profiles, risk for microvascular and macrovascular complications and mortality, and identification of risks for obstructive sleep apnea, cystic fibrosis-related diabetes mellitus, fatty liver disease, and premature mortality.

One major problem with current testing, Dr. Bergman said, is that “there is a huge disconnect between A1c and glucose values. … Only about 30% of individuals with an abnormal A1c will have an abnormal fasting glucose, and the inverse is also true. There’s a big mismatch between the two.”

Current guidelines suggest using both A1c and fasting glucose, but Dr. Bergman said that even then “you’re still missing about 20-30% who have IGT. … Part of the problem is that the criteria we use for defining abnormal fasting and 2-hour levels are too high. … 140 [mg/dL] for the 2-hour is too high and 100 [mg/dL] fasting is too high. … And that’s one of the reasons why many people progress to type 2 diabetes, because we’re using screening thresholds that are nonphysiologic.”

But Dr. Selvin disagrees, pointing to her own work showing that “using a combination of fasting glucose and A1c for screening does an excellent job at identifying high-risk individuals.”

She’s also unconvinced by other data cited in the paper. “I am deeply skeptical about 1-hour glucose being more prognostic than all other glycemic tests. … Associations of glucose tests with incident diabetes are inherently a circular analysis since diabetes is defined by elevations in those same tests. It is helpful to look at progression of diabetes, but these analyses are not simple and doing them well, especially with head-to-head comparisons against different glycemic tests, is hard,” she said.

In her view, “lifestyle interventions and weight loss should be recommended in at-risk individuals, including those with overweight and obesity, hypertension, metabolic syndrome, etc., regardless of 1-hour glucose test results.”

She added, “If we want to prevent diabetes, we need to focus on preventing weight gain and obesity and managing cardiometabolic risk factors. Lifestyle interventions are not effective unless they are intensive and patients are highly adherent. We need to make lifestyle interventions available and affordable for patients. That is the big barrier. I don’t think more screening with 1-hour glucose is going to help.”

Dr. Bergman pointed out that the International Diabetes Federation represents more than 100 countries, including many that are middle- and low-income. “They need a simple, cost-effective tool for screening effectively. A1c is more expensive, and fasting glucose alone will underestimate disease prevalence. So, the IDF felt, after doing a fairly comprehensive due diligence, that the data warranted recommendation of the 1-hour glucose.”

He’s hoping other organizations like the ADA and the World Health Organization will sign on to bring this guidance into the primary care arena. This news organization reached out to ADA for comment, but their representative hadn’t responded by press time.

Dr. Bergman had no disclosures. Dr. Selvin was supported by the National Institutes of Health.

A version of this article appeared on Medscape.com.

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

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

Four-Cohort Meta-Analysis

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

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

Excess Mortality Confirmed

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

The Earlier, the Better

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

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

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

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

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

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

Four-Cohort Meta-Analysis

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

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

Excess Mortality Confirmed

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

The Earlier, the Better

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

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

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

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

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

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

Four-Cohort Meta-Analysis

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

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

Excess Mortality Confirmed

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

The Earlier, the Better

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

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

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

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

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

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

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

CV Effects

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

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

Snoring and Hypertension

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

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

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

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

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

Implications for Practice

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

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

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

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

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

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

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

CV Effects

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

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

Snoring and Hypertension

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

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

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

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

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

Implications for Practice

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

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

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

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

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

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

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

CV Effects

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

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

Snoring and Hypertension

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

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

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

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

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

Implications for Practice

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

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

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

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

TOPLINE:

Patients on weekly glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have high residual gastric content, a major risk factor for aspiration under anesthesia, despite following fasting guidelines before undergoing elective procedures.

METHODOLOGY:

• The increasing use of GLP-1 RAs to manage weight and hyperglycemia has sparked safety concerns because of the drugs’ association with slow gastric emptying, a major risk factor for aspiration under anesthesia.
• This cross-sectional study used gastric ultrasonography to examine the link between GLP-1 RA use and the prevalence of increased residual gastric content.
• All 124 participants (median age, 56 years; 60% women) — half of whom received once-weekly GLP-1 RAs such as semaglutide, dulaglutide, or tirzepatide — adhered to the guideline-recommended fasting duration before undergoing elective procedures under anesthesia.
• The primary outcome focused on identifying increased residual gastric content, defined by the presence of solids, thick liquids, or > 1.5 mL/kg of clear liquids on ultrasound.
• An exploratory analysis examined the association between the duration of GLP-1 RA discontinuation and increased residual gastric content.

TAKEAWAY:

• The adjusted prevalence of increased residual gastric content was 30.5% (95% CI, 9.9%-51.2%) higher in participants who received GLP-1 RA than those who did not.
• Most patients took their last dose of GLP-1 RA within 5 days before their procedure, but elevated residual gastric content persisted even after 7 days of GLP-1 RA discontinuation.
• There was also no significant association between the type of GLP-1 RA used and the prevalence of increased residual gastric content.

IN PRACTICE:

“We expect healthcare professionals will encounter these classes of drugs with increasing frequency in the perioperative period. Perioperative physicians, including anesthesiologists, surgeons, and primary care physicians, should be well-informed about the safety implications of GLP-1 RA drugs,” the authors wrote.

SOURCE:

The study was led by Sudipta Sen, MD, from the Department of Anesthesiology, Critical Care and Pain Medicine, McGovern Medical School, University of Texas Health Center at Houston, Houston, Texas, and published online in JAMA Surgery.

LIMITATIONS:

Residual gastric content, the primary outcome, served as a proxy for aspiration risk and does not have an exact threshold of volume associated with increased risk. The study did not directly evaluate aspiration events. The authors also acknowledged potential bias from unmeasured confounders owing to the observational nature of this study. A small sample size limited the ability to detect a risk difference for each additional day of drug discontinuation before surgery.

DISCLOSURES:

One of the authors reported receiving a grant from the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients on weekly glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have high residual gastric content, a major risk factor for aspiration under anesthesia, despite following fasting guidelines before undergoing elective procedures.

METHODOLOGY:

• The increasing use of GLP-1 RAs to manage weight and hyperglycemia has sparked safety concerns because of the drugs’ association with slow gastric emptying, a major risk factor for aspiration under anesthesia.
• This cross-sectional study used gastric ultrasonography to examine the link between GLP-1 RA use and the prevalence of increased residual gastric content.
• All 124 participants (median age, 56 years; 60% women) — half of whom received once-weekly GLP-1 RAs such as semaglutide, dulaglutide, or tirzepatide — adhered to the guideline-recommended fasting duration before undergoing elective procedures under anesthesia.
• The primary outcome focused on identifying increased residual gastric content, defined by the presence of solids, thick liquids, or > 1.5 mL/kg of clear liquids on ultrasound.
• An exploratory analysis examined the association between the duration of GLP-1 RA discontinuation and increased residual gastric content.

TAKEAWAY:

• The adjusted prevalence of increased residual gastric content was 30.5% (95% CI, 9.9%-51.2%) higher in participants who received GLP-1 RA than those who did not.
• Most patients took their last dose of GLP-1 RA within 5 days before their procedure, but elevated residual gastric content persisted even after 7 days of GLP-1 RA discontinuation.
• There was also no significant association between the type of GLP-1 RA used and the prevalence of increased residual gastric content.

IN PRACTICE:

“We expect healthcare professionals will encounter these classes of drugs with increasing frequency in the perioperative period. Perioperative physicians, including anesthesiologists, surgeons, and primary care physicians, should be well-informed about the safety implications of GLP-1 RA drugs,” the authors wrote.

SOURCE:

The study was led by Sudipta Sen, MD, from the Department of Anesthesiology, Critical Care and Pain Medicine, McGovern Medical School, University of Texas Health Center at Houston, Houston, Texas, and published online in JAMA Surgery.

LIMITATIONS:

Residual gastric content, the primary outcome, served as a proxy for aspiration risk and does not have an exact threshold of volume associated with increased risk. The study did not directly evaluate aspiration events. The authors also acknowledged potential bias from unmeasured confounders owing to the observational nature of this study. A small sample size limited the ability to detect a risk difference for each additional day of drug discontinuation before surgery.

DISCLOSURES:

One of the authors reported receiving a grant from the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients on weekly glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have high residual gastric content, a major risk factor for aspiration under anesthesia, despite following fasting guidelines before undergoing elective procedures.

METHODOLOGY:

• The increasing use of GLP-1 RAs to manage weight and hyperglycemia has sparked safety concerns because of the drugs’ association with slow gastric emptying, a major risk factor for aspiration under anesthesia.
• This cross-sectional study used gastric ultrasonography to examine the link between GLP-1 RA use and the prevalence of increased residual gastric content.
• All 124 participants (median age, 56 years; 60% women) — half of whom received once-weekly GLP-1 RAs such as semaglutide, dulaglutide, or tirzepatide — adhered to the guideline-recommended fasting duration before undergoing elective procedures under anesthesia.
• The primary outcome focused on identifying increased residual gastric content, defined by the presence of solids, thick liquids, or > 1.5 mL/kg of clear liquids on ultrasound.
• An exploratory analysis examined the association between the duration of GLP-1 RA discontinuation and increased residual gastric content.

TAKEAWAY:

• The adjusted prevalence of increased residual gastric content was 30.5% (95% CI, 9.9%-51.2%) higher in participants who received GLP-1 RA than those who did not.
• Most patients took their last dose of GLP-1 RA within 5 days before their procedure, but elevated residual gastric content persisted even after 7 days of GLP-1 RA discontinuation.
• There was also no significant association between the type of GLP-1 RA used and the prevalence of increased residual gastric content.

IN PRACTICE:

“We expect healthcare professionals will encounter these classes of drugs with increasing frequency in the perioperative period. Perioperative physicians, including anesthesiologists, surgeons, and primary care physicians, should be well-informed about the safety implications of GLP-1 RA drugs,” the authors wrote.

SOURCE:

The study was led by Sudipta Sen, MD, from the Department of Anesthesiology, Critical Care and Pain Medicine, McGovern Medical School, University of Texas Health Center at Houston, Houston, Texas, and published online in JAMA Surgery.

LIMITATIONS:

Residual gastric content, the primary outcome, served as a proxy for aspiration risk and does not have an exact threshold of volume associated with increased risk. The study did not directly evaluate aspiration events. The authors also acknowledged potential bias from unmeasured confounders owing to the observational nature of this study. A small sample size limited the ability to detect a risk difference for each additional day of drug discontinuation before surgery.

DISCLOSURES:

One of the authors reported receiving a grant from the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

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

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

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

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

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

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

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

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

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

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

 What Are the Limitations of This Research?

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

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

What Is the Takeaway Message for Clinical Practice?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 What Are the Limitations of This Research?

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

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

What Is the Takeaway Message for Clinical Practice?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 What Are the Limitations of This Research?

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

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

What Is the Takeaway Message for Clinical Practice?

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

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

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

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

Scientists at the University of California, San Francisco, have discovered that remnants of the COVID-19 virus can linger in blood and tissue for more than a year after a person is first infected.

In their research on long COVID, the scientists found COVID antigens in the blood for up to 14 months after infection, and in tissue samples for more than 2 years after infection. 

“These two studies provide some of the strongest evidence so far that COVID antigens can persist in some people, even though we think they have normal immune responses,” Michael Peluso, MD, an infectious disease researcher in the UCSF School of Medicine, who led both studies, said in a statement. 

Scientists don’t know what causes long COVID, in which symptoms of the illness persist months or years after recovery. The most common symptoms are extreme fatigue, shortness of breath, loss of smell, and muscle aches.

The UCSF research team examined blood samples from 171 infected people and found the COVID “spike” protein was still present up to 14 months after infection in some people. The antigens were found more often in people who were hospitalized with COVID or who reported being very sick but were not hospitalized.

Researchers next looked at the UCSF Long COVID Tissue Bank, which contains samples donated by patients with and without long COVID. 

They found portions of viral RNA in the tissue up to 2 years after people were infected, though there was no evidence of reinfection. Those viral fragments were found in connective tissue where immune cells are, suggesting that the fragments caused the immune system to attack, according to the researchers. 

The UCSF team is running clinical trials to find out if monoclonal antibodies or antiviral drugs can remove the virus. 

The findings were presented in Denver this week at the Conference on Retroviruses and Opportunistic Infections.

A version of this article appeared on WebMD.com.

Scientists at the University of California, San Francisco, have discovered that remnants of the COVID-19 virus can linger in blood and tissue for more than a year after a person is first infected.

In their research on long COVID, the scientists found COVID antigens in the blood for up to 14 months after infection, and in tissue samples for more than 2 years after infection. 

“These two studies provide some of the strongest evidence so far that COVID antigens can persist in some people, even though we think they have normal immune responses,” Michael Peluso, MD, an infectious disease researcher in the UCSF School of Medicine, who led both studies, said in a statement. 

Scientists don’t know what causes long COVID, in which symptoms of the illness persist months or years after recovery. The most common symptoms are extreme fatigue, shortness of breath, loss of smell, and muscle aches.

The UCSF research team examined blood samples from 171 infected people and found the COVID “spike” protein was still present up to 14 months after infection in some people. The antigens were found more often in people who were hospitalized with COVID or who reported being very sick but were not hospitalized.

Researchers next looked at the UCSF Long COVID Tissue Bank, which contains samples donated by patients with and without long COVID. 

They found portions of viral RNA in the tissue up to 2 years after people were infected, though there was no evidence of reinfection. Those viral fragments were found in connective tissue where immune cells are, suggesting that the fragments caused the immune system to attack, according to the researchers. 

The UCSF team is running clinical trials to find out if monoclonal antibodies or antiviral drugs can remove the virus. 

The findings were presented in Denver this week at the Conference on Retroviruses and Opportunistic Infections.

A version of this article appeared on WebMD.com.

Scientists at the University of California, San Francisco, have discovered that remnants of the COVID-19 virus can linger in blood and tissue for more than a year after a person is first infected.

In their research on long COVID, the scientists found COVID antigens in the blood for up to 14 months after infection, and in tissue samples for more than 2 years after infection. 

“These two studies provide some of the strongest evidence so far that COVID antigens can persist in some people, even though we think they have normal immune responses,” Michael Peluso, MD, an infectious disease researcher in the UCSF School of Medicine, who led both studies, said in a statement. 

Scientists don’t know what causes long COVID, in which symptoms of the illness persist months or years after recovery. The most common symptoms are extreme fatigue, shortness of breath, loss of smell, and muscle aches.

The UCSF research team examined blood samples from 171 infected people and found the COVID “spike” protein was still present up to 14 months after infection in some people. The antigens were found more often in people who were hospitalized with COVID or who reported being very sick but were not hospitalized.

Researchers next looked at the UCSF Long COVID Tissue Bank, which contains samples donated by patients with and without long COVID. 

They found portions of viral RNA in the tissue up to 2 years after people were infected, though there was no evidence of reinfection. Those viral fragments were found in connective tissue where immune cells are, suggesting that the fragments caused the immune system to attack, according to the researchers. 

The UCSF team is running clinical trials to find out if monoclonal antibodies or antiviral drugs can remove the virus. 

The findings were presented in Denver this week at the Conference on Retroviruses and Opportunistic Infections.

A version of this article appeared on WebMD.com.