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Coffee drinking may cut heart disease risk, prolong survival
A trio of analyses based on the prospective UK Biobank cohort suggest that regular coffee drinking, especially a daily intake of two to three cups, is not only safe for the heart but may be cardioprotective.
People without cardiovascular disease with that level of coffee intake, compared with those who weren’t coffee drinkers, showed significantly reduced risks of death and a range of CVD endpoints, the reductions ranging from 8% to 15% over about 10 years.
In a separate analysis, participants with CVD at baseline also showed significantly improved survival with coffee intake of two to three cups daily, and no increased risk of arrhythmias.
In a third cut of the UK Biobank data, the clinical benefits of the same level of coffee drinking were observed whether the coffee consumed was the “instant” kind for reconstitution with water or brewed from ground whole beans.
Some clinicians advise their patients that coffee drinking may trigger or worsen some types of heart disease, observed Peter M. Kistler, MD, the Alfred Hospital and Baker Heart and Diabetes Institute, Melbourne. But the current analyses suggest that “daily coffee intake should not be discouraged, but rather considered part of a healthy diet.”
Dr. Kistler and colleagues are slated to present the three UK Biobank cohort analyses separately at the annual scientific sessions of the American College of Cardiology. He presented some of the data and commented on them at a press conference held in advance of the meeting.
UK Biobank study participants, who were on average in their late 50s, reported their level of daily coffee intake and preferred type of coffee on questionnaires. The researchers observed generally U-shaped relationships between daily number of cups of coffee and incident CVD, heart failure, coronary heart disease (CHD), stroke, atrial fibrillation, any arrhythmia, and death over 10 years.
“This is music to I think many of our patients’ ears, as well as many in the field of cardiology, as those of us that wake up early and stay up late in the hospital consume a fair amount of coffee,” observed Katie Berlacher, MD, associate chief of cardiology education at the University of Pittsburgh Medical Center.
The analyses were based on a large cohort and saw a consistent pattern for several cardiovascular outcomes, observed Dr. Berlacher, incoming ACC scientific session vice chair.
The findings could have a “profound impact in daily clinical care, as many of us caution patients who have or are at risk for having CV[D] against coffee consumption,” she told this news organization by email.
“These studies suggest that we do not have objective evidence to caution nor ask patients to stop drinking coffee, including patients who have arrhythmias.”
But importantly, “these studies are not causal,” she added. “So we cannot go so far as to recommend coffee consumption, though one could posit that randomized prospective studies should be done to elucidate causation.”
Coffee, Dr. Kistler observed, “is the most common cognitive enhancer. It wakes you up, makes you mentally sharper, and it’s a very important component of many people’s daily lives. The take-home message is that clinicians should NOT advise patients to stop drinking coffee up to three cups per day.”
Also, “in non–coffee drinkers, we do not have the data to suggest they should start drinking coffee,” he said. Moreover, people shouldn’t necessarily increase their coffee intake, particularly if it makes them feel anxious or uncomfortable.
Benefits with or without known heart disease
The researchers identified 382,535 participants in the UK Biobank cohort who were free of CVD at baseline. Their median age was 57, and 52% were women.
Those who reported regular daily intake of two to three cups of coffee, compared with those who were not coffee drinkers, showed significantly reduced risks of CVD (hazard ratio, 0.91; 95% confidence interval, 0.88-0.94), CHD (HR, 0.90; 95% CI, 0.87-0.93), heart failure (HR, 0.85; 95% CI, 0.81-0.90), arrhythmias (HR, 0.92; 95% CI, 0.88-0.95), and death from any cause over 10 years (HR, 0.86; 95% CI, 0.83-0.90) (P < .01 for all endpoints).
The risk of CVD death hit its lowest point at an intake of one cup per day (HR, 0.83; 95% CI, 0.75-0.93). The risk of stroke was lowest at less than one cup per day (HR, 0.85; 95% CI, 0.75-0.96).
A separate analysis found similar outcomes among a different subset of UK Biobank participants with recognized CVD at baseline. Among 34,279 such persons, those who drank two to three cups of coffee per day, compared with non–coffee drinkers, showed a reduced risk of death over 10 years (HR, 0.92; 95% CI, 0.86-0.99; P = .03).
Among the 24,111 persons diagnosed with arrhythmias at baseline, the lowest mortality risk was observed at one cup per day (HR, 0.85; 95% CI, 0.78-0.94; P < .01). Among those with atrial fibrillation or atrial flutter, one cup per day was associated with a mortality HR of 0.82 (95% CI, 0.73-0.93; P < .01).
In still another analysis of UK Biobank cohort, incident CVD and mortality during the 10-year follow-up was similarly reduced among participants who reported consumption of brewed ground coffee and, separately, instant coffee, compared with non–coffee drinkers. Decaffeinated coffee showed a mostly neutral or inconsistent effect on the clinical endpoints.
The lowest CVD risk was observed at two to three cups per day among those regularly drinking ground coffee (HR, 0.83; 95% CI, 0.79-0.87) and those predominantly taking instant coffee (HR, 0.91; 95% CI, 0.88-0.95).
Potential mechanisms, study limitations
“Caffeine blocks adenosine receptors, which may explain its potential mild antiarrhythmic properties,” Dr. Kistler said. “Regular coffee drinkers with supraventricular tachycardia coming to the emergency department often need higher adenosine doses to revert.”
Caffeine has a role in weight loss through inhibition of gut fatty acid absorption and increase in basal metabolic rate, Dr. Kistler added, and coffee has been associated with a significantly reduced risk of new-onset type 2 diabetes.
However, coffee beans contain more than 100 biologically active compounds, he noted. They include antioxidant polyphenols that reduce oxidative stress and modulate metabolism. Better survival with habitual coffee consumption may be related to improved endothelial function, circulating antioxidants, improved insulin sensitivity, or reduced inflammation, the researchers noted.
They acknowledged some limitations to the analyses. Cause and effect can’t be determined from the observational data. Also, a cup of coffee in the United Kingdom means about 200-250 mL of brew, but its actual caffeine content can vary from 90 mg to 250 mg. Also, data regarding added sugar or milk was lacking. And UK Biobank participants are predominantly White, so the findings may not be generalizable to other populations.
A version of this article first appeared on Medscape.com.
A trio of analyses based on the prospective UK Biobank cohort suggest that regular coffee drinking, especially a daily intake of two to three cups, is not only safe for the heart but may be cardioprotective.
People without cardiovascular disease with that level of coffee intake, compared with those who weren’t coffee drinkers, showed significantly reduced risks of death and a range of CVD endpoints, the reductions ranging from 8% to 15% over about 10 years.
In a separate analysis, participants with CVD at baseline also showed significantly improved survival with coffee intake of two to three cups daily, and no increased risk of arrhythmias.
In a third cut of the UK Biobank data, the clinical benefits of the same level of coffee drinking were observed whether the coffee consumed was the “instant” kind for reconstitution with water or brewed from ground whole beans.
Some clinicians advise their patients that coffee drinking may trigger or worsen some types of heart disease, observed Peter M. Kistler, MD, the Alfred Hospital and Baker Heart and Diabetes Institute, Melbourne. But the current analyses suggest that “daily coffee intake should not be discouraged, but rather considered part of a healthy diet.”
Dr. Kistler and colleagues are slated to present the three UK Biobank cohort analyses separately at the annual scientific sessions of the American College of Cardiology. He presented some of the data and commented on them at a press conference held in advance of the meeting.
UK Biobank study participants, who were on average in their late 50s, reported their level of daily coffee intake and preferred type of coffee on questionnaires. The researchers observed generally U-shaped relationships between daily number of cups of coffee and incident CVD, heart failure, coronary heart disease (CHD), stroke, atrial fibrillation, any arrhythmia, and death over 10 years.
“This is music to I think many of our patients’ ears, as well as many in the field of cardiology, as those of us that wake up early and stay up late in the hospital consume a fair amount of coffee,” observed Katie Berlacher, MD, associate chief of cardiology education at the University of Pittsburgh Medical Center.
The analyses were based on a large cohort and saw a consistent pattern for several cardiovascular outcomes, observed Dr. Berlacher, incoming ACC scientific session vice chair.
The findings could have a “profound impact in daily clinical care, as many of us caution patients who have or are at risk for having CV[D] against coffee consumption,” she told this news organization by email.
“These studies suggest that we do not have objective evidence to caution nor ask patients to stop drinking coffee, including patients who have arrhythmias.”
But importantly, “these studies are not causal,” she added. “So we cannot go so far as to recommend coffee consumption, though one could posit that randomized prospective studies should be done to elucidate causation.”
Coffee, Dr. Kistler observed, “is the most common cognitive enhancer. It wakes you up, makes you mentally sharper, and it’s a very important component of many people’s daily lives. The take-home message is that clinicians should NOT advise patients to stop drinking coffee up to three cups per day.”
Also, “in non–coffee drinkers, we do not have the data to suggest they should start drinking coffee,” he said. Moreover, people shouldn’t necessarily increase their coffee intake, particularly if it makes them feel anxious or uncomfortable.
Benefits with or without known heart disease
The researchers identified 382,535 participants in the UK Biobank cohort who were free of CVD at baseline. Their median age was 57, and 52% were women.
Those who reported regular daily intake of two to three cups of coffee, compared with those who were not coffee drinkers, showed significantly reduced risks of CVD (hazard ratio, 0.91; 95% confidence interval, 0.88-0.94), CHD (HR, 0.90; 95% CI, 0.87-0.93), heart failure (HR, 0.85; 95% CI, 0.81-0.90), arrhythmias (HR, 0.92; 95% CI, 0.88-0.95), and death from any cause over 10 years (HR, 0.86; 95% CI, 0.83-0.90) (P < .01 for all endpoints).
The risk of CVD death hit its lowest point at an intake of one cup per day (HR, 0.83; 95% CI, 0.75-0.93). The risk of stroke was lowest at less than one cup per day (HR, 0.85; 95% CI, 0.75-0.96).
A separate analysis found similar outcomes among a different subset of UK Biobank participants with recognized CVD at baseline. Among 34,279 such persons, those who drank two to three cups of coffee per day, compared with non–coffee drinkers, showed a reduced risk of death over 10 years (HR, 0.92; 95% CI, 0.86-0.99; P = .03).
Among the 24,111 persons diagnosed with arrhythmias at baseline, the lowest mortality risk was observed at one cup per day (HR, 0.85; 95% CI, 0.78-0.94; P < .01). Among those with atrial fibrillation or atrial flutter, one cup per day was associated with a mortality HR of 0.82 (95% CI, 0.73-0.93; P < .01).
In still another analysis of UK Biobank cohort, incident CVD and mortality during the 10-year follow-up was similarly reduced among participants who reported consumption of brewed ground coffee and, separately, instant coffee, compared with non–coffee drinkers. Decaffeinated coffee showed a mostly neutral or inconsistent effect on the clinical endpoints.
The lowest CVD risk was observed at two to three cups per day among those regularly drinking ground coffee (HR, 0.83; 95% CI, 0.79-0.87) and those predominantly taking instant coffee (HR, 0.91; 95% CI, 0.88-0.95).
Potential mechanisms, study limitations
“Caffeine blocks adenosine receptors, which may explain its potential mild antiarrhythmic properties,” Dr. Kistler said. “Regular coffee drinkers with supraventricular tachycardia coming to the emergency department often need higher adenosine doses to revert.”
Caffeine has a role in weight loss through inhibition of gut fatty acid absorption and increase in basal metabolic rate, Dr. Kistler added, and coffee has been associated with a significantly reduced risk of new-onset type 2 diabetes.
However, coffee beans contain more than 100 biologically active compounds, he noted. They include antioxidant polyphenols that reduce oxidative stress and modulate metabolism. Better survival with habitual coffee consumption may be related to improved endothelial function, circulating antioxidants, improved insulin sensitivity, or reduced inflammation, the researchers noted.
They acknowledged some limitations to the analyses. Cause and effect can’t be determined from the observational data. Also, a cup of coffee in the United Kingdom means about 200-250 mL of brew, but its actual caffeine content can vary from 90 mg to 250 mg. Also, data regarding added sugar or milk was lacking. And UK Biobank participants are predominantly White, so the findings may not be generalizable to other populations.
A version of this article first appeared on Medscape.com.
A trio of analyses based on the prospective UK Biobank cohort suggest that regular coffee drinking, especially a daily intake of two to three cups, is not only safe for the heart but may be cardioprotective.
People without cardiovascular disease with that level of coffee intake, compared with those who weren’t coffee drinkers, showed significantly reduced risks of death and a range of CVD endpoints, the reductions ranging from 8% to 15% over about 10 years.
In a separate analysis, participants with CVD at baseline also showed significantly improved survival with coffee intake of two to three cups daily, and no increased risk of arrhythmias.
In a third cut of the UK Biobank data, the clinical benefits of the same level of coffee drinking were observed whether the coffee consumed was the “instant” kind for reconstitution with water or brewed from ground whole beans.
Some clinicians advise their patients that coffee drinking may trigger or worsen some types of heart disease, observed Peter M. Kistler, MD, the Alfred Hospital and Baker Heart and Diabetes Institute, Melbourne. But the current analyses suggest that “daily coffee intake should not be discouraged, but rather considered part of a healthy diet.”
Dr. Kistler and colleagues are slated to present the three UK Biobank cohort analyses separately at the annual scientific sessions of the American College of Cardiology. He presented some of the data and commented on them at a press conference held in advance of the meeting.
UK Biobank study participants, who were on average in their late 50s, reported their level of daily coffee intake and preferred type of coffee on questionnaires. The researchers observed generally U-shaped relationships between daily number of cups of coffee and incident CVD, heart failure, coronary heart disease (CHD), stroke, atrial fibrillation, any arrhythmia, and death over 10 years.
“This is music to I think many of our patients’ ears, as well as many in the field of cardiology, as those of us that wake up early and stay up late in the hospital consume a fair amount of coffee,” observed Katie Berlacher, MD, associate chief of cardiology education at the University of Pittsburgh Medical Center.
The analyses were based on a large cohort and saw a consistent pattern for several cardiovascular outcomes, observed Dr. Berlacher, incoming ACC scientific session vice chair.
The findings could have a “profound impact in daily clinical care, as many of us caution patients who have or are at risk for having CV[D] against coffee consumption,” she told this news organization by email.
“These studies suggest that we do not have objective evidence to caution nor ask patients to stop drinking coffee, including patients who have arrhythmias.”
But importantly, “these studies are not causal,” she added. “So we cannot go so far as to recommend coffee consumption, though one could posit that randomized prospective studies should be done to elucidate causation.”
Coffee, Dr. Kistler observed, “is the most common cognitive enhancer. It wakes you up, makes you mentally sharper, and it’s a very important component of many people’s daily lives. The take-home message is that clinicians should NOT advise patients to stop drinking coffee up to three cups per day.”
Also, “in non–coffee drinkers, we do not have the data to suggest they should start drinking coffee,” he said. Moreover, people shouldn’t necessarily increase their coffee intake, particularly if it makes them feel anxious or uncomfortable.
Benefits with or without known heart disease
The researchers identified 382,535 participants in the UK Biobank cohort who were free of CVD at baseline. Their median age was 57, and 52% were women.
Those who reported regular daily intake of two to three cups of coffee, compared with those who were not coffee drinkers, showed significantly reduced risks of CVD (hazard ratio, 0.91; 95% confidence interval, 0.88-0.94), CHD (HR, 0.90; 95% CI, 0.87-0.93), heart failure (HR, 0.85; 95% CI, 0.81-0.90), arrhythmias (HR, 0.92; 95% CI, 0.88-0.95), and death from any cause over 10 years (HR, 0.86; 95% CI, 0.83-0.90) (P < .01 for all endpoints).
The risk of CVD death hit its lowest point at an intake of one cup per day (HR, 0.83; 95% CI, 0.75-0.93). The risk of stroke was lowest at less than one cup per day (HR, 0.85; 95% CI, 0.75-0.96).
A separate analysis found similar outcomes among a different subset of UK Biobank participants with recognized CVD at baseline. Among 34,279 such persons, those who drank two to three cups of coffee per day, compared with non–coffee drinkers, showed a reduced risk of death over 10 years (HR, 0.92; 95% CI, 0.86-0.99; P = .03).
Among the 24,111 persons diagnosed with arrhythmias at baseline, the lowest mortality risk was observed at one cup per day (HR, 0.85; 95% CI, 0.78-0.94; P < .01). Among those with atrial fibrillation or atrial flutter, one cup per day was associated with a mortality HR of 0.82 (95% CI, 0.73-0.93; P < .01).
In still another analysis of UK Biobank cohort, incident CVD and mortality during the 10-year follow-up was similarly reduced among participants who reported consumption of brewed ground coffee and, separately, instant coffee, compared with non–coffee drinkers. Decaffeinated coffee showed a mostly neutral or inconsistent effect on the clinical endpoints.
The lowest CVD risk was observed at two to three cups per day among those regularly drinking ground coffee (HR, 0.83; 95% CI, 0.79-0.87) and those predominantly taking instant coffee (HR, 0.91; 95% CI, 0.88-0.95).
Potential mechanisms, study limitations
“Caffeine blocks adenosine receptors, which may explain its potential mild antiarrhythmic properties,” Dr. Kistler said. “Regular coffee drinkers with supraventricular tachycardia coming to the emergency department often need higher adenosine doses to revert.”
Caffeine has a role in weight loss through inhibition of gut fatty acid absorption and increase in basal metabolic rate, Dr. Kistler added, and coffee has been associated with a significantly reduced risk of new-onset type 2 diabetes.
However, coffee beans contain more than 100 biologically active compounds, he noted. They include antioxidant polyphenols that reduce oxidative stress and modulate metabolism. Better survival with habitual coffee consumption may be related to improved endothelial function, circulating antioxidants, improved insulin sensitivity, or reduced inflammation, the researchers noted.
They acknowledged some limitations to the analyses. Cause and effect can’t be determined from the observational data. Also, a cup of coffee in the United Kingdom means about 200-250 mL of brew, but its actual caffeine content can vary from 90 mg to 250 mg. Also, data regarding added sugar or milk was lacking. And UK Biobank participants are predominantly White, so the findings may not be generalizable to other populations.
A version of this article first appeared on Medscape.com.
FROM ACC 2022
Intermittent fasting good for weight loss, at least short term
The health benefits of intermittent fasting are slowly being clarified as more evidence continues to emerge, say the authors of a new review of 21 studies. Initial findings suggest that fasting might be effective for mild to moderate weight loss for certain groups of people, at least in the short term.
And data so far at least dispel the myth that “people are going to feel weak and not be able to concentrate during fasting,” lead researcher Krista A. Varady, PhD, professor of nutrition in the University of Illinois at Chicago, noted in a press release from her university.
“We’ve shown it is the opposite,” she said. “They actually have a better ability to concentrate.”
Yet much longer-term data are needed on issues such as safety, Dr. Varady and colleagues note in their review in Nature Reviews: Endocrinology .
The trials so far have only been conducted in adults – generally with overweight or obesity and sometimes hypertension, dyslipidemia, and/or diabetes – but some have been performed in those of normal weight.
Dr. Varady and colleague recommend that those with type 1 diabetes, type 2 diabetes, or other comorbidities, or patients who need to take medications with meals at certain times of the day, should seek clinical supervision when considering intermittent fasting.
And currently, based on existing evidence, intermittent fasting is contraindicated for children under age 12 and those who have a history of an eating disorder or a body mass index <18.5 kg/m2. Opinions vary about the safety of supervised fasting in adolescents with obesity. Also, safety has not been evaluated in those older than age 70, and in women who are pregnant or lactating.
‘A few studies’ show 3%-8% weight loss over 2-3 months
Despite the recent surge in the popularity of intermittent fasting, “only a few studies have examined the health benefits of these diets in humans,” Dr. Varady and coauthors emphasize.
They identified 21 clinical trials of three types of intermittent fasting strategies:
Alternate day fasting (alternating between consuming 0-500 kcal on “fasting” days, followed by unlimited food on “feasting” days), six trials.
5:2 diet (“feasting” on 5 days and “fasting” on 2 days), seven trials.
Time-restricted eating (eating during a 4- to 8- hour window), nine trials.
The trials were short (mostly 5-12 weeks long) and small (10-150 participants), and mostly conducted in the United States.
They found these strategies can all produce a mild to moderate 3%-8% weight loss during 8-12 weeks, similar to that attained with a calorie-restricted diet.
Some studies found that patients had improvements in blood pressure, LDL cholesterol, triglycerides, insulin resistance, and hemoglobin A1c.
These weight-loss strategies produced few gastrointestinal, neurological, hormonal, or metabolic adverse effects; “however, as adverse outcomes are not regularly assessed in human trials of fasting, definitive conclusions regarding the safety of these diets are difficult to draw at present,” the researchers caution.
Practical advice, great anecdotes
Typically, 1-2 weeks of adjustment is needed when individuals start intermittent fasting, the researchers say.
While following this eating pattern, patients should be encouraged to consume plenty of fruits, vegetables, and whole grains to boost their fiber and micronutrient intake.
On fasting days, they should consume at least 50 g of lean protein to help control hunger and prevent excessive loss of lean mass. On those days, alcohol is permitted but not recommended. Energy drinks and coffee or tea without sugar, milk, or cream are allowed, and diet soda should be limited to two servings a day because it can increase sugar cravings.
Ideally, clinicians should regularly assess patients for adverse effects during the first 3 months of intermittent fasting. They should also monitor patients for deficiencies in vitamin D, vitamin B12, and electrolytes, as well as for changes in medications for blood pressure, lipids, and glucose that may be needed if patients lose weight.
Patients who reach their weight-loss goals and wish to stop intermittent fasting need to transition to a weight-maintenance program, possibly by increasing energy intake on fasting days to 1,000-1,200 kcal/day or widening the eating window to 12 hours in time-restricted eating.
“I get lots of emails from people saying that they have been on the diet for 10-15 years, and it reversed their type 2 diabetes, and they lost 60 pounds, and it was the only diet they could stick to,” Dr. Varady noted.
“That is always nice to hear, but we really do need long-term data to see if people can do intermittent fasting for the long term,” she reiterated.
The review was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Varady received author fees from the Hachette Book Group for the book, “The Every Other Day Diet.” The other authors have declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The health benefits of intermittent fasting are slowly being clarified as more evidence continues to emerge, say the authors of a new review of 21 studies. Initial findings suggest that fasting might be effective for mild to moderate weight loss for certain groups of people, at least in the short term.
And data so far at least dispel the myth that “people are going to feel weak and not be able to concentrate during fasting,” lead researcher Krista A. Varady, PhD, professor of nutrition in the University of Illinois at Chicago, noted in a press release from her university.
“We’ve shown it is the opposite,” she said. “They actually have a better ability to concentrate.”
Yet much longer-term data are needed on issues such as safety, Dr. Varady and colleagues note in their review in Nature Reviews: Endocrinology .
The trials so far have only been conducted in adults – generally with overweight or obesity and sometimes hypertension, dyslipidemia, and/or diabetes – but some have been performed in those of normal weight.
Dr. Varady and colleague recommend that those with type 1 diabetes, type 2 diabetes, or other comorbidities, or patients who need to take medications with meals at certain times of the day, should seek clinical supervision when considering intermittent fasting.
And currently, based on existing evidence, intermittent fasting is contraindicated for children under age 12 and those who have a history of an eating disorder or a body mass index <18.5 kg/m2. Opinions vary about the safety of supervised fasting in adolescents with obesity. Also, safety has not been evaluated in those older than age 70, and in women who are pregnant or lactating.
‘A few studies’ show 3%-8% weight loss over 2-3 months
Despite the recent surge in the popularity of intermittent fasting, “only a few studies have examined the health benefits of these diets in humans,” Dr. Varady and coauthors emphasize.
They identified 21 clinical trials of three types of intermittent fasting strategies:
Alternate day fasting (alternating between consuming 0-500 kcal on “fasting” days, followed by unlimited food on “feasting” days), six trials.
5:2 diet (“feasting” on 5 days and “fasting” on 2 days), seven trials.
Time-restricted eating (eating during a 4- to 8- hour window), nine trials.
The trials were short (mostly 5-12 weeks long) and small (10-150 participants), and mostly conducted in the United States.
They found these strategies can all produce a mild to moderate 3%-8% weight loss during 8-12 weeks, similar to that attained with a calorie-restricted diet.
Some studies found that patients had improvements in blood pressure, LDL cholesterol, triglycerides, insulin resistance, and hemoglobin A1c.
These weight-loss strategies produced few gastrointestinal, neurological, hormonal, or metabolic adverse effects; “however, as adverse outcomes are not regularly assessed in human trials of fasting, definitive conclusions regarding the safety of these diets are difficult to draw at present,” the researchers caution.
Practical advice, great anecdotes
Typically, 1-2 weeks of adjustment is needed when individuals start intermittent fasting, the researchers say.
While following this eating pattern, patients should be encouraged to consume plenty of fruits, vegetables, and whole grains to boost their fiber and micronutrient intake.
On fasting days, they should consume at least 50 g of lean protein to help control hunger and prevent excessive loss of lean mass. On those days, alcohol is permitted but not recommended. Energy drinks and coffee or tea without sugar, milk, or cream are allowed, and diet soda should be limited to two servings a day because it can increase sugar cravings.
Ideally, clinicians should regularly assess patients for adverse effects during the first 3 months of intermittent fasting. They should also monitor patients for deficiencies in vitamin D, vitamin B12, and electrolytes, as well as for changes in medications for blood pressure, lipids, and glucose that may be needed if patients lose weight.
Patients who reach their weight-loss goals and wish to stop intermittent fasting need to transition to a weight-maintenance program, possibly by increasing energy intake on fasting days to 1,000-1,200 kcal/day or widening the eating window to 12 hours in time-restricted eating.
“I get lots of emails from people saying that they have been on the diet for 10-15 years, and it reversed their type 2 diabetes, and they lost 60 pounds, and it was the only diet they could stick to,” Dr. Varady noted.
“That is always nice to hear, but we really do need long-term data to see if people can do intermittent fasting for the long term,” she reiterated.
The review was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Varady received author fees from the Hachette Book Group for the book, “The Every Other Day Diet.” The other authors have declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The health benefits of intermittent fasting are slowly being clarified as more evidence continues to emerge, say the authors of a new review of 21 studies. Initial findings suggest that fasting might be effective for mild to moderate weight loss for certain groups of people, at least in the short term.
And data so far at least dispel the myth that “people are going to feel weak and not be able to concentrate during fasting,” lead researcher Krista A. Varady, PhD, professor of nutrition in the University of Illinois at Chicago, noted in a press release from her university.
“We’ve shown it is the opposite,” she said. “They actually have a better ability to concentrate.”
Yet much longer-term data are needed on issues such as safety, Dr. Varady and colleagues note in their review in Nature Reviews: Endocrinology .
The trials so far have only been conducted in adults – generally with overweight or obesity and sometimes hypertension, dyslipidemia, and/or diabetes – but some have been performed in those of normal weight.
Dr. Varady and colleague recommend that those with type 1 diabetes, type 2 diabetes, or other comorbidities, or patients who need to take medications with meals at certain times of the day, should seek clinical supervision when considering intermittent fasting.
And currently, based on existing evidence, intermittent fasting is contraindicated for children under age 12 and those who have a history of an eating disorder or a body mass index <18.5 kg/m2. Opinions vary about the safety of supervised fasting in adolescents with obesity. Also, safety has not been evaluated in those older than age 70, and in women who are pregnant or lactating.
‘A few studies’ show 3%-8% weight loss over 2-3 months
Despite the recent surge in the popularity of intermittent fasting, “only a few studies have examined the health benefits of these diets in humans,” Dr. Varady and coauthors emphasize.
They identified 21 clinical trials of three types of intermittent fasting strategies:
Alternate day fasting (alternating between consuming 0-500 kcal on “fasting” days, followed by unlimited food on “feasting” days), six trials.
5:2 diet (“feasting” on 5 days and “fasting” on 2 days), seven trials.
Time-restricted eating (eating during a 4- to 8- hour window), nine trials.
The trials were short (mostly 5-12 weeks long) and small (10-150 participants), and mostly conducted in the United States.
They found these strategies can all produce a mild to moderate 3%-8% weight loss during 8-12 weeks, similar to that attained with a calorie-restricted diet.
Some studies found that patients had improvements in blood pressure, LDL cholesterol, triglycerides, insulin resistance, and hemoglobin A1c.
These weight-loss strategies produced few gastrointestinal, neurological, hormonal, or metabolic adverse effects; “however, as adverse outcomes are not regularly assessed in human trials of fasting, definitive conclusions regarding the safety of these diets are difficult to draw at present,” the researchers caution.
Practical advice, great anecdotes
Typically, 1-2 weeks of adjustment is needed when individuals start intermittent fasting, the researchers say.
While following this eating pattern, patients should be encouraged to consume plenty of fruits, vegetables, and whole grains to boost their fiber and micronutrient intake.
On fasting days, they should consume at least 50 g of lean protein to help control hunger and prevent excessive loss of lean mass. On those days, alcohol is permitted but not recommended. Energy drinks and coffee or tea without sugar, milk, or cream are allowed, and diet soda should be limited to two servings a day because it can increase sugar cravings.
Ideally, clinicians should regularly assess patients for adverse effects during the first 3 months of intermittent fasting. They should also monitor patients for deficiencies in vitamin D, vitamin B12, and electrolytes, as well as for changes in medications for blood pressure, lipids, and glucose that may be needed if patients lose weight.
Patients who reach their weight-loss goals and wish to stop intermittent fasting need to transition to a weight-maintenance program, possibly by increasing energy intake on fasting days to 1,000-1,200 kcal/day or widening the eating window to 12 hours in time-restricted eating.
“I get lots of emails from people saying that they have been on the diet for 10-15 years, and it reversed their type 2 diabetes, and they lost 60 pounds, and it was the only diet they could stick to,” Dr. Varady noted.
“That is always nice to hear, but we really do need long-term data to see if people can do intermittent fasting for the long term,” she reiterated.
The review was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Varady received author fees from the Hachette Book Group for the book, “The Every Other Day Diet.” The other authors have declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NATURE REVIEWS: ENDOCRINOLOGY
Brown fat, white fat. Is one better than the other?
“Adipose tissue is an underappreciated and misunderstood organ.” It’s with these words that Aaron M. Cypess, MD, PhD, begins his recent review published in the New England Journal of Medicine.
As obesity rates steadily rise, “the riskiest approach to human adipose tissue is to dismiss its importance,” he adds, especially because there has been “an explosive growth” in our understanding of white and brown adipose tissue over the past 5 to 10 years.
This news organization asked Dr. Cypess, a National Institutes of Health (NIH) scientist whose research focuses on brown fat, to discuss some of the main points in his review, titled, “Reassessing Human Adipose Tissue,” and clear up some misconceptions about fat.
You write that, for people who struggle to lose weight, “fat is often a source of misery, not marvel.” Why is fat a marvel?
When I started medical school in 1992, fat was just a thing that stored calories. You had to get it out of the way when you operated on the stomach or intestines. Now we know it’s not just one cell, it’s multiple types of cells, including immune cells and some blood cells. There’s cell turnover, and cells can get bigger or smaller, so it’s a dynamic tissue. It impacts the immune system and affects insulin sensitivity.
Why use the term “adipose tissue” and not just “fat”?
People think of fat cells and that’s it. However, adipose tissue (fat) has multiple cell types, and they each matter. There are adipocytes (fat cells) – which can be white, brown, beige, or pink – as well as immune cells, fibroblasts, blood vessels, and parts of nerve cells.
The main function of white adipose tissue is to store energy in the form of triglycerides. Brown adipose tissue consumes glucose and triglycerides, generating heat. Brown fat cells within depots of white fat are termed brite cells (a portmanteau of brown and white) or beige cells. Pink fat cells have been found in breast tissue in mice.
What do we now know about white fat and brown fat? Can brown fat change to white fat or vice versa?
White adipose tissue is commonly separated into visceral fat and subcutaneous fat, which have negative and neutral or positive metabolic effects, respectively. It is capable of more than doubling in mass and then returning to baseline.
White adipocyte-derived hormones include leptin, which is low in starvation, and adiponectin, which regulates glucose and lipid metabolism. White adipose tissue is essential for the proper function of the reproductive system, including secretion of hormones and lactation.
Brown adipose tissue protects newborns from cold as they develop the ability to shiver, and in adults it is found in depots in the neck, shoulders, posterior thorax, and abdomen. The amount of brown adipose tissue varies according to sex and lowers with increasing age and increasing body mass index.
There is much more white fat in the body than brown fat. It appears that activating brown fat leads to beneficial effects on metabolism, though we don’t know yet all the steps for how that happens.
In mice, you’ve got white fat depots and brown fat depots, and some brown fat can be found in the white fat.
With humans it’s much more complicated, and I’ve seen this in the operating room myself, and on slides. Where you find brown fat cells you also find a certain proportion of white fat cells, not an exclusive brown fat depot like you see in a mouse.
It is hotly debated right now whether brown fat can change to white fat and vice versa (transdifferentiation). The beige fat cells are supposed to be the kind that can shuttle between more white-like or brown-like. They can sometimes be white or sometimes brown. It can be very contentious in [scientific] papers and meetings.
Are humans born with all the fat cells they will ever have?
No. New fat cells are made throughout our lives. When the white adipocytes store too much triglyceride, they get really big and they get “sick” and die faster. It’s the rate at which the white cells take up the fat to store it and then get rid of it that can impact whether someone gains a lot of weight and whether they can successfully lose it after reasonable effort.
The average lifespan of a white fat cell is 15 years. We have no idea yet of the lifespan of a brown fat cell.
Is there a single “fat gene”? What role do fat genes play in the likelihood of developing metabolic diseases and type 2 diabetes?
Genes are very important for influencing the development of obesity and probably influence 50%-70% of obesity, based on studies in populations of predominantly European origin. But that high percentage reflects the impact of hundreds of genes. For most people, there is no one gene that exerts all of the effects. There are extremely rare diseases where one gene is responsible. Currently, only 20% of the entire phenotypic variation in obesity can be explained by the thousands of loci identified so far.
Why is it “correct but too simplistic” to attribute the increasing rates of obesity to excessive triglyceride storage in white adipose tissue?
Saying obesity is caused by too much triglyceride storage ignores the reasons how and why the triglycerides got there. There are likely to be multiple contributing factors to drive obesity, and those have billions of dollars of policy implications. Is obesity resulting from portion sizes? Then we should work on educating the public on how to estimate their caloric intake. Is it the types of foods, such as ultra-processed foods? Then we can discourage eating certain food groups while promoting others. Is it about physical activity? Then we should prioritize exercise programs.
Why is obesity “not simply a failure of will power”?
Genetic factors in adipose tissue impact how easy it is to store triglycerides, how easy it is to get fat out of the tissue and burn it up, and what kinds of hormones are released by the tissue to regulate appetite, insulin resistance, and inflammation. Ten different people can all overeat the same amount of the same foods, yet there will be differences in the amount of weight gain and metabolic complications experienced. And at the brain level, some people will feel “full” sooner than others.
How can excess adipose tissue lead to disease? Do some people have “metabolically healthy obesity”?
Excess adipose tissue leads to chronic inflammation that can then cause insulin resistance, hypertension, fatty liver disease, and other complications. It appears that there are metabolically healthy obese people, but it is not clear if that is only a temporary state.
Could long-term brown adipose tissue activation help treat obesity or related metabolic disease?
Our research group at the NIH and others have shown that long-term brown adipose tissue activation produces metabolic benefit such as improved insulin resistance, lower plasma glucose, and higher HDL [good] cholesterol. However, there is no evidence yet that it will lead to actual weight loss.
We are trying to use brown adipose tissue activation to treat obesity-related metabolic disease to see if it could lead to reduction in inflammation, improvement in the cholesterol profile, and decrease in blood pressure.
A large observational study published Jan. 4, 2021, in Nature Medicine by Paul Cohen’s group at Rockefeller University, in tens of thousands of people at Memorial Sloan Kettering Cancer Center, showed that people who had brown fat were generally healthier and had less high blood pressure and less cardiovascular disease. This study could not show causation, but at every BMI, people were healthier if they had more brown fat than if they had less. So, there’s something going on. We’re still trying to figure that out.
Dr. Cypess has no reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“Adipose tissue is an underappreciated and misunderstood organ.” It’s with these words that Aaron M. Cypess, MD, PhD, begins his recent review published in the New England Journal of Medicine.
As obesity rates steadily rise, “the riskiest approach to human adipose tissue is to dismiss its importance,” he adds, especially because there has been “an explosive growth” in our understanding of white and brown adipose tissue over the past 5 to 10 years.
This news organization asked Dr. Cypess, a National Institutes of Health (NIH) scientist whose research focuses on brown fat, to discuss some of the main points in his review, titled, “Reassessing Human Adipose Tissue,” and clear up some misconceptions about fat.
You write that, for people who struggle to lose weight, “fat is often a source of misery, not marvel.” Why is fat a marvel?
When I started medical school in 1992, fat was just a thing that stored calories. You had to get it out of the way when you operated on the stomach or intestines. Now we know it’s not just one cell, it’s multiple types of cells, including immune cells and some blood cells. There’s cell turnover, and cells can get bigger or smaller, so it’s a dynamic tissue. It impacts the immune system and affects insulin sensitivity.
Why use the term “adipose tissue” and not just “fat”?
People think of fat cells and that’s it. However, adipose tissue (fat) has multiple cell types, and they each matter. There are adipocytes (fat cells) – which can be white, brown, beige, or pink – as well as immune cells, fibroblasts, blood vessels, and parts of nerve cells.
The main function of white adipose tissue is to store energy in the form of triglycerides. Brown adipose tissue consumes glucose and triglycerides, generating heat. Brown fat cells within depots of white fat are termed brite cells (a portmanteau of brown and white) or beige cells. Pink fat cells have been found in breast tissue in mice.
What do we now know about white fat and brown fat? Can brown fat change to white fat or vice versa?
White adipose tissue is commonly separated into visceral fat and subcutaneous fat, which have negative and neutral or positive metabolic effects, respectively. It is capable of more than doubling in mass and then returning to baseline.
White adipocyte-derived hormones include leptin, which is low in starvation, and adiponectin, which regulates glucose and lipid metabolism. White adipose tissue is essential for the proper function of the reproductive system, including secretion of hormones and lactation.
Brown adipose tissue protects newborns from cold as they develop the ability to shiver, and in adults it is found in depots in the neck, shoulders, posterior thorax, and abdomen. The amount of brown adipose tissue varies according to sex and lowers with increasing age and increasing body mass index.
There is much more white fat in the body than brown fat. It appears that activating brown fat leads to beneficial effects on metabolism, though we don’t know yet all the steps for how that happens.
In mice, you’ve got white fat depots and brown fat depots, and some brown fat can be found in the white fat.
With humans it’s much more complicated, and I’ve seen this in the operating room myself, and on slides. Where you find brown fat cells you also find a certain proportion of white fat cells, not an exclusive brown fat depot like you see in a mouse.
It is hotly debated right now whether brown fat can change to white fat and vice versa (transdifferentiation). The beige fat cells are supposed to be the kind that can shuttle between more white-like or brown-like. They can sometimes be white or sometimes brown. It can be very contentious in [scientific] papers and meetings.
Are humans born with all the fat cells they will ever have?
No. New fat cells are made throughout our lives. When the white adipocytes store too much triglyceride, they get really big and they get “sick” and die faster. It’s the rate at which the white cells take up the fat to store it and then get rid of it that can impact whether someone gains a lot of weight and whether they can successfully lose it after reasonable effort.
The average lifespan of a white fat cell is 15 years. We have no idea yet of the lifespan of a brown fat cell.
Is there a single “fat gene”? What role do fat genes play in the likelihood of developing metabolic diseases and type 2 diabetes?
Genes are very important for influencing the development of obesity and probably influence 50%-70% of obesity, based on studies in populations of predominantly European origin. But that high percentage reflects the impact of hundreds of genes. For most people, there is no one gene that exerts all of the effects. There are extremely rare diseases where one gene is responsible. Currently, only 20% of the entire phenotypic variation in obesity can be explained by the thousands of loci identified so far.
Why is it “correct but too simplistic” to attribute the increasing rates of obesity to excessive triglyceride storage in white adipose tissue?
Saying obesity is caused by too much triglyceride storage ignores the reasons how and why the triglycerides got there. There are likely to be multiple contributing factors to drive obesity, and those have billions of dollars of policy implications. Is obesity resulting from portion sizes? Then we should work on educating the public on how to estimate their caloric intake. Is it the types of foods, such as ultra-processed foods? Then we can discourage eating certain food groups while promoting others. Is it about physical activity? Then we should prioritize exercise programs.
Why is obesity “not simply a failure of will power”?
Genetic factors in adipose tissue impact how easy it is to store triglycerides, how easy it is to get fat out of the tissue and burn it up, and what kinds of hormones are released by the tissue to regulate appetite, insulin resistance, and inflammation. Ten different people can all overeat the same amount of the same foods, yet there will be differences in the amount of weight gain and metabolic complications experienced. And at the brain level, some people will feel “full” sooner than others.
How can excess adipose tissue lead to disease? Do some people have “metabolically healthy obesity”?
Excess adipose tissue leads to chronic inflammation that can then cause insulin resistance, hypertension, fatty liver disease, and other complications. It appears that there are metabolically healthy obese people, but it is not clear if that is only a temporary state.
Could long-term brown adipose tissue activation help treat obesity or related metabolic disease?
Our research group at the NIH and others have shown that long-term brown adipose tissue activation produces metabolic benefit such as improved insulin resistance, lower plasma glucose, and higher HDL [good] cholesterol. However, there is no evidence yet that it will lead to actual weight loss.
We are trying to use brown adipose tissue activation to treat obesity-related metabolic disease to see if it could lead to reduction in inflammation, improvement in the cholesterol profile, and decrease in blood pressure.
A large observational study published Jan. 4, 2021, in Nature Medicine by Paul Cohen’s group at Rockefeller University, in tens of thousands of people at Memorial Sloan Kettering Cancer Center, showed that people who had brown fat were generally healthier and had less high blood pressure and less cardiovascular disease. This study could not show causation, but at every BMI, people were healthier if they had more brown fat than if they had less. So, there’s something going on. We’re still trying to figure that out.
Dr. Cypess has no reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“Adipose tissue is an underappreciated and misunderstood organ.” It’s with these words that Aaron M. Cypess, MD, PhD, begins his recent review published in the New England Journal of Medicine.
As obesity rates steadily rise, “the riskiest approach to human adipose tissue is to dismiss its importance,” he adds, especially because there has been “an explosive growth” in our understanding of white and brown adipose tissue over the past 5 to 10 years.
This news organization asked Dr. Cypess, a National Institutes of Health (NIH) scientist whose research focuses on brown fat, to discuss some of the main points in his review, titled, “Reassessing Human Adipose Tissue,” and clear up some misconceptions about fat.
You write that, for people who struggle to lose weight, “fat is often a source of misery, not marvel.” Why is fat a marvel?
When I started medical school in 1992, fat was just a thing that stored calories. You had to get it out of the way when you operated on the stomach or intestines. Now we know it’s not just one cell, it’s multiple types of cells, including immune cells and some blood cells. There’s cell turnover, and cells can get bigger or smaller, so it’s a dynamic tissue. It impacts the immune system and affects insulin sensitivity.
Why use the term “adipose tissue” and not just “fat”?
People think of fat cells and that’s it. However, adipose tissue (fat) has multiple cell types, and they each matter. There are adipocytes (fat cells) – which can be white, brown, beige, or pink – as well as immune cells, fibroblasts, blood vessels, and parts of nerve cells.
The main function of white adipose tissue is to store energy in the form of triglycerides. Brown adipose tissue consumes glucose and triglycerides, generating heat. Brown fat cells within depots of white fat are termed brite cells (a portmanteau of brown and white) or beige cells. Pink fat cells have been found in breast tissue in mice.
What do we now know about white fat and brown fat? Can brown fat change to white fat or vice versa?
White adipose tissue is commonly separated into visceral fat and subcutaneous fat, which have negative and neutral or positive metabolic effects, respectively. It is capable of more than doubling in mass and then returning to baseline.
White adipocyte-derived hormones include leptin, which is low in starvation, and adiponectin, which regulates glucose and lipid metabolism. White adipose tissue is essential for the proper function of the reproductive system, including secretion of hormones and lactation.
Brown adipose tissue protects newborns from cold as they develop the ability to shiver, and in adults it is found in depots in the neck, shoulders, posterior thorax, and abdomen. The amount of brown adipose tissue varies according to sex and lowers with increasing age and increasing body mass index.
There is much more white fat in the body than brown fat. It appears that activating brown fat leads to beneficial effects on metabolism, though we don’t know yet all the steps for how that happens.
In mice, you’ve got white fat depots and brown fat depots, and some brown fat can be found in the white fat.
With humans it’s much more complicated, and I’ve seen this in the operating room myself, and on slides. Where you find brown fat cells you also find a certain proportion of white fat cells, not an exclusive brown fat depot like you see in a mouse.
It is hotly debated right now whether brown fat can change to white fat and vice versa (transdifferentiation). The beige fat cells are supposed to be the kind that can shuttle between more white-like or brown-like. They can sometimes be white or sometimes brown. It can be very contentious in [scientific] papers and meetings.
Are humans born with all the fat cells they will ever have?
No. New fat cells are made throughout our lives. When the white adipocytes store too much triglyceride, they get really big and they get “sick” and die faster. It’s the rate at which the white cells take up the fat to store it and then get rid of it that can impact whether someone gains a lot of weight and whether they can successfully lose it after reasonable effort.
The average lifespan of a white fat cell is 15 years. We have no idea yet of the lifespan of a brown fat cell.
Is there a single “fat gene”? What role do fat genes play in the likelihood of developing metabolic diseases and type 2 diabetes?
Genes are very important for influencing the development of obesity and probably influence 50%-70% of obesity, based on studies in populations of predominantly European origin. But that high percentage reflects the impact of hundreds of genes. For most people, there is no one gene that exerts all of the effects. There are extremely rare diseases where one gene is responsible. Currently, only 20% of the entire phenotypic variation in obesity can be explained by the thousands of loci identified so far.
Why is it “correct but too simplistic” to attribute the increasing rates of obesity to excessive triglyceride storage in white adipose tissue?
Saying obesity is caused by too much triglyceride storage ignores the reasons how and why the triglycerides got there. There are likely to be multiple contributing factors to drive obesity, and those have billions of dollars of policy implications. Is obesity resulting from portion sizes? Then we should work on educating the public on how to estimate their caloric intake. Is it the types of foods, such as ultra-processed foods? Then we can discourage eating certain food groups while promoting others. Is it about physical activity? Then we should prioritize exercise programs.
Why is obesity “not simply a failure of will power”?
Genetic factors in adipose tissue impact how easy it is to store triglycerides, how easy it is to get fat out of the tissue and burn it up, and what kinds of hormones are released by the tissue to regulate appetite, insulin resistance, and inflammation. Ten different people can all overeat the same amount of the same foods, yet there will be differences in the amount of weight gain and metabolic complications experienced. And at the brain level, some people will feel “full” sooner than others.
How can excess adipose tissue lead to disease? Do some people have “metabolically healthy obesity”?
Excess adipose tissue leads to chronic inflammation that can then cause insulin resistance, hypertension, fatty liver disease, and other complications. It appears that there are metabolically healthy obese people, but it is not clear if that is only a temporary state.
Could long-term brown adipose tissue activation help treat obesity or related metabolic disease?
Our research group at the NIH and others have shown that long-term brown adipose tissue activation produces metabolic benefit such as improved insulin resistance, lower plasma glucose, and higher HDL [good] cholesterol. However, there is no evidence yet that it will lead to actual weight loss.
We are trying to use brown adipose tissue activation to treat obesity-related metabolic disease to see if it could lead to reduction in inflammation, improvement in the cholesterol profile, and decrease in blood pressure.
A large observational study published Jan. 4, 2021, in Nature Medicine by Paul Cohen’s group at Rockefeller University, in tens of thousands of people at Memorial Sloan Kettering Cancer Center, showed that people who had brown fat were generally healthier and had less high blood pressure and less cardiovascular disease. This study could not show causation, but at every BMI, people were healthier if they had more brown fat than if they had less. So, there’s something going on. We’re still trying to figure that out.
Dr. Cypess has no reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Sports experts on T2D: Boost activity, cut sedentary time
The American College of Sports Medicine (ACSM) has issued new recommendations for exercise/physical activity in people with type 2 diabetes, which update a 2010 joint ACSM/American Diabetes Association position statement.
The guidance has been published in the February issue of Medicine & Science in Sports & Exercise.
“This consensus statement provides a brief summary of the current evidence and extends and updates the prior recommendations,” the authors explain.
In the past decade, there has been a “considerable amount” of research about exercise in people with type 2 diabetes, they add, while the prevalence of diabetes has steadily increased.
The updated recommendations have been “expanded to include physical activity – a broader, more comprehensive definition of human movement than planned exercise – and reducing sedentary time,” the authors note.
“The latest guidelines are applicable to most individuals with diabetes, including youth, with a few exceptions and modifications,” lead author Jill A. Kanaley, PhD, said in a press release from the ACSM.
The key takeaway is that “all individuals [with type 2 diabetes] should engage in regular physical activity, reduce sedentary time, and break up sitting time with frequent activity breaks,” said Dr. Kanaley, a professor in the department of nutrition and exercise physiology, University of Missouri, Columbia.
“Exercise can play an important role in managing type 2 diabetes, and workouts can be modified to fit the abilities of most people,” she stressed.
And those with type 2 diabetes who want to lose weight “should consider workouts of moderately high volume for 4 to 5 days per week,” she added.
Six key tips for physical activity in adults with type 2 diabetes
The consensus statement gives six key tips for physical activity in adults with type 2 diabetes, as follows.
- Regular aerobic exercise improves glycemic management; meta-analyses have reported fewer daily hyperglycemic episodes and reductions in A1c of 0.5%-0.7%.
- High-intensity resistance exercise, when performed safely, is better than low-to-moderate intensity resistance exercise for glucose management and attenuation of insulin levels. Resistance exercise typically results in improvements of 10% to 15% in strength, bone mineral density, blood pressure, lipid profile, skeletal muscle mass, and insulin sensitivity.
- Exercise after meals, such as taking a walk after dinner at one’s own pace, takes advantage of the blood glucose-stabilizing effects of exercise.
- Reduce sedentary time by taking regular breaks for small “doses” of physical activity, which can modestly attenuate postprandial glucose and insulin levels, particularly in individuals with insulin resistance and a higher body mass index.
- To prevent hypoglycemia during or after exercise, people taking insulin or insulin secretagogues should increase carbohydrate intake, or if possible, reduce insulin.
- People who are taking beta blockers should not rely on a heart monitor to measure workout intensity. They could ask a certified exercise professional about using ratings of perceived exertion to track how a workout feels.
Other recommendations
The consensus statement also summarizes precautions that people with complications of type 2 diabetes (such as neuropathy, retinopathy, kidney disease, and hypertension) should take.
Low impact exercises for flexibility can help introduce sedentary people to physical activity, the consensus group writes. Balance exercises can be helpful for older adults.
Weight loss greater than 5% can benefit A1c, blood lipid, and blood pressure levels. Moderate exercise 4 to 5 days a week can reduce visceral fat.
In studies of youth with type 2 diabetes, intensive lifestyle interventions plus metformin were not superior to metformin alone for managing glycemia. Physical activity goals are the same for youth with or without diabetes.
Pregnant women with diabetes should participate in at least 20 to 30 minutes of moderate-intensity exercise most days of the week.
Participating in an exercise program before and after bariatric surgery may enhance surgical outcomes.
Dr. Kanaley has reported receiving a grant from the National Institutes of Health. Disclosures for the other authors are listed in the article.
A version of this article first appeared on Medscape.com.
The American College of Sports Medicine (ACSM) has issued new recommendations for exercise/physical activity in people with type 2 diabetes, which update a 2010 joint ACSM/American Diabetes Association position statement.
The guidance has been published in the February issue of Medicine & Science in Sports & Exercise.
“This consensus statement provides a brief summary of the current evidence and extends and updates the prior recommendations,” the authors explain.
In the past decade, there has been a “considerable amount” of research about exercise in people with type 2 diabetes, they add, while the prevalence of diabetes has steadily increased.
The updated recommendations have been “expanded to include physical activity – a broader, more comprehensive definition of human movement than planned exercise – and reducing sedentary time,” the authors note.
“The latest guidelines are applicable to most individuals with diabetes, including youth, with a few exceptions and modifications,” lead author Jill A. Kanaley, PhD, said in a press release from the ACSM.
The key takeaway is that “all individuals [with type 2 diabetes] should engage in regular physical activity, reduce sedentary time, and break up sitting time with frequent activity breaks,” said Dr. Kanaley, a professor in the department of nutrition and exercise physiology, University of Missouri, Columbia.
“Exercise can play an important role in managing type 2 diabetes, and workouts can be modified to fit the abilities of most people,” she stressed.
And those with type 2 diabetes who want to lose weight “should consider workouts of moderately high volume for 4 to 5 days per week,” she added.
Six key tips for physical activity in adults with type 2 diabetes
The consensus statement gives six key tips for physical activity in adults with type 2 diabetes, as follows.
- Regular aerobic exercise improves glycemic management; meta-analyses have reported fewer daily hyperglycemic episodes and reductions in A1c of 0.5%-0.7%.
- High-intensity resistance exercise, when performed safely, is better than low-to-moderate intensity resistance exercise for glucose management and attenuation of insulin levels. Resistance exercise typically results in improvements of 10% to 15% in strength, bone mineral density, blood pressure, lipid profile, skeletal muscle mass, and insulin sensitivity.
- Exercise after meals, such as taking a walk after dinner at one’s own pace, takes advantage of the blood glucose-stabilizing effects of exercise.
- Reduce sedentary time by taking regular breaks for small “doses” of physical activity, which can modestly attenuate postprandial glucose and insulin levels, particularly in individuals with insulin resistance and a higher body mass index.
- To prevent hypoglycemia during or after exercise, people taking insulin or insulin secretagogues should increase carbohydrate intake, or if possible, reduce insulin.
- People who are taking beta blockers should not rely on a heart monitor to measure workout intensity. They could ask a certified exercise professional about using ratings of perceived exertion to track how a workout feels.
Other recommendations
The consensus statement also summarizes precautions that people with complications of type 2 diabetes (such as neuropathy, retinopathy, kidney disease, and hypertension) should take.
Low impact exercises for flexibility can help introduce sedentary people to physical activity, the consensus group writes. Balance exercises can be helpful for older adults.
Weight loss greater than 5% can benefit A1c, blood lipid, and blood pressure levels. Moderate exercise 4 to 5 days a week can reduce visceral fat.
In studies of youth with type 2 diabetes, intensive lifestyle interventions plus metformin were not superior to metformin alone for managing glycemia. Physical activity goals are the same for youth with or without diabetes.
Pregnant women with diabetes should participate in at least 20 to 30 minutes of moderate-intensity exercise most days of the week.
Participating in an exercise program before and after bariatric surgery may enhance surgical outcomes.
Dr. Kanaley has reported receiving a grant from the National Institutes of Health. Disclosures for the other authors are listed in the article.
A version of this article first appeared on Medscape.com.
The American College of Sports Medicine (ACSM) has issued new recommendations for exercise/physical activity in people with type 2 diabetes, which update a 2010 joint ACSM/American Diabetes Association position statement.
The guidance has been published in the February issue of Medicine & Science in Sports & Exercise.
“This consensus statement provides a brief summary of the current evidence and extends and updates the prior recommendations,” the authors explain.
In the past decade, there has been a “considerable amount” of research about exercise in people with type 2 diabetes, they add, while the prevalence of diabetes has steadily increased.
The updated recommendations have been “expanded to include physical activity – a broader, more comprehensive definition of human movement than planned exercise – and reducing sedentary time,” the authors note.
“The latest guidelines are applicable to most individuals with diabetes, including youth, with a few exceptions and modifications,” lead author Jill A. Kanaley, PhD, said in a press release from the ACSM.
The key takeaway is that “all individuals [with type 2 diabetes] should engage in regular physical activity, reduce sedentary time, and break up sitting time with frequent activity breaks,” said Dr. Kanaley, a professor in the department of nutrition and exercise physiology, University of Missouri, Columbia.
“Exercise can play an important role in managing type 2 diabetes, and workouts can be modified to fit the abilities of most people,” she stressed.
And those with type 2 diabetes who want to lose weight “should consider workouts of moderately high volume for 4 to 5 days per week,” she added.
Six key tips for physical activity in adults with type 2 diabetes
The consensus statement gives six key tips for physical activity in adults with type 2 diabetes, as follows.
- Regular aerobic exercise improves glycemic management; meta-analyses have reported fewer daily hyperglycemic episodes and reductions in A1c of 0.5%-0.7%.
- High-intensity resistance exercise, when performed safely, is better than low-to-moderate intensity resistance exercise for glucose management and attenuation of insulin levels. Resistance exercise typically results in improvements of 10% to 15% in strength, bone mineral density, blood pressure, lipid profile, skeletal muscle mass, and insulin sensitivity.
- Exercise after meals, such as taking a walk after dinner at one’s own pace, takes advantage of the blood glucose-stabilizing effects of exercise.
- Reduce sedentary time by taking regular breaks for small “doses” of physical activity, which can modestly attenuate postprandial glucose and insulin levels, particularly in individuals with insulin resistance and a higher body mass index.
- To prevent hypoglycemia during or after exercise, people taking insulin or insulin secretagogues should increase carbohydrate intake, or if possible, reduce insulin.
- People who are taking beta blockers should not rely on a heart monitor to measure workout intensity. They could ask a certified exercise professional about using ratings of perceived exertion to track how a workout feels.
Other recommendations
The consensus statement also summarizes precautions that people with complications of type 2 diabetes (such as neuropathy, retinopathy, kidney disease, and hypertension) should take.
Low impact exercises for flexibility can help introduce sedentary people to physical activity, the consensus group writes. Balance exercises can be helpful for older adults.
Weight loss greater than 5% can benefit A1c, blood lipid, and blood pressure levels. Moderate exercise 4 to 5 days a week can reduce visceral fat.
In studies of youth with type 2 diabetes, intensive lifestyle interventions plus metformin were not superior to metformin alone for managing glycemia. Physical activity goals are the same for youth with or without diabetes.
Pregnant women with diabetes should participate in at least 20 to 30 minutes of moderate-intensity exercise most days of the week.
Participating in an exercise program before and after bariatric surgery may enhance surgical outcomes.
Dr. Kanaley has reported receiving a grant from the National Institutes of Health. Disclosures for the other authors are listed in the article.
A version of this article first appeared on Medscape.com.
Eating dinner late ups diabetes risk; melatonin involved
which increase the risk of type 2 diabetes.
And people who are carriers of the G allele of the MTNR1B gene have greater impairment in glucose tolerance after eating a late dinner.
“In natural late eaters [in Spain], we simulated early and late dinner timing by administering a glucose drink and compared effects on blood sugar control over 2 hours,” said senior author Richa Saxena, PhD, a principal investigator at the Center for Genomic Medicine at Massachusetts General Hospital, Boston.
The study also compared outcomes in carriers and noncarriers of the G allele variant of the melatonin receptor gene, Dr. Saxena pointed out in a press release from the hospital.
“We found that late eating disturbed blood sugar control in the whole group,” added lead author Marta Garaulet, PhD.
“This impaired glucose control was predominantly seen in genetic risk variant carriers, representing about half of the cohort,” said Dr. Garaulet, professor of physiology and nutrition, University of Murcia (Spain).
The study results “may be important in the effort toward prevention of type 2 diabetes,” according to co–senior author Frank A.J.L. Scheer, PhD.
“Our findings are applicable to about a third of the population in the industrialized world who consume food close to bedtime, as well as other populations who eat at night, including shift workers, or those experiencing jet lag or night-eating disorders, as well as those who routinely use melatonin supplements close to food intake,” said Dr. Scheer, director of the medical chronobiology program at Brigham and Women’s Hospital, Boston.
The results suggest people should not eat within 2 hours of bedtime, said the researchers.
“Notably, our study does not include patients with diabetes, so additional studies are needed to examine the impact of food timing and its link with melatonin and receptor variation in patients with diabetes,” Dr. Scheer said.
The findings, from the MTNR1B SNP*Food Timing Interaction on Glucose Control (ONTIME-MT) randomized crossover study, were recently published in Diabetes Care.
Melatonin plays a key role in glucose metabolism
Melatonin, a hormone primarily released at night that helps control the sleep-wake cycle, typically rises around 2 hours before bedtime, the researchers explained.
The discovery of MTNR1B as a type 2 diabetes–associated gene “suggests that, beyond sleep and circadian regulation, melatonin plays a key role in glucose metabolism,” they noted. However, whether melatonin improves or impairs glucose control is controversial, and the effect of MTNR1B genotypes on glucose control is not clear.
“We decided to test if late eating that usually occurs with elevated melatonin levels results in disturbed blood sugar control,” Dr. Saxena explained.
To investigate this, researchers enrolled 845 adults in Spain who were 18-70 years old and did not have diabetes. Participants were a mean age of 38 years and 71% were women. They had a mean body mass index of 25.7 kg/m2 and 18% had obesity.
On average, they typically ate dinner at 21:38 (9:38 p.m.) and went to bed at 24:32 (12:32 a.m.).
DNA analysis from participants’ blood samples determined that 50% had the CC genotype of the MTNR1B gene, 40% had the CG genotype, and 10% had the GG genotype.
Each participant underwent two oral glucose tolerance tests. They fasted for 8 hours and then had a 2-hour 75-g oral glucose tolerance test either 1 hour before bedtime (simulating a late dinner) or 4 hours before bedtime (simulating an early dinner). Then they repeated the test at the opposite dinner time on another night.
The average serum melatonin values were 3.5-fold higher after the late dinner than after the early dinner, resulting in 6.7% lower insulin area under the curve and 8.3% higher glucose AUC.
Genotype differences in glucose tolerance were attributed to reductions in beta-cell function.
“Our results confirm that late eating acutely impairs glucose tolerance through a defect in insulin secretion,” the researchers reiterated.
ONTIME-MT was funded by the National Institutes of Health; the Spanish Government of Investigation, Development, and Innovation; and the Seneca Foundation. The researchers reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
which increase the risk of type 2 diabetes.
And people who are carriers of the G allele of the MTNR1B gene have greater impairment in glucose tolerance after eating a late dinner.
“In natural late eaters [in Spain], we simulated early and late dinner timing by administering a glucose drink and compared effects on blood sugar control over 2 hours,” said senior author Richa Saxena, PhD, a principal investigator at the Center for Genomic Medicine at Massachusetts General Hospital, Boston.
The study also compared outcomes in carriers and noncarriers of the G allele variant of the melatonin receptor gene, Dr. Saxena pointed out in a press release from the hospital.
“We found that late eating disturbed blood sugar control in the whole group,” added lead author Marta Garaulet, PhD.
“This impaired glucose control was predominantly seen in genetic risk variant carriers, representing about half of the cohort,” said Dr. Garaulet, professor of physiology and nutrition, University of Murcia (Spain).
The study results “may be important in the effort toward prevention of type 2 diabetes,” according to co–senior author Frank A.J.L. Scheer, PhD.
“Our findings are applicable to about a third of the population in the industrialized world who consume food close to bedtime, as well as other populations who eat at night, including shift workers, or those experiencing jet lag or night-eating disorders, as well as those who routinely use melatonin supplements close to food intake,” said Dr. Scheer, director of the medical chronobiology program at Brigham and Women’s Hospital, Boston.
The results suggest people should not eat within 2 hours of bedtime, said the researchers.
“Notably, our study does not include patients with diabetes, so additional studies are needed to examine the impact of food timing and its link with melatonin and receptor variation in patients with diabetes,” Dr. Scheer said.
The findings, from the MTNR1B SNP*Food Timing Interaction on Glucose Control (ONTIME-MT) randomized crossover study, were recently published in Diabetes Care.
Melatonin plays a key role in glucose metabolism
Melatonin, a hormone primarily released at night that helps control the sleep-wake cycle, typically rises around 2 hours before bedtime, the researchers explained.
The discovery of MTNR1B as a type 2 diabetes–associated gene “suggests that, beyond sleep and circadian regulation, melatonin plays a key role in glucose metabolism,” they noted. However, whether melatonin improves or impairs glucose control is controversial, and the effect of MTNR1B genotypes on glucose control is not clear.
“We decided to test if late eating that usually occurs with elevated melatonin levels results in disturbed blood sugar control,” Dr. Saxena explained.
To investigate this, researchers enrolled 845 adults in Spain who were 18-70 years old and did not have diabetes. Participants were a mean age of 38 years and 71% were women. They had a mean body mass index of 25.7 kg/m2 and 18% had obesity.
On average, they typically ate dinner at 21:38 (9:38 p.m.) and went to bed at 24:32 (12:32 a.m.).
DNA analysis from participants’ blood samples determined that 50% had the CC genotype of the MTNR1B gene, 40% had the CG genotype, and 10% had the GG genotype.
Each participant underwent two oral glucose tolerance tests. They fasted for 8 hours and then had a 2-hour 75-g oral glucose tolerance test either 1 hour before bedtime (simulating a late dinner) or 4 hours before bedtime (simulating an early dinner). Then they repeated the test at the opposite dinner time on another night.
The average serum melatonin values were 3.5-fold higher after the late dinner than after the early dinner, resulting in 6.7% lower insulin area under the curve and 8.3% higher glucose AUC.
Genotype differences in glucose tolerance were attributed to reductions in beta-cell function.
“Our results confirm that late eating acutely impairs glucose tolerance through a defect in insulin secretion,” the researchers reiterated.
ONTIME-MT was funded by the National Institutes of Health; the Spanish Government of Investigation, Development, and Innovation; and the Seneca Foundation. The researchers reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
which increase the risk of type 2 diabetes.
And people who are carriers of the G allele of the MTNR1B gene have greater impairment in glucose tolerance after eating a late dinner.
“In natural late eaters [in Spain], we simulated early and late dinner timing by administering a glucose drink and compared effects on blood sugar control over 2 hours,” said senior author Richa Saxena, PhD, a principal investigator at the Center for Genomic Medicine at Massachusetts General Hospital, Boston.
The study also compared outcomes in carriers and noncarriers of the G allele variant of the melatonin receptor gene, Dr. Saxena pointed out in a press release from the hospital.
“We found that late eating disturbed blood sugar control in the whole group,” added lead author Marta Garaulet, PhD.
“This impaired glucose control was predominantly seen in genetic risk variant carriers, representing about half of the cohort,” said Dr. Garaulet, professor of physiology and nutrition, University of Murcia (Spain).
The study results “may be important in the effort toward prevention of type 2 diabetes,” according to co–senior author Frank A.J.L. Scheer, PhD.
“Our findings are applicable to about a third of the population in the industrialized world who consume food close to bedtime, as well as other populations who eat at night, including shift workers, or those experiencing jet lag or night-eating disorders, as well as those who routinely use melatonin supplements close to food intake,” said Dr. Scheer, director of the medical chronobiology program at Brigham and Women’s Hospital, Boston.
The results suggest people should not eat within 2 hours of bedtime, said the researchers.
“Notably, our study does not include patients with diabetes, so additional studies are needed to examine the impact of food timing and its link with melatonin and receptor variation in patients with diabetes,” Dr. Scheer said.
The findings, from the MTNR1B SNP*Food Timing Interaction on Glucose Control (ONTIME-MT) randomized crossover study, were recently published in Diabetes Care.
Melatonin plays a key role in glucose metabolism
Melatonin, a hormone primarily released at night that helps control the sleep-wake cycle, typically rises around 2 hours before bedtime, the researchers explained.
The discovery of MTNR1B as a type 2 diabetes–associated gene “suggests that, beyond sleep and circadian regulation, melatonin plays a key role in glucose metabolism,” they noted. However, whether melatonin improves or impairs glucose control is controversial, and the effect of MTNR1B genotypes on glucose control is not clear.
“We decided to test if late eating that usually occurs with elevated melatonin levels results in disturbed blood sugar control,” Dr. Saxena explained.
To investigate this, researchers enrolled 845 adults in Spain who were 18-70 years old and did not have diabetes. Participants were a mean age of 38 years and 71% were women. They had a mean body mass index of 25.7 kg/m2 and 18% had obesity.
On average, they typically ate dinner at 21:38 (9:38 p.m.) and went to bed at 24:32 (12:32 a.m.).
DNA analysis from participants’ blood samples determined that 50% had the CC genotype of the MTNR1B gene, 40% had the CG genotype, and 10% had the GG genotype.
Each participant underwent two oral glucose tolerance tests. They fasted for 8 hours and then had a 2-hour 75-g oral glucose tolerance test either 1 hour before bedtime (simulating a late dinner) or 4 hours before bedtime (simulating an early dinner). Then they repeated the test at the opposite dinner time on another night.
The average serum melatonin values were 3.5-fold higher after the late dinner than after the early dinner, resulting in 6.7% lower insulin area under the curve and 8.3% higher glucose AUC.
Genotype differences in glucose tolerance were attributed to reductions in beta-cell function.
“Our results confirm that late eating acutely impairs glucose tolerance through a defect in insulin secretion,” the researchers reiterated.
ONTIME-MT was funded by the National Institutes of Health; the Spanish Government of Investigation, Development, and Innovation; and the Seneca Foundation. The researchers reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
FROM DIABETES CARE
Anxiety in men tied to risk factors for CVD, diabetes
Among healthy middle-aged men, those who were more anxious were more likely to develop high levels of multiple biomarkers of cardiometabolic risk over a 40-year follow-up in a new study.
“By middle adulthood, higher anxiety levels are associated with stable differences” in biomarkers of risk for coronary artery disease (CAD), stroke, and type 2 diabetes, which “are maintained into older ages,” the researchers wrote.
Anxious individuals “may experience deteriorations in cardiometabolic health earlier in life and remain on a stable trajectory of heightened risk into older ages,” they concluded.
The study, led by Lewina Lee, PhD, was published online Jan. 24, 2022, in the Journal of the American Heart Association.
“Men who had higher levels of anxiety at the beginning of the study had consistently higher biological risk for cardiometabolic disease than less anxious men from midlife into old age,” Dr. Lee, assistant professor of psychiatry, Boston University, summarized in an email.
Clinicians may not screen for heart disease and diabetes, and/or only discuss lifestyle modifications when patients are older or have the first signs of disease, she added.
However, the study findings “suggest that worries and anxiety are associated with preclinical pathophysiological processes that tend to culminate in cardiometabolic disease” and show “the importance of screening for mental health difficulties, such as worries and anxiety, in men as early as in their 30s and 40s,” she stressed.
Since most of the men were White (97%) and veterans (94%), “it would be important for future studies to evaluate if these associations exist among women, people from diverse racial and ethnic groups, and in more socioeconomically varying samples, and to consider how anxiety may relate to the development of cardiometabolic risk in much younger individuals than those in our study,” Dr. Lee said in a press release from the American Heart Association.
“This study adds to the growing body of research that link psychological health to cardiovascular risk,” Glenn N. Levine, MD, who was not involved with this research, told this news organization in an email.
“We know that factors such as depression and stress can increase cardiac risk; this study further supports that anxiety can as well,” added Dr. Levine, chief of cardiology, Michael E. DeBakey Veterans Affairs Medical Center, Houston.
“Everyone experiences some anxiety in their life,” he added. However, “if a provider senses that a patient’s anxiety is far beyond the ‘normal’ that we all have from time to time, and it is seemingly adversely impacting both their psychological and physical health, it would be reasonable to suggest to the patient that it might be useful to speak with a mental health professional, and if the patient is receptive, to then make a formal consultation or referral,” said Dr. Levine, who was writing group chair of a recent AHA Scientific Statement on mind-heart-body connection.
Neuroticism and worry
Several studies have linked anxiety to a greater risk of cardiometabolic disease onset, Dr. Lee and colleagues wrote, but it is unclear if anxious individuals have a steadily worsening risk as they age, or if they have a higher risk in middle age, which stays the same in older age.
To investigate this, they analyzed data from 1561 men who were seen at the VA Boston outpatient clinic and did not have CAD, type 2 diabetes, stroke, or cancer when they enrolled in the Normative Aging Study.
The men had a mean age of 53 years (range, 33-84) in 1975 and were followed until 2015 or until dropout from the study or death.
At baseline, the study participants filled in the Eysenck Personality Inventory, which assesses neuroticism, and also responded to a scale indicating how much they worry about 20 issues (excluding health).
“Neuroticism,” the researchers explained, “is a tendency to perceive experiences as threatening, feel that challenges are uncontrollable, and experience frequent and disproportionately intense negative emotions,” such as fear, anxiety, sadness, and anger, “across many situations.”
“Worry refers to attempts to solve a problem where future outcome is uncertain and potentially positive or negative,” Dr. Lee noted. Although worry can be healthy and lead to constructive solutions, “it may be unhealthy, especially when it becomes uncontrollable and interferes with day-to-day functioning.”
Of note, in 1980, the American Psychiatric Association removed the term neurosis from its diagnostic manual. What was previously called neurosis is included as part of generalized anxiety disorder; GAD also encompasses excessive worry.
Cardiometabolic risk from midlife to old age
The men in the current study had on-site physical examinations every 3-5 years.
The researchers calculated the men’s cardiometabolic risk score (from 0 to 7) by assigning 1 point each for the following: systolic blood pressure greater than 130 mm Hg, diastolic blood pressure greater than 85 mm Hg, total cholesterol of at least 240 mg/dL, triglycerides of at least 150 mg/dL, body mass index of at least 30 kg/m2, glucose of at least 100 mg/dL, and erythrocyte sedimentation rate of at least 14 mm/hour.
Alternatively, patients were assigned a point each for taking medication that could affect these markers (except for body mass index).
Overall, on average, at baseline, the men had a cardiometabolic risk score of 2.9. From age 33-65, this score increased to 3.8, and then it did not increase as much later on.
That is, the cardiometabolic risk score increased by 0.8 per decade until age 65, followed by a slower increase of 0.5 per decade.
At all ages, men with higher levels of neuroticism or worry had a higher cardiometabolic risk score
Each additional standard deviation of neuroticism was associated with a 13% increased risk of having six or more of the seven cardiometabolic risk markers during follow-up, after adjusting for age, demographics, and family history of CAD, but the relationship was attenuated after also adjusting for health behaviors (for example, smoking, alcohol consumption, physical activity, and past-year physician visit at baseline).
Similarly, each additional standard deviation of worry was associated with a 10% increased risk of having six or more of the seven cardiometabolic risk markers during follow-up after the same adjustments, and was also no longer significantly different after the same further adjustments.
The research was supported by grants from the National Institutes of Health and a Senior Research Career Scientist Award from the Office of Research and Development, Department of Veterans Affairs. The Normative Aging Study is a research component of the Massachusetts Veterans Epidemiology Research and Information Center and is supported by the VA Cooperative Studies Program/Epidemiological Research Centers. The study authors and Dr. Levine disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Among healthy middle-aged men, those who were more anxious were more likely to develop high levels of multiple biomarkers of cardiometabolic risk over a 40-year follow-up in a new study.
“By middle adulthood, higher anxiety levels are associated with stable differences” in biomarkers of risk for coronary artery disease (CAD), stroke, and type 2 diabetes, which “are maintained into older ages,” the researchers wrote.
Anxious individuals “may experience deteriorations in cardiometabolic health earlier in life and remain on a stable trajectory of heightened risk into older ages,” they concluded.
The study, led by Lewina Lee, PhD, was published online Jan. 24, 2022, in the Journal of the American Heart Association.
“Men who had higher levels of anxiety at the beginning of the study had consistently higher biological risk for cardiometabolic disease than less anxious men from midlife into old age,” Dr. Lee, assistant professor of psychiatry, Boston University, summarized in an email.
Clinicians may not screen for heart disease and diabetes, and/or only discuss lifestyle modifications when patients are older or have the first signs of disease, she added.
However, the study findings “suggest that worries and anxiety are associated with preclinical pathophysiological processes that tend to culminate in cardiometabolic disease” and show “the importance of screening for mental health difficulties, such as worries and anxiety, in men as early as in their 30s and 40s,” she stressed.
Since most of the men were White (97%) and veterans (94%), “it would be important for future studies to evaluate if these associations exist among women, people from diverse racial and ethnic groups, and in more socioeconomically varying samples, and to consider how anxiety may relate to the development of cardiometabolic risk in much younger individuals than those in our study,” Dr. Lee said in a press release from the American Heart Association.
“This study adds to the growing body of research that link psychological health to cardiovascular risk,” Glenn N. Levine, MD, who was not involved with this research, told this news organization in an email.
“We know that factors such as depression and stress can increase cardiac risk; this study further supports that anxiety can as well,” added Dr. Levine, chief of cardiology, Michael E. DeBakey Veterans Affairs Medical Center, Houston.
“Everyone experiences some anxiety in their life,” he added. However, “if a provider senses that a patient’s anxiety is far beyond the ‘normal’ that we all have from time to time, and it is seemingly adversely impacting both their psychological and physical health, it would be reasonable to suggest to the patient that it might be useful to speak with a mental health professional, and if the patient is receptive, to then make a formal consultation or referral,” said Dr. Levine, who was writing group chair of a recent AHA Scientific Statement on mind-heart-body connection.
Neuroticism and worry
Several studies have linked anxiety to a greater risk of cardiometabolic disease onset, Dr. Lee and colleagues wrote, but it is unclear if anxious individuals have a steadily worsening risk as they age, or if they have a higher risk in middle age, which stays the same in older age.
To investigate this, they analyzed data from 1561 men who were seen at the VA Boston outpatient clinic and did not have CAD, type 2 diabetes, stroke, or cancer when they enrolled in the Normative Aging Study.
The men had a mean age of 53 years (range, 33-84) in 1975 and were followed until 2015 or until dropout from the study or death.
At baseline, the study participants filled in the Eysenck Personality Inventory, which assesses neuroticism, and also responded to a scale indicating how much they worry about 20 issues (excluding health).
“Neuroticism,” the researchers explained, “is a tendency to perceive experiences as threatening, feel that challenges are uncontrollable, and experience frequent and disproportionately intense negative emotions,” such as fear, anxiety, sadness, and anger, “across many situations.”
“Worry refers to attempts to solve a problem where future outcome is uncertain and potentially positive or negative,” Dr. Lee noted. Although worry can be healthy and lead to constructive solutions, “it may be unhealthy, especially when it becomes uncontrollable and interferes with day-to-day functioning.”
Of note, in 1980, the American Psychiatric Association removed the term neurosis from its diagnostic manual. What was previously called neurosis is included as part of generalized anxiety disorder; GAD also encompasses excessive worry.
Cardiometabolic risk from midlife to old age
The men in the current study had on-site physical examinations every 3-5 years.
The researchers calculated the men’s cardiometabolic risk score (from 0 to 7) by assigning 1 point each for the following: systolic blood pressure greater than 130 mm Hg, diastolic blood pressure greater than 85 mm Hg, total cholesterol of at least 240 mg/dL, triglycerides of at least 150 mg/dL, body mass index of at least 30 kg/m2, glucose of at least 100 mg/dL, and erythrocyte sedimentation rate of at least 14 mm/hour.
Alternatively, patients were assigned a point each for taking medication that could affect these markers (except for body mass index).
Overall, on average, at baseline, the men had a cardiometabolic risk score of 2.9. From age 33-65, this score increased to 3.8, and then it did not increase as much later on.
That is, the cardiometabolic risk score increased by 0.8 per decade until age 65, followed by a slower increase of 0.5 per decade.
At all ages, men with higher levels of neuroticism or worry had a higher cardiometabolic risk score
Each additional standard deviation of neuroticism was associated with a 13% increased risk of having six or more of the seven cardiometabolic risk markers during follow-up, after adjusting for age, demographics, and family history of CAD, but the relationship was attenuated after also adjusting for health behaviors (for example, smoking, alcohol consumption, physical activity, and past-year physician visit at baseline).
Similarly, each additional standard deviation of worry was associated with a 10% increased risk of having six or more of the seven cardiometabolic risk markers during follow-up after the same adjustments, and was also no longer significantly different after the same further adjustments.
The research was supported by grants from the National Institutes of Health and a Senior Research Career Scientist Award from the Office of Research and Development, Department of Veterans Affairs. The Normative Aging Study is a research component of the Massachusetts Veterans Epidemiology Research and Information Center and is supported by the VA Cooperative Studies Program/Epidemiological Research Centers. The study authors and Dr. Levine disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Among healthy middle-aged men, those who were more anxious were more likely to develop high levels of multiple biomarkers of cardiometabolic risk over a 40-year follow-up in a new study.
“By middle adulthood, higher anxiety levels are associated with stable differences” in biomarkers of risk for coronary artery disease (CAD), stroke, and type 2 diabetes, which “are maintained into older ages,” the researchers wrote.
Anxious individuals “may experience deteriorations in cardiometabolic health earlier in life and remain on a stable trajectory of heightened risk into older ages,” they concluded.
The study, led by Lewina Lee, PhD, was published online Jan. 24, 2022, in the Journal of the American Heart Association.
“Men who had higher levels of anxiety at the beginning of the study had consistently higher biological risk for cardiometabolic disease than less anxious men from midlife into old age,” Dr. Lee, assistant professor of psychiatry, Boston University, summarized in an email.
Clinicians may not screen for heart disease and diabetes, and/or only discuss lifestyle modifications when patients are older or have the first signs of disease, she added.
However, the study findings “suggest that worries and anxiety are associated with preclinical pathophysiological processes that tend to culminate in cardiometabolic disease” and show “the importance of screening for mental health difficulties, such as worries and anxiety, in men as early as in their 30s and 40s,” she stressed.
Since most of the men were White (97%) and veterans (94%), “it would be important for future studies to evaluate if these associations exist among women, people from diverse racial and ethnic groups, and in more socioeconomically varying samples, and to consider how anxiety may relate to the development of cardiometabolic risk in much younger individuals than those in our study,” Dr. Lee said in a press release from the American Heart Association.
“This study adds to the growing body of research that link psychological health to cardiovascular risk,” Glenn N. Levine, MD, who was not involved with this research, told this news organization in an email.
“We know that factors such as depression and stress can increase cardiac risk; this study further supports that anxiety can as well,” added Dr. Levine, chief of cardiology, Michael E. DeBakey Veterans Affairs Medical Center, Houston.
“Everyone experiences some anxiety in their life,” he added. However, “if a provider senses that a patient’s anxiety is far beyond the ‘normal’ that we all have from time to time, and it is seemingly adversely impacting both their psychological and physical health, it would be reasonable to suggest to the patient that it might be useful to speak with a mental health professional, and if the patient is receptive, to then make a formal consultation or referral,” said Dr. Levine, who was writing group chair of a recent AHA Scientific Statement on mind-heart-body connection.
Neuroticism and worry
Several studies have linked anxiety to a greater risk of cardiometabolic disease onset, Dr. Lee and colleagues wrote, but it is unclear if anxious individuals have a steadily worsening risk as they age, or if they have a higher risk in middle age, which stays the same in older age.
To investigate this, they analyzed data from 1561 men who were seen at the VA Boston outpatient clinic and did not have CAD, type 2 diabetes, stroke, or cancer when they enrolled in the Normative Aging Study.
The men had a mean age of 53 years (range, 33-84) in 1975 and were followed until 2015 or until dropout from the study or death.
At baseline, the study participants filled in the Eysenck Personality Inventory, which assesses neuroticism, and also responded to a scale indicating how much they worry about 20 issues (excluding health).
“Neuroticism,” the researchers explained, “is a tendency to perceive experiences as threatening, feel that challenges are uncontrollable, and experience frequent and disproportionately intense negative emotions,” such as fear, anxiety, sadness, and anger, “across many situations.”
“Worry refers to attempts to solve a problem where future outcome is uncertain and potentially positive or negative,” Dr. Lee noted. Although worry can be healthy and lead to constructive solutions, “it may be unhealthy, especially when it becomes uncontrollable and interferes with day-to-day functioning.”
Of note, in 1980, the American Psychiatric Association removed the term neurosis from its diagnostic manual. What was previously called neurosis is included as part of generalized anxiety disorder; GAD also encompasses excessive worry.
Cardiometabolic risk from midlife to old age
The men in the current study had on-site physical examinations every 3-5 years.
The researchers calculated the men’s cardiometabolic risk score (from 0 to 7) by assigning 1 point each for the following: systolic blood pressure greater than 130 mm Hg, diastolic blood pressure greater than 85 mm Hg, total cholesterol of at least 240 mg/dL, triglycerides of at least 150 mg/dL, body mass index of at least 30 kg/m2, glucose of at least 100 mg/dL, and erythrocyte sedimentation rate of at least 14 mm/hour.
Alternatively, patients were assigned a point each for taking medication that could affect these markers (except for body mass index).
Overall, on average, at baseline, the men had a cardiometabolic risk score of 2.9. From age 33-65, this score increased to 3.8, and then it did not increase as much later on.
That is, the cardiometabolic risk score increased by 0.8 per decade until age 65, followed by a slower increase of 0.5 per decade.
At all ages, men with higher levels of neuroticism or worry had a higher cardiometabolic risk score
Each additional standard deviation of neuroticism was associated with a 13% increased risk of having six or more of the seven cardiometabolic risk markers during follow-up, after adjusting for age, demographics, and family history of CAD, but the relationship was attenuated after also adjusting for health behaviors (for example, smoking, alcohol consumption, physical activity, and past-year physician visit at baseline).
Similarly, each additional standard deviation of worry was associated with a 10% increased risk of having six or more of the seven cardiometabolic risk markers during follow-up after the same adjustments, and was also no longer significantly different after the same further adjustments.
The research was supported by grants from the National Institutes of Health and a Senior Research Career Scientist Award from the Office of Research and Development, Department of Veterans Affairs. The Normative Aging Study is a research component of the Massachusetts Veterans Epidemiology Research and Information Center and is supported by the VA Cooperative Studies Program/Epidemiological Research Centers. The study authors and Dr. Levine disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN HEART ASSOCIATION
‘Lucky genes’ may protect against some obesity-related diseases
in a large new genetics study.
That is, people with unfavorable adiposity gene variants had fat stored under the skin throughout the body, but they also had more ectopic fat (fat in the “wrong place”) surrounding the pancreas and liver, which is associated with a higher risk of metabolic diseases such as heart disease and type 2 diabetes.
In contrast, people with favorable adiposity gene variants had more subcutaneous fat (such as a paunch or a double chin).
The study by Susan Martin, PhD, a postdoctoral research associate at the University of Exeter (England) and colleagues, was recently published in eLife.
“Some people have ‘unlucky fat genes,’ meaning they store higher levels of fat everywhere, including under the skin [and around the] liver and pancreas. That’s associated with a higher risk of diseases such as type 2 diabetes,” senior author Hanieh Yaghootkar, MD, PhD, summarized in a press release from the University of Exeter.
“Others are luckier and have genes that mean higher fat under the skin but lower liver fat and a lower risk of diseases like type 2 diabetes,” added Dr. Yaghootkar, from Brunel University London.
Among 37 chronic diseases that are associated with obesity, the researchers found the metabolic effects of adiposity are likely the main cause of the following 11: type 2 diabetes, polycystic ovary syndrome, coronary artery disease, peripheral artery disease, hypertension, stroke, heart failure, atrial fibrillation, chronic kidney disease, renal cancer, and gout.
On the other hand, excess weight itself (such as a heavy load on the joints) rather than a metabolic effect is associated with nine other obesity-related diseases: osteoarthritis, rheumatoid arthritis, osteoporosis, gastro-esophageal reflux disease, gallstones, adult-onset asthma, psoriasis, deep vein thrombosis, and venous thromboembolism.
Good genes no substitute for a healthy lifestyle
“People with more favorable adiposity gene variants are still at risk of the nine diseases” that are not caused by metabolic effects – such as osteoarthritis – but are caused by the effect of excess weight on the joints, another author, Timothy M. Frayling, PhD, stressed.
“People with obesity and unfavorable adiposity gene variants are at higher risk of all 20 diseases because they have the double hit of the excess mechanical effects and the adverse metabolic effects,” Dr. Frayling of the University of Exeter, told this news organization in an email.
The main clinical message, he said, is that “this research helps inform which conditions may respond better to therapies that lower the adverse effects” of risk factors such as high cholesterol and blood glucose levels, “and high blood pressure, even with no weight loss.”
“In contrast, other conditions really require the weight loss.”
“These results emphasize that many people in the community who are of higher body mass index are at risk of multiple chronic conditions that can severely impair their quality of life or cause morbidity or mortality, even if their metabolic parameters appear relatively normal,” the researchers conclude.
“Whilst it’s important that we identify the causes of obesity-related disease, good genes [are] still no substitute for a healthy lifestyle,” Dr. Martin stressed.
“A favorable adiposity will only go so far. If you’re obese, the advice is to still try and shift the excess weight where you can,” she said.
“The authors have conducted a robust and very comprehensive study using Mendelian randomization to disentangle metabolic and nonmetabolic effects of overweight on a long list of disease outcomes,” reviewing editor Edward D. Janus, MD, PhD, of the University of Melbourne summarized.
“This is an important topic and can help us better understand how overweight influences risk of several important outcomes.”
Metabolic and nonmetabolic diseases caused by obesity
The researchers aimed to investigate the effects of adiposity on metabolic and nonmetabolic diseases caused by obesity.
They used data from 176,899 individuals in the FinnGen project in Finland and from over 500,000 individuals in the UK Biobank database.
They performed Mendelian randomization studies to investigate the causal association between BMI, body fat percentage, favorable adiposity alleles, and unfavorable adiposity alleles with 37 disease outcomes.
Of these 37 chronic diseases associated with obesity, 11 diseases were directly related to the metabolic effect of adiposity (where favorable adiposity or unfavorable adiposity gene variants had opposite effects). Nine other diseases were unrelated to the metabolic effects of adiposity.
For most of the remaining diseases – for example, Alzheimer’s disease and different cancers – it was difficult to draw firm conclusions about the respective roles of favorable adiposity and unfavorable adiposity gene variants.
The study was funded by Diabetes UK, the UK Medical Research Council, the World Cancer Research Fund, and the National Cancer Institute. Author disclosures are listed with the article.
A version of this article first appeared on Medscape.com.
in a large new genetics study.
That is, people with unfavorable adiposity gene variants had fat stored under the skin throughout the body, but they also had more ectopic fat (fat in the “wrong place”) surrounding the pancreas and liver, which is associated with a higher risk of metabolic diseases such as heart disease and type 2 diabetes.
In contrast, people with favorable adiposity gene variants had more subcutaneous fat (such as a paunch or a double chin).
The study by Susan Martin, PhD, a postdoctoral research associate at the University of Exeter (England) and colleagues, was recently published in eLife.
“Some people have ‘unlucky fat genes,’ meaning they store higher levels of fat everywhere, including under the skin [and around the] liver and pancreas. That’s associated with a higher risk of diseases such as type 2 diabetes,” senior author Hanieh Yaghootkar, MD, PhD, summarized in a press release from the University of Exeter.
“Others are luckier and have genes that mean higher fat under the skin but lower liver fat and a lower risk of diseases like type 2 diabetes,” added Dr. Yaghootkar, from Brunel University London.
Among 37 chronic diseases that are associated with obesity, the researchers found the metabolic effects of adiposity are likely the main cause of the following 11: type 2 diabetes, polycystic ovary syndrome, coronary artery disease, peripheral artery disease, hypertension, stroke, heart failure, atrial fibrillation, chronic kidney disease, renal cancer, and gout.
On the other hand, excess weight itself (such as a heavy load on the joints) rather than a metabolic effect is associated with nine other obesity-related diseases: osteoarthritis, rheumatoid arthritis, osteoporosis, gastro-esophageal reflux disease, gallstones, adult-onset asthma, psoriasis, deep vein thrombosis, and venous thromboembolism.
Good genes no substitute for a healthy lifestyle
“People with more favorable adiposity gene variants are still at risk of the nine diseases” that are not caused by metabolic effects – such as osteoarthritis – but are caused by the effect of excess weight on the joints, another author, Timothy M. Frayling, PhD, stressed.
“People with obesity and unfavorable adiposity gene variants are at higher risk of all 20 diseases because they have the double hit of the excess mechanical effects and the adverse metabolic effects,” Dr. Frayling of the University of Exeter, told this news organization in an email.
The main clinical message, he said, is that “this research helps inform which conditions may respond better to therapies that lower the adverse effects” of risk factors such as high cholesterol and blood glucose levels, “and high blood pressure, even with no weight loss.”
“In contrast, other conditions really require the weight loss.”
“These results emphasize that many people in the community who are of higher body mass index are at risk of multiple chronic conditions that can severely impair their quality of life or cause morbidity or mortality, even if their metabolic parameters appear relatively normal,” the researchers conclude.
“Whilst it’s important that we identify the causes of obesity-related disease, good genes [are] still no substitute for a healthy lifestyle,” Dr. Martin stressed.
“A favorable adiposity will only go so far. If you’re obese, the advice is to still try and shift the excess weight where you can,” she said.
“The authors have conducted a robust and very comprehensive study using Mendelian randomization to disentangle metabolic and nonmetabolic effects of overweight on a long list of disease outcomes,” reviewing editor Edward D. Janus, MD, PhD, of the University of Melbourne summarized.
“This is an important topic and can help us better understand how overweight influences risk of several important outcomes.”
Metabolic and nonmetabolic diseases caused by obesity
The researchers aimed to investigate the effects of adiposity on metabolic and nonmetabolic diseases caused by obesity.
They used data from 176,899 individuals in the FinnGen project in Finland and from over 500,000 individuals in the UK Biobank database.
They performed Mendelian randomization studies to investigate the causal association between BMI, body fat percentage, favorable adiposity alleles, and unfavorable adiposity alleles with 37 disease outcomes.
Of these 37 chronic diseases associated with obesity, 11 diseases were directly related to the metabolic effect of adiposity (where favorable adiposity or unfavorable adiposity gene variants had opposite effects). Nine other diseases were unrelated to the metabolic effects of adiposity.
For most of the remaining diseases – for example, Alzheimer’s disease and different cancers – it was difficult to draw firm conclusions about the respective roles of favorable adiposity and unfavorable adiposity gene variants.
The study was funded by Diabetes UK, the UK Medical Research Council, the World Cancer Research Fund, and the National Cancer Institute. Author disclosures are listed with the article.
A version of this article first appeared on Medscape.com.
in a large new genetics study.
That is, people with unfavorable adiposity gene variants had fat stored under the skin throughout the body, but they also had more ectopic fat (fat in the “wrong place”) surrounding the pancreas and liver, which is associated with a higher risk of metabolic diseases such as heart disease and type 2 diabetes.
In contrast, people with favorable adiposity gene variants had more subcutaneous fat (such as a paunch or a double chin).
The study by Susan Martin, PhD, a postdoctoral research associate at the University of Exeter (England) and colleagues, was recently published in eLife.
“Some people have ‘unlucky fat genes,’ meaning they store higher levels of fat everywhere, including under the skin [and around the] liver and pancreas. That’s associated with a higher risk of diseases such as type 2 diabetes,” senior author Hanieh Yaghootkar, MD, PhD, summarized in a press release from the University of Exeter.
“Others are luckier and have genes that mean higher fat under the skin but lower liver fat and a lower risk of diseases like type 2 diabetes,” added Dr. Yaghootkar, from Brunel University London.
Among 37 chronic diseases that are associated with obesity, the researchers found the metabolic effects of adiposity are likely the main cause of the following 11: type 2 diabetes, polycystic ovary syndrome, coronary artery disease, peripheral artery disease, hypertension, stroke, heart failure, atrial fibrillation, chronic kidney disease, renal cancer, and gout.
On the other hand, excess weight itself (such as a heavy load on the joints) rather than a metabolic effect is associated with nine other obesity-related diseases: osteoarthritis, rheumatoid arthritis, osteoporosis, gastro-esophageal reflux disease, gallstones, adult-onset asthma, psoriasis, deep vein thrombosis, and venous thromboembolism.
Good genes no substitute for a healthy lifestyle
“People with more favorable adiposity gene variants are still at risk of the nine diseases” that are not caused by metabolic effects – such as osteoarthritis – but are caused by the effect of excess weight on the joints, another author, Timothy M. Frayling, PhD, stressed.
“People with obesity and unfavorable adiposity gene variants are at higher risk of all 20 diseases because they have the double hit of the excess mechanical effects and the adverse metabolic effects,” Dr. Frayling of the University of Exeter, told this news organization in an email.
The main clinical message, he said, is that “this research helps inform which conditions may respond better to therapies that lower the adverse effects” of risk factors such as high cholesterol and blood glucose levels, “and high blood pressure, even with no weight loss.”
“In contrast, other conditions really require the weight loss.”
“These results emphasize that many people in the community who are of higher body mass index are at risk of multiple chronic conditions that can severely impair their quality of life or cause morbidity or mortality, even if their metabolic parameters appear relatively normal,” the researchers conclude.
“Whilst it’s important that we identify the causes of obesity-related disease, good genes [are] still no substitute for a healthy lifestyle,” Dr. Martin stressed.
“A favorable adiposity will only go so far. If you’re obese, the advice is to still try and shift the excess weight where you can,” she said.
“The authors have conducted a robust and very comprehensive study using Mendelian randomization to disentangle metabolic and nonmetabolic effects of overweight on a long list of disease outcomes,” reviewing editor Edward D. Janus, MD, PhD, of the University of Melbourne summarized.
“This is an important topic and can help us better understand how overweight influences risk of several important outcomes.”
Metabolic and nonmetabolic diseases caused by obesity
The researchers aimed to investigate the effects of adiposity on metabolic and nonmetabolic diseases caused by obesity.
They used data from 176,899 individuals in the FinnGen project in Finland and from over 500,000 individuals in the UK Biobank database.
They performed Mendelian randomization studies to investigate the causal association between BMI, body fat percentage, favorable adiposity alleles, and unfavorable adiposity alleles with 37 disease outcomes.
Of these 37 chronic diseases associated with obesity, 11 diseases were directly related to the metabolic effect of adiposity (where favorable adiposity or unfavorable adiposity gene variants had opposite effects). Nine other diseases were unrelated to the metabolic effects of adiposity.
For most of the remaining diseases – for example, Alzheimer’s disease and different cancers – it was difficult to draw firm conclusions about the respective roles of favorable adiposity and unfavorable adiposity gene variants.
The study was funded by Diabetes UK, the UK Medical Research Council, the World Cancer Research Fund, and the National Cancer Institute. Author disclosures are listed with the article.
A version of this article first appeared on Medscape.com.
‘Physiology fights back’ when people are trying to lose weight
Metabolic adaptation – slowing of metabolism in response to weight loss – increases the length of time needed to achieve a target lower weight, a new study of premenopausal women with overweight reports.
All of the 65 sedentary young and middle-aged women with overweight who were on a low-calorie diet (800 calories/day) attained their target lower weight – corresponding to a body mass index (BMI) of 25 kg/m2 or less – after 66-252 days.
But a woman with the largest metabolic adaptation needed to stay on the diet for an extra 70 days, compared with a woman with no metabolic adaptation, to reach the target BMI, after adjusting for dietary adherence.
The study by Catia Martins, PhD, and colleagues was published Jan. 27, 2022, in Obesity.
“Even though adherence to the diet is clearly the most important determinant of time to reach weight loss goals,” wrote Dr. Martins and colleagues, “the present findings are of great clinical relevance as they mean that individuals who are struggling to achieve weight-loss goals, despite assuring compliance with the diet, may indeed be ‘suffering’ from metabolic adaptation during active weight loss.”
Therefore, “clinicians need to consider metabolic adaptation when assessing resistance to weight loss,” they concluded.
Good news: Metabolic adaption ceases when weight stabilizes
“This study shows that a longer than expected duration of intervention to achieve weight loss targets might be due to metabolic adaptation, even after controlling for adherence to the diet,” Dr. Martins said in an interview.
Metabolic adaptation while on a diet makes it harder to lose the last pound than to lose the first pound because as weight loss progresses metabolic adaptation increases, she noted.
However, “the good news is that this mechanism disappears once weight is stabilized (a new energy balance is established), and it is not a predictor of weight regain in the long term,” noted Dr. Martins, associate professor, nutrition sciences research, University of Alabama at Birmingham.
The group published a study in 2020 showing that metabolic adaptation does not predict weight regain at 1 year, and another study, published a few months earlier, showed it is not a barrier to weight-loss maintenance.
The current study findings “provide further evidence of the ways that physiology fights back when people are trying to lose weight,” David B. Sarwer, PhD, who was not involved with this research, said in a press release from the Obesity Society.
“A countless number of environmental variables and other social determinants of health also make weight loss and maintenance challenging for many individuals,” added Dr. Sarwer, director of the Center for Obesity Research and Education at Temple University, Philadelphia.
“Nevertheless, it is import to remember that even a modest weight loss of 5% of initial body weight – much smaller than seen in this study – is associated with clinically significant improvements in weight-related health issues for many individuals,” he stressed.
16% weight loss at 5 weeks with 800-calorie/day diet
It is unclear whether metabolic adaptation contributes to resistance to weight loss by increasing the time necessary to achieve weight-loss goals.
To investigate this, Dr. Martins and associates analyzed data from 36 White women and 29 Black women, aged 20-41 years (mean age, 36), who had a mean BMI of 28.6 and had participated in the diet arms of two studies (ROMEO and JULIET) conducted at Martins’ institution.
Participants received food containing 20% to 22% fat, 20% to 22% protein, and 56% to 58% carbohydrate provided by the center’s research kitchen.
On average, the women were 64% compliant with the diet and lost 12.5 kg (27.6 pounds), a 16% weight loss, over 155 days.
Metabolic adaption was measured 4 weeks after weight stabilization after reaching the weight-loss target.
On average, participants’ resting metabolic rate after weight loss was 46 kcal lower than what would be expected for their lower body weight.
Metabolic adaptation after weight loss was a significant predictor of time to reach the weight-loss goal, after adjusting for target weight loss, energy deficit, and adherence to the diet (R2 adjusted, 0.63; P < .001).
The study findings may not be generalizable to men, older patients, or people with a higher BMI, so further research is needed in a broader population, the researchers concluded.
The research was supported by National Institutes of Health grants. Dr. Martins was supported by a sabbatical grant from the Liaison Committee for Education, Research, and Innovation in Central Norway and the Norwegian University of Science and Technology. The researchers have no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
Metabolic adaptation – slowing of metabolism in response to weight loss – increases the length of time needed to achieve a target lower weight, a new study of premenopausal women with overweight reports.
All of the 65 sedentary young and middle-aged women with overweight who were on a low-calorie diet (800 calories/day) attained their target lower weight – corresponding to a body mass index (BMI) of 25 kg/m2 or less – after 66-252 days.
But a woman with the largest metabolic adaptation needed to stay on the diet for an extra 70 days, compared with a woman with no metabolic adaptation, to reach the target BMI, after adjusting for dietary adherence.
The study by Catia Martins, PhD, and colleagues was published Jan. 27, 2022, in Obesity.
“Even though adherence to the diet is clearly the most important determinant of time to reach weight loss goals,” wrote Dr. Martins and colleagues, “the present findings are of great clinical relevance as they mean that individuals who are struggling to achieve weight-loss goals, despite assuring compliance with the diet, may indeed be ‘suffering’ from metabolic adaptation during active weight loss.”
Therefore, “clinicians need to consider metabolic adaptation when assessing resistance to weight loss,” they concluded.
Good news: Metabolic adaption ceases when weight stabilizes
“This study shows that a longer than expected duration of intervention to achieve weight loss targets might be due to metabolic adaptation, even after controlling for adherence to the diet,” Dr. Martins said in an interview.
Metabolic adaptation while on a diet makes it harder to lose the last pound than to lose the first pound because as weight loss progresses metabolic adaptation increases, she noted.
However, “the good news is that this mechanism disappears once weight is stabilized (a new energy balance is established), and it is not a predictor of weight regain in the long term,” noted Dr. Martins, associate professor, nutrition sciences research, University of Alabama at Birmingham.
The group published a study in 2020 showing that metabolic adaptation does not predict weight regain at 1 year, and another study, published a few months earlier, showed it is not a barrier to weight-loss maintenance.
The current study findings “provide further evidence of the ways that physiology fights back when people are trying to lose weight,” David B. Sarwer, PhD, who was not involved with this research, said in a press release from the Obesity Society.
“A countless number of environmental variables and other social determinants of health also make weight loss and maintenance challenging for many individuals,” added Dr. Sarwer, director of the Center for Obesity Research and Education at Temple University, Philadelphia.
“Nevertheless, it is import to remember that even a modest weight loss of 5% of initial body weight – much smaller than seen in this study – is associated with clinically significant improvements in weight-related health issues for many individuals,” he stressed.
16% weight loss at 5 weeks with 800-calorie/day diet
It is unclear whether metabolic adaptation contributes to resistance to weight loss by increasing the time necessary to achieve weight-loss goals.
To investigate this, Dr. Martins and associates analyzed data from 36 White women and 29 Black women, aged 20-41 years (mean age, 36), who had a mean BMI of 28.6 and had participated in the diet arms of two studies (ROMEO and JULIET) conducted at Martins’ institution.
Participants received food containing 20% to 22% fat, 20% to 22% protein, and 56% to 58% carbohydrate provided by the center’s research kitchen.
On average, the women were 64% compliant with the diet and lost 12.5 kg (27.6 pounds), a 16% weight loss, over 155 days.
Metabolic adaption was measured 4 weeks after weight stabilization after reaching the weight-loss target.
On average, participants’ resting metabolic rate after weight loss was 46 kcal lower than what would be expected for their lower body weight.
Metabolic adaptation after weight loss was a significant predictor of time to reach the weight-loss goal, after adjusting for target weight loss, energy deficit, and adherence to the diet (R2 adjusted, 0.63; P < .001).
The study findings may not be generalizable to men, older patients, or people with a higher BMI, so further research is needed in a broader population, the researchers concluded.
The research was supported by National Institutes of Health grants. Dr. Martins was supported by a sabbatical grant from the Liaison Committee for Education, Research, and Innovation in Central Norway and the Norwegian University of Science and Technology. The researchers have no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
Metabolic adaptation – slowing of metabolism in response to weight loss – increases the length of time needed to achieve a target lower weight, a new study of premenopausal women with overweight reports.
All of the 65 sedentary young and middle-aged women with overweight who were on a low-calorie diet (800 calories/day) attained their target lower weight – corresponding to a body mass index (BMI) of 25 kg/m2 or less – after 66-252 days.
But a woman with the largest metabolic adaptation needed to stay on the diet for an extra 70 days, compared with a woman with no metabolic adaptation, to reach the target BMI, after adjusting for dietary adherence.
The study by Catia Martins, PhD, and colleagues was published Jan. 27, 2022, in Obesity.
“Even though adherence to the diet is clearly the most important determinant of time to reach weight loss goals,” wrote Dr. Martins and colleagues, “the present findings are of great clinical relevance as they mean that individuals who are struggling to achieve weight-loss goals, despite assuring compliance with the diet, may indeed be ‘suffering’ from metabolic adaptation during active weight loss.”
Therefore, “clinicians need to consider metabolic adaptation when assessing resistance to weight loss,” they concluded.
Good news: Metabolic adaption ceases when weight stabilizes
“This study shows that a longer than expected duration of intervention to achieve weight loss targets might be due to metabolic adaptation, even after controlling for adherence to the diet,” Dr. Martins said in an interview.
Metabolic adaptation while on a diet makes it harder to lose the last pound than to lose the first pound because as weight loss progresses metabolic adaptation increases, she noted.
However, “the good news is that this mechanism disappears once weight is stabilized (a new energy balance is established), and it is not a predictor of weight regain in the long term,” noted Dr. Martins, associate professor, nutrition sciences research, University of Alabama at Birmingham.
The group published a study in 2020 showing that metabolic adaptation does not predict weight regain at 1 year, and another study, published a few months earlier, showed it is not a barrier to weight-loss maintenance.
The current study findings “provide further evidence of the ways that physiology fights back when people are trying to lose weight,” David B. Sarwer, PhD, who was not involved with this research, said in a press release from the Obesity Society.
“A countless number of environmental variables and other social determinants of health also make weight loss and maintenance challenging for many individuals,” added Dr. Sarwer, director of the Center for Obesity Research and Education at Temple University, Philadelphia.
“Nevertheless, it is import to remember that even a modest weight loss of 5% of initial body weight – much smaller than seen in this study – is associated with clinically significant improvements in weight-related health issues for many individuals,” he stressed.
16% weight loss at 5 weeks with 800-calorie/day diet
It is unclear whether metabolic adaptation contributes to resistance to weight loss by increasing the time necessary to achieve weight-loss goals.
To investigate this, Dr. Martins and associates analyzed data from 36 White women and 29 Black women, aged 20-41 years (mean age, 36), who had a mean BMI of 28.6 and had participated in the diet arms of two studies (ROMEO and JULIET) conducted at Martins’ institution.
Participants received food containing 20% to 22% fat, 20% to 22% protein, and 56% to 58% carbohydrate provided by the center’s research kitchen.
On average, the women were 64% compliant with the diet and lost 12.5 kg (27.6 pounds), a 16% weight loss, over 155 days.
Metabolic adaption was measured 4 weeks after weight stabilization after reaching the weight-loss target.
On average, participants’ resting metabolic rate after weight loss was 46 kcal lower than what would be expected for their lower body weight.
Metabolic adaptation after weight loss was a significant predictor of time to reach the weight-loss goal, after adjusting for target weight loss, energy deficit, and adherence to the diet (R2 adjusted, 0.63; P < .001).
The study findings may not be generalizable to men, older patients, or people with a higher BMI, so further research is needed in a broader population, the researchers concluded.
The research was supported by National Institutes of Health grants. Dr. Martins was supported by a sabbatical grant from the Liaison Committee for Education, Research, and Innovation in Central Norway and the Norwegian University of Science and Technology. The researchers have no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
FROM OBESITY
Breastfeeding linked to lower CVD risk in later life
In a meta-analysis of more than 1 million mothers, those who breastfed their children had an 11% to 17% lower risk of developing cardiovascular disease (CVD), coronary heart disease (CHD), or stroke, and of dying from CVD, in later life than mothers who did not.
On average, the women had two children and had breastfed for 15.9 months in total. Longer breastfeeding was associated with greater CV health benefit.
This meta-analysis of eight studies from different countries was published online Jan. 11 in an issue of the Journal of the American Heart Association devoted to the impact of pregnancy on CV health in the mother and child.
Breastfeeding is known to be associated with a lower risk for death from infectious disease and with fewer respiratory infections in babies, the researchers write, but what is less well known is that it is also associated with a reduced risk for breast and ovarian cancer and type 2 diabetes in mothers.
The current study showed a clear association between breastfeeding and reduced risk for CVD in later life, lead author Lena Tschiderer, Dipl.-Ing., PhD, and senior author Peter Willeit, MD, MPhil, PhD, summarized in a joint email to this news organization.
Specifically, mothers who had breastfed their children at any time had an 11% lower risk for CVD, a 14% lower risk for CHD, a 12% lower risk for stroke, and a 17% lower risk of dying from CVD in later life, compared with other mothers.
On the basis of existing evidence, the researchers write, the World Health Organization recommends exclusive breastfeeding until a baby is 6 months old, followed by breastfeeding plus complementary feeding until the baby is 2 years or older.
“We believe that [breastfeeding] benefits for the mother are communicated poorly,” said Dr. Tschiderer and Dr. Willeit, from the University of Innsbruck, Austria.
“Positive effects of breastfeeding on mothers need to be communicated effectively, awareness for breastfeeding recommendations needs to be raised, and interventions to promote and facilitate breastfeeding need to be implemented and reinforced,” the researchers conclude.
‘Should not be ignored’
Two cardiologists invited to comment, who were not involved with the research, noted that this study provides insight into an important topic.
“This is yet another body of evidence [and the largest population to date] to show that breastfeeding is protective for women and may show important beneficial effects in terms of CV risk,” Roxana Mehran, MD, said in an email.
“The risk reductions were 11% for CVD events and 14% for CHD events; these are impressive numbers,” said Dr. Mehran, from Icahn School of Medicine at Mount Sinai, New York.
“The caveat,” she said, “is that these are data from several trials, but nonetheless, this is a very important observation that should not be ignored.”
The study did not address the definitive amount of time of breastfeeding and its correlation to the improvement of CVD risk, but it did show that for the lifetime duration, the longer the better.
“The beneficial effects,” she noted, “can be linked to hormones during breastfeeding, as well as weight loss associated with breastfeeding, and resetting the maternal metabolism, as the authors suggest.”
Clinicians and employers “must provide ways to educate women about breastfeeding and make it easy for women who are in the workplace to pump, and to provide them with resources” where possible, Dr. Mehran said.
Michelle O’Donoghue, MD, MPH, noted that over the past several years, there has been intense interest in the possible health benefits of breastfeeding for both mother and child.
There is biologic plausibility for some of the possible maternal benefits because the favorable CV effects of both prolactin and oxytocin are only now being better understood, said Dr. O’Donoghue, from Brigham and Women’s Hospital and Harvard Medical School, Boston.
“The current meta-analysis provides a large dataset that helps support the concept that breastfeeding may offer some cardiovascular benefit for the mother,” she agreed.
“However, ultimately more research will be necessary since this method of combining data across trials relies upon the robustness of the statistical method in each study,” Dr. O’Donoghue said. “I applaud the authors for shining a spotlight on this important topic.”
Although the benefits of breastfeeding appear to continue over time, “it is incredibly difficult for women to continue breastfeeding once they return to work,” she added. “Women in some countries outside the U.S. have an advantage due to longer durations of maternity leave.
“If we want to encourage breastfeeding,” Dr. O’Donoghue stressed, “we need to make sure that we put the right supports in place. Women need protected places to breastfeed in the workplace and places to store their milk. Most importantly, women need to be allowed dedicated time to make it happen.”
First large study of CVD in mothers
Emerging individual studies suggest that mothers who breastfeed may have a lower risk for CVD in later life, but studies have been inconsistent, and it is not clear if longer breastfeeding would strengthen this benefit, the authors note.
To examine this, they pooled data from the following eight studies (with study acronym, country, and baseline enrolment dates in brackets): 45&Up (Australia, 2006-2009), China Kadoorie Biobank (CKB, China, 2004-2008), European Prospective Investigation into Cancer and Nutrition (EPIC, multinational, 1992-2000), Gallagher et al. (China, 1989-1991), Nord-Trøndelag Health Survey 2 (HUNT2, Norway, 1995-1997), Japan Public Health Center-based Prospective Study (JPHC, Japan, 1990-1994), Nurses’ Health Study (NHS, U.S., 1986), and the Woman’s Health Initiative (WHI, U.S., 1993-1998).
On average, the women were 51.3 years old (range, 40-65 years) when they enrolled in the study, and they were followed for a median of 10.3 years (range, 7.9-20.9 years, in the individual studies).
On average, they had their first child at age 25 and had two to three children (mean, 2.3); 82% had breastfed at some point (ranging from 58% of women in the two U.S. studies to 97% in CKB and HUNT2).
The women had breastfed for a mean of 7.4 to 18.9 months during their lifetimes (except women in the CKB study, who had breastfed for a median of 24 months).
Among the 1,192,700 women, there were 54,226 incident CVD events, 26,913 incident CHD events, 30,843 incident strokes, and 10,766 deaths from CVD during follow-up.
The researchers acknowledge that study limitations include the fact that there could have been publication bias, since fewer than 10 studies were available for pooling. There was significant between-study heterogeneity for CVD, CHD, and stroke outcomes.
Participant-level data were also lacking, and breastfeeding was self-reported. There may have been unaccounted residual confounding, and the benefits of lifetime breastfeeding that is longer than 2 years are not clear, because few women in this population breastfed that long.
The research was funded by the Austrian Science Fund. The researchers and Dr. Mehran and Dr. O’Donoghue have no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
In a meta-analysis of more than 1 million mothers, those who breastfed their children had an 11% to 17% lower risk of developing cardiovascular disease (CVD), coronary heart disease (CHD), or stroke, and of dying from CVD, in later life than mothers who did not.
On average, the women had two children and had breastfed for 15.9 months in total. Longer breastfeeding was associated with greater CV health benefit.
This meta-analysis of eight studies from different countries was published online Jan. 11 in an issue of the Journal of the American Heart Association devoted to the impact of pregnancy on CV health in the mother and child.
Breastfeeding is known to be associated with a lower risk for death from infectious disease and with fewer respiratory infections in babies, the researchers write, but what is less well known is that it is also associated with a reduced risk for breast and ovarian cancer and type 2 diabetes in mothers.
The current study showed a clear association between breastfeeding and reduced risk for CVD in later life, lead author Lena Tschiderer, Dipl.-Ing., PhD, and senior author Peter Willeit, MD, MPhil, PhD, summarized in a joint email to this news organization.
Specifically, mothers who had breastfed their children at any time had an 11% lower risk for CVD, a 14% lower risk for CHD, a 12% lower risk for stroke, and a 17% lower risk of dying from CVD in later life, compared with other mothers.
On the basis of existing evidence, the researchers write, the World Health Organization recommends exclusive breastfeeding until a baby is 6 months old, followed by breastfeeding plus complementary feeding until the baby is 2 years or older.
“We believe that [breastfeeding] benefits for the mother are communicated poorly,” said Dr. Tschiderer and Dr. Willeit, from the University of Innsbruck, Austria.
“Positive effects of breastfeeding on mothers need to be communicated effectively, awareness for breastfeeding recommendations needs to be raised, and interventions to promote and facilitate breastfeeding need to be implemented and reinforced,” the researchers conclude.
‘Should not be ignored’
Two cardiologists invited to comment, who were not involved with the research, noted that this study provides insight into an important topic.
“This is yet another body of evidence [and the largest population to date] to show that breastfeeding is protective for women and may show important beneficial effects in terms of CV risk,” Roxana Mehran, MD, said in an email.
“The risk reductions were 11% for CVD events and 14% for CHD events; these are impressive numbers,” said Dr. Mehran, from Icahn School of Medicine at Mount Sinai, New York.
“The caveat,” she said, “is that these are data from several trials, but nonetheless, this is a very important observation that should not be ignored.”
The study did not address the definitive amount of time of breastfeeding and its correlation to the improvement of CVD risk, but it did show that for the lifetime duration, the longer the better.
“The beneficial effects,” she noted, “can be linked to hormones during breastfeeding, as well as weight loss associated with breastfeeding, and resetting the maternal metabolism, as the authors suggest.”
Clinicians and employers “must provide ways to educate women about breastfeeding and make it easy for women who are in the workplace to pump, and to provide them with resources” where possible, Dr. Mehran said.
Michelle O’Donoghue, MD, MPH, noted that over the past several years, there has been intense interest in the possible health benefits of breastfeeding for both mother and child.
There is biologic plausibility for some of the possible maternal benefits because the favorable CV effects of both prolactin and oxytocin are only now being better understood, said Dr. O’Donoghue, from Brigham and Women’s Hospital and Harvard Medical School, Boston.
“The current meta-analysis provides a large dataset that helps support the concept that breastfeeding may offer some cardiovascular benefit for the mother,” she agreed.
“However, ultimately more research will be necessary since this method of combining data across trials relies upon the robustness of the statistical method in each study,” Dr. O’Donoghue said. “I applaud the authors for shining a spotlight on this important topic.”
Although the benefits of breastfeeding appear to continue over time, “it is incredibly difficult for women to continue breastfeeding once they return to work,” she added. “Women in some countries outside the U.S. have an advantage due to longer durations of maternity leave.
“If we want to encourage breastfeeding,” Dr. O’Donoghue stressed, “we need to make sure that we put the right supports in place. Women need protected places to breastfeed in the workplace and places to store their milk. Most importantly, women need to be allowed dedicated time to make it happen.”
First large study of CVD in mothers
Emerging individual studies suggest that mothers who breastfeed may have a lower risk for CVD in later life, but studies have been inconsistent, and it is not clear if longer breastfeeding would strengthen this benefit, the authors note.
To examine this, they pooled data from the following eight studies (with study acronym, country, and baseline enrolment dates in brackets): 45&Up (Australia, 2006-2009), China Kadoorie Biobank (CKB, China, 2004-2008), European Prospective Investigation into Cancer and Nutrition (EPIC, multinational, 1992-2000), Gallagher et al. (China, 1989-1991), Nord-Trøndelag Health Survey 2 (HUNT2, Norway, 1995-1997), Japan Public Health Center-based Prospective Study (JPHC, Japan, 1990-1994), Nurses’ Health Study (NHS, U.S., 1986), and the Woman’s Health Initiative (WHI, U.S., 1993-1998).
On average, the women were 51.3 years old (range, 40-65 years) when they enrolled in the study, and they were followed for a median of 10.3 years (range, 7.9-20.9 years, in the individual studies).
On average, they had their first child at age 25 and had two to three children (mean, 2.3); 82% had breastfed at some point (ranging from 58% of women in the two U.S. studies to 97% in CKB and HUNT2).
The women had breastfed for a mean of 7.4 to 18.9 months during their lifetimes (except women in the CKB study, who had breastfed for a median of 24 months).
Among the 1,192,700 women, there were 54,226 incident CVD events, 26,913 incident CHD events, 30,843 incident strokes, and 10,766 deaths from CVD during follow-up.
The researchers acknowledge that study limitations include the fact that there could have been publication bias, since fewer than 10 studies were available for pooling. There was significant between-study heterogeneity for CVD, CHD, and stroke outcomes.
Participant-level data were also lacking, and breastfeeding was self-reported. There may have been unaccounted residual confounding, and the benefits of lifetime breastfeeding that is longer than 2 years are not clear, because few women in this population breastfed that long.
The research was funded by the Austrian Science Fund. The researchers and Dr. Mehran and Dr. O’Donoghue have no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
In a meta-analysis of more than 1 million mothers, those who breastfed their children had an 11% to 17% lower risk of developing cardiovascular disease (CVD), coronary heart disease (CHD), or stroke, and of dying from CVD, in later life than mothers who did not.
On average, the women had two children and had breastfed for 15.9 months in total. Longer breastfeeding was associated with greater CV health benefit.
This meta-analysis of eight studies from different countries was published online Jan. 11 in an issue of the Journal of the American Heart Association devoted to the impact of pregnancy on CV health in the mother and child.
Breastfeeding is known to be associated with a lower risk for death from infectious disease and with fewer respiratory infections in babies, the researchers write, but what is less well known is that it is also associated with a reduced risk for breast and ovarian cancer and type 2 diabetes in mothers.
The current study showed a clear association between breastfeeding and reduced risk for CVD in later life, lead author Lena Tschiderer, Dipl.-Ing., PhD, and senior author Peter Willeit, MD, MPhil, PhD, summarized in a joint email to this news organization.
Specifically, mothers who had breastfed their children at any time had an 11% lower risk for CVD, a 14% lower risk for CHD, a 12% lower risk for stroke, and a 17% lower risk of dying from CVD in later life, compared with other mothers.
On the basis of existing evidence, the researchers write, the World Health Organization recommends exclusive breastfeeding until a baby is 6 months old, followed by breastfeeding plus complementary feeding until the baby is 2 years or older.
“We believe that [breastfeeding] benefits for the mother are communicated poorly,” said Dr. Tschiderer and Dr. Willeit, from the University of Innsbruck, Austria.
“Positive effects of breastfeeding on mothers need to be communicated effectively, awareness for breastfeeding recommendations needs to be raised, and interventions to promote and facilitate breastfeeding need to be implemented and reinforced,” the researchers conclude.
‘Should not be ignored’
Two cardiologists invited to comment, who were not involved with the research, noted that this study provides insight into an important topic.
“This is yet another body of evidence [and the largest population to date] to show that breastfeeding is protective for women and may show important beneficial effects in terms of CV risk,” Roxana Mehran, MD, said in an email.
“The risk reductions were 11% for CVD events and 14% for CHD events; these are impressive numbers,” said Dr. Mehran, from Icahn School of Medicine at Mount Sinai, New York.
“The caveat,” she said, “is that these are data from several trials, but nonetheless, this is a very important observation that should not be ignored.”
The study did not address the definitive amount of time of breastfeeding and its correlation to the improvement of CVD risk, but it did show that for the lifetime duration, the longer the better.
“The beneficial effects,” she noted, “can be linked to hormones during breastfeeding, as well as weight loss associated with breastfeeding, and resetting the maternal metabolism, as the authors suggest.”
Clinicians and employers “must provide ways to educate women about breastfeeding and make it easy for women who are in the workplace to pump, and to provide them with resources” where possible, Dr. Mehran said.
Michelle O’Donoghue, MD, MPH, noted that over the past several years, there has been intense interest in the possible health benefits of breastfeeding for both mother and child.
There is biologic plausibility for some of the possible maternal benefits because the favorable CV effects of both prolactin and oxytocin are only now being better understood, said Dr. O’Donoghue, from Brigham and Women’s Hospital and Harvard Medical School, Boston.
“The current meta-analysis provides a large dataset that helps support the concept that breastfeeding may offer some cardiovascular benefit for the mother,” she agreed.
“However, ultimately more research will be necessary since this method of combining data across trials relies upon the robustness of the statistical method in each study,” Dr. O’Donoghue said. “I applaud the authors for shining a spotlight on this important topic.”
Although the benefits of breastfeeding appear to continue over time, “it is incredibly difficult for women to continue breastfeeding once they return to work,” she added. “Women in some countries outside the U.S. have an advantage due to longer durations of maternity leave.
“If we want to encourage breastfeeding,” Dr. O’Donoghue stressed, “we need to make sure that we put the right supports in place. Women need protected places to breastfeed in the workplace and places to store their milk. Most importantly, women need to be allowed dedicated time to make it happen.”
First large study of CVD in mothers
Emerging individual studies suggest that mothers who breastfeed may have a lower risk for CVD in later life, but studies have been inconsistent, and it is not clear if longer breastfeeding would strengthen this benefit, the authors note.
To examine this, they pooled data from the following eight studies (with study acronym, country, and baseline enrolment dates in brackets): 45&Up (Australia, 2006-2009), China Kadoorie Biobank (CKB, China, 2004-2008), European Prospective Investigation into Cancer and Nutrition (EPIC, multinational, 1992-2000), Gallagher et al. (China, 1989-1991), Nord-Trøndelag Health Survey 2 (HUNT2, Norway, 1995-1997), Japan Public Health Center-based Prospective Study (JPHC, Japan, 1990-1994), Nurses’ Health Study (NHS, U.S., 1986), and the Woman’s Health Initiative (WHI, U.S., 1993-1998).
On average, the women were 51.3 years old (range, 40-65 years) when they enrolled in the study, and they were followed for a median of 10.3 years (range, 7.9-20.9 years, in the individual studies).
On average, they had their first child at age 25 and had two to three children (mean, 2.3); 82% had breastfed at some point (ranging from 58% of women in the two U.S. studies to 97% in CKB and HUNT2).
The women had breastfed for a mean of 7.4 to 18.9 months during their lifetimes (except women in the CKB study, who had breastfed for a median of 24 months).
Among the 1,192,700 women, there were 54,226 incident CVD events, 26,913 incident CHD events, 30,843 incident strokes, and 10,766 deaths from CVD during follow-up.
The researchers acknowledge that study limitations include the fact that there could have been publication bias, since fewer than 10 studies were available for pooling. There was significant between-study heterogeneity for CVD, CHD, and stroke outcomes.
Participant-level data were also lacking, and breastfeeding was self-reported. There may have been unaccounted residual confounding, and the benefits of lifetime breastfeeding that is longer than 2 years are not clear, because few women in this population breastfed that long.
The research was funded by the Austrian Science Fund. The researchers and Dr. Mehran and Dr. O’Donoghue have no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
Preschool boys’ behaviors traced back to moms’ thyroid hormones
Pregnant women’s thyroid hormone trajectories (levels in the first, second, and third trimester) may predict whether their male offspring are aggressive or withdrawn at age 4.
Certain maternal thyroid hormone trajectories were associated with problem behaviors in preschool boys in a study of close to 2,000 mother-child pairs in China.
The researchers identified low, moderate, and high thyroid-stimulating hormone (TSH) and free thyroxine (FT4) trajectories.
Most women had a low TSH trajectory and moderate FT4 trajectory, which the researchers deemed to be reference (normal) trajectories.
The children’s primary caregiver (parent or grandparent) completed an extensive questionnaire about their child’s behavior at age 4.
The 4-year-old boys whose mothers had a high TSH trajectory during pregnancy were more likely to be withdrawn and to externalize problems (odds ratio, 2.01 and 2.69, respectively).
Boys whose mothers had a high FT4 trajectory during pregnancy were more likely to be anxious/depressed (OR, 2.22).
And boys whose mothers had a moderate TSH trajectory or low FT4 trajectory were more likely to show aggressive behavior (OR, 3.76 and 4.17, respectively), compared with boys whose mothers had normal TSH and FT4 trajectories, after adjusting for potential confounders.
However, there was no association between abnormal maternal thyroid hormone trajectories and behavior problems in 4-year-old girls.
The study by Peixuan Li, BM, and colleagues was published online Jan. 6 in the Journal of Clinical Endocrinology & Metabolism.
‘Study supports monitoring thyroid function in pregnancy’
“Our findings highlight the significance of close monitoring and management of maternal thyroid function during pregnancy,” senior author Kun Huang, PhD, said in a press release from the Endocrine Society.
“This research presents a new perspective in early intervention of children’s emotional and behavioral problems,” added Dr. Huang, from Anhui Medical University, Hefei, China.
The results add to a growing body of literature about a controversial link between maternal thyroid hormones in pregnancy, when the fetal brain is developing, and subsequent behavior in preschool children, Caroline T. Nguyen, MD, who was not involved with this research, commented in an email.
“Some studies show an association between thyroid levels and behavioral outcomes, others not,” added Dr. Nguyen, assistant professor of clinical medicine, Keck School of Medicine, University of Southern California, Los Angeles. And “some studies have found sex-specific associations with maternal thyroid levels and neurocognitive/behavioral outcomes, others have not.”
Women considering pregnancy should be evaluated for possible thyroid disease, she continued. Currently, no universal screening mandates exist for thyroid disease in pregnancy, but the 2017 American Thyroid Association guidelines do recommend screening women at risk for thyroid dysfunction.
“I think screening for thyroid peroxidase antibody (TPOAb) positivity is helpful in women desiring pregnancy,” Dr. Nguyen continued, “because we know that patients with TPOAb positivity are at increased risk for miscarriage and have a blunted response to the increased demands of pregnancy for thyroid hormone production.”
TPOAb positivity is also associated with the increased risk of postpartum and long-term thyroid dysfunction.
This current study, Dr. Nguyen summarized, “adds to a growing body of research of the relationship of thyroid hormone levels and neurocognitive outcomes [in offspring] and supports the monitoring of thyroid disease in pregnancy.”
“However, we do not have sufficient data to demonstrate the benefits of intervention with levothyroxine treatment,” she noted.
Nevertheless, the lack of positive data does not suggest there is no theoretical benefit of intervention, she said, as such studies are very challenging to do.
“Physicians can help reduce stress and anxiety in patients desiring pregnancy by [recommending] preconception counseling, screening patients at risk for thyroid disease, and optimizing thyroid hormone levels before and during pregnancy,” according to Dr. Nguyen.
Maternal TSH and FT4 trajectories and preschoolers’ behaviors
Previous studies have reported that during pregnancy, maternal subclinical hypothyroidism (elevated TSH with normal FT4) as well as isolated hypothyroxinemia (decreased FT4 with normal TSH) are associated with adverse maternal and child outcomes, including preterm delivery and low birth weight.
However, most studies have not determined maternal thyroid hormone levels in different trimesters.
Researchers recruited pregnant women going for their first antenatal checkup at the Ma’anshan Maternal and Child Health Hospital in China from May 2013 to September 2014 and identified 1,860 mother-child pairs.
They determined maternal thyroid hormone levels from blood samples taken during the first, second, and third trimester: on average, gestational week 10, 25, and 34, respectively.
The researchers found that TSH levels increased somewhat from trimester 1 to trimester 2 and then decreased slightly in trimester 3. Most women (68%) had a low TSH trajectory, 28% had a moderate TSH trajectory, and 4% had a high TSH trajectory.
FT4 levels dropped sharply from trimester 1 to trimester 2 and then increased somewhat in trimester 3. About half of the women (52%) had a moderate FT4 trajectory, 33% had a low FT4 trajectory, and 15% had a high FT4 trajectory.
Most women (96.5%) had a low and stable TPOAb level, and the rest (3.5%) had high and decreasing TPOAb levels.
When the children in the study were 4 years old, their main caregiver (parent or grandparent) completed the 100-question Achenbach Child Behavior checklist to identify whether the child often, sometimes, or never displayed three internalizing problem behaviors (emotionally reactive, anxious/depressed, or withdrawn) and/or two externalizing problem behaviors (attention problems or aggressive behavior).
Study limitations, more research needed
It is not clear why the associations between maternal hormones and offspring behavior were only seen in boys. Perhaps male fetuses are more sensitive than female fetuses to changing maternal thyroid hormone levels in pregnancy, the researchers speculate.
They acknowledge that study limitations include there were few children with aggressive behavior, so the confidence interval for the association of the moderate TSH trajectory with aggressive behavior was very wide.
In addition, evaluation of children’s behavior by caregivers was subjective. Also, the researchers did not have information about iodine levels, and low iodine levels can impair child brain development.
And there may have been residual confounders that researchers did not account for, such as differences in family upbringing, parental marital status, and the mother’s exposure to endocrine disruptors.
Therefore, further research is needed.
The study was supported by grants from the National Natural Science Foundation of China, the University Synergy Innovation Program of Anhui Province, the Sci-Tech Basic Resources Research Program of China, the National Key Research and Development Program, the Chinese Academy of Medical Sciences, and the Research Fund of Anhui Institute of Translational Medicine. The researchers and Dr. Nguyen have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Pregnant women’s thyroid hormone trajectories (levels in the first, second, and third trimester) may predict whether their male offspring are aggressive or withdrawn at age 4.
Certain maternal thyroid hormone trajectories were associated with problem behaviors in preschool boys in a study of close to 2,000 mother-child pairs in China.
The researchers identified low, moderate, and high thyroid-stimulating hormone (TSH) and free thyroxine (FT4) trajectories.
Most women had a low TSH trajectory and moderate FT4 trajectory, which the researchers deemed to be reference (normal) trajectories.
The children’s primary caregiver (parent or grandparent) completed an extensive questionnaire about their child’s behavior at age 4.
The 4-year-old boys whose mothers had a high TSH trajectory during pregnancy were more likely to be withdrawn and to externalize problems (odds ratio, 2.01 and 2.69, respectively).
Boys whose mothers had a high FT4 trajectory during pregnancy were more likely to be anxious/depressed (OR, 2.22).
And boys whose mothers had a moderate TSH trajectory or low FT4 trajectory were more likely to show aggressive behavior (OR, 3.76 and 4.17, respectively), compared with boys whose mothers had normal TSH and FT4 trajectories, after adjusting for potential confounders.
However, there was no association between abnormal maternal thyroid hormone trajectories and behavior problems in 4-year-old girls.
The study by Peixuan Li, BM, and colleagues was published online Jan. 6 in the Journal of Clinical Endocrinology & Metabolism.
‘Study supports monitoring thyroid function in pregnancy’
“Our findings highlight the significance of close monitoring and management of maternal thyroid function during pregnancy,” senior author Kun Huang, PhD, said in a press release from the Endocrine Society.
“This research presents a new perspective in early intervention of children’s emotional and behavioral problems,” added Dr. Huang, from Anhui Medical University, Hefei, China.
The results add to a growing body of literature about a controversial link between maternal thyroid hormones in pregnancy, when the fetal brain is developing, and subsequent behavior in preschool children, Caroline T. Nguyen, MD, who was not involved with this research, commented in an email.
“Some studies show an association between thyroid levels and behavioral outcomes, others not,” added Dr. Nguyen, assistant professor of clinical medicine, Keck School of Medicine, University of Southern California, Los Angeles. And “some studies have found sex-specific associations with maternal thyroid levels and neurocognitive/behavioral outcomes, others have not.”
Women considering pregnancy should be evaluated for possible thyroid disease, she continued. Currently, no universal screening mandates exist for thyroid disease in pregnancy, but the 2017 American Thyroid Association guidelines do recommend screening women at risk for thyroid dysfunction.
“I think screening for thyroid peroxidase antibody (TPOAb) positivity is helpful in women desiring pregnancy,” Dr. Nguyen continued, “because we know that patients with TPOAb positivity are at increased risk for miscarriage and have a blunted response to the increased demands of pregnancy for thyroid hormone production.”
TPOAb positivity is also associated with the increased risk of postpartum and long-term thyroid dysfunction.
This current study, Dr. Nguyen summarized, “adds to a growing body of research of the relationship of thyroid hormone levels and neurocognitive outcomes [in offspring] and supports the monitoring of thyroid disease in pregnancy.”
“However, we do not have sufficient data to demonstrate the benefits of intervention with levothyroxine treatment,” she noted.
Nevertheless, the lack of positive data does not suggest there is no theoretical benefit of intervention, she said, as such studies are very challenging to do.
“Physicians can help reduce stress and anxiety in patients desiring pregnancy by [recommending] preconception counseling, screening patients at risk for thyroid disease, and optimizing thyroid hormone levels before and during pregnancy,” according to Dr. Nguyen.
Maternal TSH and FT4 trajectories and preschoolers’ behaviors
Previous studies have reported that during pregnancy, maternal subclinical hypothyroidism (elevated TSH with normal FT4) as well as isolated hypothyroxinemia (decreased FT4 with normal TSH) are associated with adverse maternal and child outcomes, including preterm delivery and low birth weight.
However, most studies have not determined maternal thyroid hormone levels in different trimesters.
Researchers recruited pregnant women going for their first antenatal checkup at the Ma’anshan Maternal and Child Health Hospital in China from May 2013 to September 2014 and identified 1,860 mother-child pairs.
They determined maternal thyroid hormone levels from blood samples taken during the first, second, and third trimester: on average, gestational week 10, 25, and 34, respectively.
The researchers found that TSH levels increased somewhat from trimester 1 to trimester 2 and then decreased slightly in trimester 3. Most women (68%) had a low TSH trajectory, 28% had a moderate TSH trajectory, and 4% had a high TSH trajectory.
FT4 levels dropped sharply from trimester 1 to trimester 2 and then increased somewhat in trimester 3. About half of the women (52%) had a moderate FT4 trajectory, 33% had a low FT4 trajectory, and 15% had a high FT4 trajectory.
Most women (96.5%) had a low and stable TPOAb level, and the rest (3.5%) had high and decreasing TPOAb levels.
When the children in the study were 4 years old, their main caregiver (parent or grandparent) completed the 100-question Achenbach Child Behavior checklist to identify whether the child often, sometimes, or never displayed three internalizing problem behaviors (emotionally reactive, anxious/depressed, or withdrawn) and/or two externalizing problem behaviors (attention problems or aggressive behavior).
Study limitations, more research needed
It is not clear why the associations between maternal hormones and offspring behavior were only seen in boys. Perhaps male fetuses are more sensitive than female fetuses to changing maternal thyroid hormone levels in pregnancy, the researchers speculate.
They acknowledge that study limitations include there were few children with aggressive behavior, so the confidence interval for the association of the moderate TSH trajectory with aggressive behavior was very wide.
In addition, evaluation of children’s behavior by caregivers was subjective. Also, the researchers did not have information about iodine levels, and low iodine levels can impair child brain development.
And there may have been residual confounders that researchers did not account for, such as differences in family upbringing, parental marital status, and the mother’s exposure to endocrine disruptors.
Therefore, further research is needed.
The study was supported by grants from the National Natural Science Foundation of China, the University Synergy Innovation Program of Anhui Province, the Sci-Tech Basic Resources Research Program of China, the National Key Research and Development Program, the Chinese Academy of Medical Sciences, and the Research Fund of Anhui Institute of Translational Medicine. The researchers and Dr. Nguyen have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Pregnant women’s thyroid hormone trajectories (levels in the first, second, and third trimester) may predict whether their male offspring are aggressive or withdrawn at age 4.
Certain maternal thyroid hormone trajectories were associated with problem behaviors in preschool boys in a study of close to 2,000 mother-child pairs in China.
The researchers identified low, moderate, and high thyroid-stimulating hormone (TSH) and free thyroxine (FT4) trajectories.
Most women had a low TSH trajectory and moderate FT4 trajectory, which the researchers deemed to be reference (normal) trajectories.
The children’s primary caregiver (parent or grandparent) completed an extensive questionnaire about their child’s behavior at age 4.
The 4-year-old boys whose mothers had a high TSH trajectory during pregnancy were more likely to be withdrawn and to externalize problems (odds ratio, 2.01 and 2.69, respectively).
Boys whose mothers had a high FT4 trajectory during pregnancy were more likely to be anxious/depressed (OR, 2.22).
And boys whose mothers had a moderate TSH trajectory or low FT4 trajectory were more likely to show aggressive behavior (OR, 3.76 and 4.17, respectively), compared with boys whose mothers had normal TSH and FT4 trajectories, after adjusting for potential confounders.
However, there was no association between abnormal maternal thyroid hormone trajectories and behavior problems in 4-year-old girls.
The study by Peixuan Li, BM, and colleagues was published online Jan. 6 in the Journal of Clinical Endocrinology & Metabolism.
‘Study supports monitoring thyroid function in pregnancy’
“Our findings highlight the significance of close monitoring and management of maternal thyroid function during pregnancy,” senior author Kun Huang, PhD, said in a press release from the Endocrine Society.
“This research presents a new perspective in early intervention of children’s emotional and behavioral problems,” added Dr. Huang, from Anhui Medical University, Hefei, China.
The results add to a growing body of literature about a controversial link between maternal thyroid hormones in pregnancy, when the fetal brain is developing, and subsequent behavior in preschool children, Caroline T. Nguyen, MD, who was not involved with this research, commented in an email.
“Some studies show an association between thyroid levels and behavioral outcomes, others not,” added Dr. Nguyen, assistant professor of clinical medicine, Keck School of Medicine, University of Southern California, Los Angeles. And “some studies have found sex-specific associations with maternal thyroid levels and neurocognitive/behavioral outcomes, others have not.”
Women considering pregnancy should be evaluated for possible thyroid disease, she continued. Currently, no universal screening mandates exist for thyroid disease in pregnancy, but the 2017 American Thyroid Association guidelines do recommend screening women at risk for thyroid dysfunction.
“I think screening for thyroid peroxidase antibody (TPOAb) positivity is helpful in women desiring pregnancy,” Dr. Nguyen continued, “because we know that patients with TPOAb positivity are at increased risk for miscarriage and have a blunted response to the increased demands of pregnancy for thyroid hormone production.”
TPOAb positivity is also associated with the increased risk of postpartum and long-term thyroid dysfunction.
This current study, Dr. Nguyen summarized, “adds to a growing body of research of the relationship of thyroid hormone levels and neurocognitive outcomes [in offspring] and supports the monitoring of thyroid disease in pregnancy.”
“However, we do not have sufficient data to demonstrate the benefits of intervention with levothyroxine treatment,” she noted.
Nevertheless, the lack of positive data does not suggest there is no theoretical benefit of intervention, she said, as such studies are very challenging to do.
“Physicians can help reduce stress and anxiety in patients desiring pregnancy by [recommending] preconception counseling, screening patients at risk for thyroid disease, and optimizing thyroid hormone levels before and during pregnancy,” according to Dr. Nguyen.
Maternal TSH and FT4 trajectories and preschoolers’ behaviors
Previous studies have reported that during pregnancy, maternal subclinical hypothyroidism (elevated TSH with normal FT4) as well as isolated hypothyroxinemia (decreased FT4 with normal TSH) are associated with adverse maternal and child outcomes, including preterm delivery and low birth weight.
However, most studies have not determined maternal thyroid hormone levels in different trimesters.
Researchers recruited pregnant women going for their first antenatal checkup at the Ma’anshan Maternal and Child Health Hospital in China from May 2013 to September 2014 and identified 1,860 mother-child pairs.
They determined maternal thyroid hormone levels from blood samples taken during the first, second, and third trimester: on average, gestational week 10, 25, and 34, respectively.
The researchers found that TSH levels increased somewhat from trimester 1 to trimester 2 and then decreased slightly in trimester 3. Most women (68%) had a low TSH trajectory, 28% had a moderate TSH trajectory, and 4% had a high TSH trajectory.
FT4 levels dropped sharply from trimester 1 to trimester 2 and then increased somewhat in trimester 3. About half of the women (52%) had a moderate FT4 trajectory, 33% had a low FT4 trajectory, and 15% had a high FT4 trajectory.
Most women (96.5%) had a low and stable TPOAb level, and the rest (3.5%) had high and decreasing TPOAb levels.
When the children in the study were 4 years old, their main caregiver (parent or grandparent) completed the 100-question Achenbach Child Behavior checklist to identify whether the child often, sometimes, or never displayed three internalizing problem behaviors (emotionally reactive, anxious/depressed, or withdrawn) and/or two externalizing problem behaviors (attention problems or aggressive behavior).
Study limitations, more research needed
It is not clear why the associations between maternal hormones and offspring behavior were only seen in boys. Perhaps male fetuses are more sensitive than female fetuses to changing maternal thyroid hormone levels in pregnancy, the researchers speculate.
They acknowledge that study limitations include there were few children with aggressive behavior, so the confidence interval for the association of the moderate TSH trajectory with aggressive behavior was very wide.
In addition, evaluation of children’s behavior by caregivers was subjective. Also, the researchers did not have information about iodine levels, and low iodine levels can impair child brain development.
And there may have been residual confounders that researchers did not account for, such as differences in family upbringing, parental marital status, and the mother’s exposure to endocrine disruptors.
Therefore, further research is needed.
The study was supported by grants from the National Natural Science Foundation of China, the University Synergy Innovation Program of Anhui Province, the Sci-Tech Basic Resources Research Program of China, the National Key Research and Development Program, the Chinese Academy of Medical Sciences, and the Research Fund of Anhui Institute of Translational Medicine. The researchers and Dr. Nguyen have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM