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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
New test for Lp(a) allows more accurate LDL-cholesterol results
A new study has drawn attention to inaccurate measurement of LDL-cholesterol levels in some patients with current assays, which could lead to incorrect therapeutic approaches.
The patient groups most affected are those with high levels of the lipoprotein Lp(a), in whom LDL-cholesterol levels are being overestimated in current laboratory tests, the authors say.
“Current laboratory assays all have the limitation that they cannot measure or report LDL cholesterol accurately. They are actually measuring the combination of LDL and Lp(a),” senior study author Sotirios Tsimikas, MD, University of California, San Diego, explained to this news organization.
“While this may not matter much in individuals with normal Lp(a) levels, in those with elevated Lp(a), the Lp(a) cholesterol may constitute a substantial proportion of the reported LDL cholesterol, and the actual LDL-cholesterol levels could be much lower that the value the lab is telling us,” he said.
Dr. Tsimikas gave the example of a patient with an LDL-cholesterol lab measurement of 75 mg/dL. “If that patient has an Lp(a) level of zero, then they do actually have an LDL level of 75. But as the Lp(a) increases, then the proportion of the result accounted for by LDL cholesterol decreases. So, if a patient with a measured LDL cholesterol of 75 has an Lp(a)-cholesterol level of 20, then their actual LDL level is 55.”
Dr. Tsimikas said it is important to know levels of both lipoproteins individually, so the correct therapeutic approach is used in situations where the Lp(a) cholesterol might be elevated.
“By understanding the actual values of LDL cholesterol and Lp(a) cholesterol, this will allow us to personalize the use of cholesterol-lowering medications and decide where to focus treatment. In the patient with a high level of Lp(a), their residual risk could be coming from Lp(a) cholesterol and less so from LDL cholesterol,” he added. “As we develop drugs to lower Lp(a), this patient might be better off on one of these rather than increasing efforts to lower LDL cholesterol, which might already be at goal.”
The study was published in the March 22 issue of the Journal of the American College of Cardiology.
Dr. Tsimikas noted that Lp(a) is now accepted as a genetic, independent, causal risk factor for cardiovascular disease, but current LDL-lowering drugs do not have much effect on Lp(a).
“Lp(a) can be lowered a little with niacin and PCSK9 inhibitors, but both have a quite a weak effect, and statins increase Lp(a). However, there are now multiple RNA-based therapeutics specifically targeting Lp(a) in clinical development,” he said.
At present, Lp(a) cholesterol has to be mathematically estimated, most commonly with the Dahlén formula, because of the lack of a validated, quantitative method to measure Lp(a) cholesterol, Dr. Tsimikas says.
For the current study, the researchers used a novel, quantitative, sensitive method to directly measure Lp(a) cholesterol, then applied this method to data from a recent study with the one of the new Lp(a)-lowering drugs in development – pelacarsen – which was conducted in patients with elevated Lp(a) levels.
Results showed that direct Lp(a)-cholesterol assessment, and subtracting this value from the laboratory LDL-cholesterol value, provides a more accurate reflection of the baseline and change in LDL cholesterol, the authors report. In the current study, corrected LDL cholesterol was 13 to 16 mg/dL lower than laboratory-reported LDL cholesterol.
Using the corrected LDL-cholesterol results, the study showed that pelacarsen significantly decreases Lp(a) cholesterol, with neutral to modest effects on LDL.
The study also suggests that the current method of calculating Lp(a) cholesterol, and then deriving a corrected LDL cholesterol – the Dahlén formula – is not accurate.
“The Dahlén formula relies on the assumption that Lp(a) cholesterol is universally a fixed 30% of Lp(a) mass, but this usually isn’t the case. The Dahlén formula needs to be discontinued. It can be highly inaccurate,” Dr. Tsimikas said.
Important implications
In an accompanying editorial, Guillaume Paré, MD, Michael Chong, PhD student, and Pedrum Mohammadi-Shemirani, BSc, all of McMaster University, Hamilton, Ont., say the current findings have three important clinical implications.
“First, they provide further proof that in individuals with elevated Lp(a), the contribution of Lp(a)-cholesterol to LDL-cholesterol is non-negligible using standard assays, with 13-16 mg/dL lower LDL-cholesterol post-correction.”
Secondly, the editorialists point out that these new findings confirm that the effect of Lp(a) inhibitors is likely to be mostly confined to Lp(a), “as would be expected.”
Finally, “and perhaps more importantly, the authors highlight the need to improve clinical reporting of lipid fractions to properly treat LDL-cholesterol and Lp(a) in high-risk patients,” they note.
“The report paves the way for future studies investigating the clinical utility of these additional measurements to initiate and monitor lipid-lowering therapy,” they conclude.
The clinical trial was funded by Ionis Pharmaceuticals, and the direct Lp(a)-cholesterol measurements were funded by Novartis through a research grant to the University of California, San Diego. Dr. Tsimikas is an employee of Ionis Pharmaceuticals and of the University of California, San Diego, and he is a cofounder of Covicept Therapeutics. He is also a coinventor and receives royalties from patents owned by UCSD on oxidation-specific antibodies and on biomarkers related to oxidized lipoproteins, as well as a cofounder and has equity interest in Oxitope and Kleanthi Diagnostics.
A version of this article first appeared on Medscape.com.
A new study has drawn attention to inaccurate measurement of LDL-cholesterol levels in some patients with current assays, which could lead to incorrect therapeutic approaches.
The patient groups most affected are those with high levels of the lipoprotein Lp(a), in whom LDL-cholesterol levels are being overestimated in current laboratory tests, the authors say.
“Current laboratory assays all have the limitation that they cannot measure or report LDL cholesterol accurately. They are actually measuring the combination of LDL and Lp(a),” senior study author Sotirios Tsimikas, MD, University of California, San Diego, explained to this news organization.
“While this may not matter much in individuals with normal Lp(a) levels, in those with elevated Lp(a), the Lp(a) cholesterol may constitute a substantial proportion of the reported LDL cholesterol, and the actual LDL-cholesterol levels could be much lower that the value the lab is telling us,” he said.
Dr. Tsimikas gave the example of a patient with an LDL-cholesterol lab measurement of 75 mg/dL. “If that patient has an Lp(a) level of zero, then they do actually have an LDL level of 75. But as the Lp(a) increases, then the proportion of the result accounted for by LDL cholesterol decreases. So, if a patient with a measured LDL cholesterol of 75 has an Lp(a)-cholesterol level of 20, then their actual LDL level is 55.”
Dr. Tsimikas said it is important to know levels of both lipoproteins individually, so the correct therapeutic approach is used in situations where the Lp(a) cholesterol might be elevated.
“By understanding the actual values of LDL cholesterol and Lp(a) cholesterol, this will allow us to personalize the use of cholesterol-lowering medications and decide where to focus treatment. In the patient with a high level of Lp(a), their residual risk could be coming from Lp(a) cholesterol and less so from LDL cholesterol,” he added. “As we develop drugs to lower Lp(a), this patient might be better off on one of these rather than increasing efforts to lower LDL cholesterol, which might already be at goal.”
The study was published in the March 22 issue of the Journal of the American College of Cardiology.
Dr. Tsimikas noted that Lp(a) is now accepted as a genetic, independent, causal risk factor for cardiovascular disease, but current LDL-lowering drugs do not have much effect on Lp(a).
“Lp(a) can be lowered a little with niacin and PCSK9 inhibitors, but both have a quite a weak effect, and statins increase Lp(a). However, there are now multiple RNA-based therapeutics specifically targeting Lp(a) in clinical development,” he said.
At present, Lp(a) cholesterol has to be mathematically estimated, most commonly with the Dahlén formula, because of the lack of a validated, quantitative method to measure Lp(a) cholesterol, Dr. Tsimikas says.
For the current study, the researchers used a novel, quantitative, sensitive method to directly measure Lp(a) cholesterol, then applied this method to data from a recent study with the one of the new Lp(a)-lowering drugs in development – pelacarsen – which was conducted in patients with elevated Lp(a) levels.
Results showed that direct Lp(a)-cholesterol assessment, and subtracting this value from the laboratory LDL-cholesterol value, provides a more accurate reflection of the baseline and change in LDL cholesterol, the authors report. In the current study, corrected LDL cholesterol was 13 to 16 mg/dL lower than laboratory-reported LDL cholesterol.
Using the corrected LDL-cholesterol results, the study showed that pelacarsen significantly decreases Lp(a) cholesterol, with neutral to modest effects on LDL.
The study also suggests that the current method of calculating Lp(a) cholesterol, and then deriving a corrected LDL cholesterol – the Dahlén formula – is not accurate.
“The Dahlén formula relies on the assumption that Lp(a) cholesterol is universally a fixed 30% of Lp(a) mass, but this usually isn’t the case. The Dahlén formula needs to be discontinued. It can be highly inaccurate,” Dr. Tsimikas said.
Important implications
In an accompanying editorial, Guillaume Paré, MD, Michael Chong, PhD student, and Pedrum Mohammadi-Shemirani, BSc, all of McMaster University, Hamilton, Ont., say the current findings have three important clinical implications.
“First, they provide further proof that in individuals with elevated Lp(a), the contribution of Lp(a)-cholesterol to LDL-cholesterol is non-negligible using standard assays, with 13-16 mg/dL lower LDL-cholesterol post-correction.”
Secondly, the editorialists point out that these new findings confirm that the effect of Lp(a) inhibitors is likely to be mostly confined to Lp(a), “as would be expected.”
Finally, “and perhaps more importantly, the authors highlight the need to improve clinical reporting of lipid fractions to properly treat LDL-cholesterol and Lp(a) in high-risk patients,” they note.
“The report paves the way for future studies investigating the clinical utility of these additional measurements to initiate and monitor lipid-lowering therapy,” they conclude.
The clinical trial was funded by Ionis Pharmaceuticals, and the direct Lp(a)-cholesterol measurements were funded by Novartis through a research grant to the University of California, San Diego. Dr. Tsimikas is an employee of Ionis Pharmaceuticals and of the University of California, San Diego, and he is a cofounder of Covicept Therapeutics. He is also a coinventor and receives royalties from patents owned by UCSD on oxidation-specific antibodies and on biomarkers related to oxidized lipoproteins, as well as a cofounder and has equity interest in Oxitope and Kleanthi Diagnostics.
A version of this article first appeared on Medscape.com.
A new study has drawn attention to inaccurate measurement of LDL-cholesterol levels in some patients with current assays, which could lead to incorrect therapeutic approaches.
The patient groups most affected are those with high levels of the lipoprotein Lp(a), in whom LDL-cholesterol levels are being overestimated in current laboratory tests, the authors say.
“Current laboratory assays all have the limitation that they cannot measure or report LDL cholesterol accurately. They are actually measuring the combination of LDL and Lp(a),” senior study author Sotirios Tsimikas, MD, University of California, San Diego, explained to this news organization.
“While this may not matter much in individuals with normal Lp(a) levels, in those with elevated Lp(a), the Lp(a) cholesterol may constitute a substantial proportion of the reported LDL cholesterol, and the actual LDL-cholesterol levels could be much lower that the value the lab is telling us,” he said.
Dr. Tsimikas gave the example of a patient with an LDL-cholesterol lab measurement of 75 mg/dL. “If that patient has an Lp(a) level of zero, then they do actually have an LDL level of 75. But as the Lp(a) increases, then the proportion of the result accounted for by LDL cholesterol decreases. So, if a patient with a measured LDL cholesterol of 75 has an Lp(a)-cholesterol level of 20, then their actual LDL level is 55.”
Dr. Tsimikas said it is important to know levels of both lipoproteins individually, so the correct therapeutic approach is used in situations where the Lp(a) cholesterol might be elevated.
“By understanding the actual values of LDL cholesterol and Lp(a) cholesterol, this will allow us to personalize the use of cholesterol-lowering medications and decide where to focus treatment. In the patient with a high level of Lp(a), their residual risk could be coming from Lp(a) cholesterol and less so from LDL cholesterol,” he added. “As we develop drugs to lower Lp(a), this patient might be better off on one of these rather than increasing efforts to lower LDL cholesterol, which might already be at goal.”
The study was published in the March 22 issue of the Journal of the American College of Cardiology.
Dr. Tsimikas noted that Lp(a) is now accepted as a genetic, independent, causal risk factor for cardiovascular disease, but current LDL-lowering drugs do not have much effect on Lp(a).
“Lp(a) can be lowered a little with niacin and PCSK9 inhibitors, but both have a quite a weak effect, and statins increase Lp(a). However, there are now multiple RNA-based therapeutics specifically targeting Lp(a) in clinical development,” he said.
At present, Lp(a) cholesterol has to be mathematically estimated, most commonly with the Dahlén formula, because of the lack of a validated, quantitative method to measure Lp(a) cholesterol, Dr. Tsimikas says.
For the current study, the researchers used a novel, quantitative, sensitive method to directly measure Lp(a) cholesterol, then applied this method to data from a recent study with the one of the new Lp(a)-lowering drugs in development – pelacarsen – which was conducted in patients with elevated Lp(a) levels.
Results showed that direct Lp(a)-cholesterol assessment, and subtracting this value from the laboratory LDL-cholesterol value, provides a more accurate reflection of the baseline and change in LDL cholesterol, the authors report. In the current study, corrected LDL cholesterol was 13 to 16 mg/dL lower than laboratory-reported LDL cholesterol.
Using the corrected LDL-cholesterol results, the study showed that pelacarsen significantly decreases Lp(a) cholesterol, with neutral to modest effects on LDL.
The study also suggests that the current method of calculating Lp(a) cholesterol, and then deriving a corrected LDL cholesterol – the Dahlén formula – is not accurate.
“The Dahlén formula relies on the assumption that Lp(a) cholesterol is universally a fixed 30% of Lp(a) mass, but this usually isn’t the case. The Dahlén formula needs to be discontinued. It can be highly inaccurate,” Dr. Tsimikas said.
Important implications
In an accompanying editorial, Guillaume Paré, MD, Michael Chong, PhD student, and Pedrum Mohammadi-Shemirani, BSc, all of McMaster University, Hamilton, Ont., say the current findings have three important clinical implications.
“First, they provide further proof that in individuals with elevated Lp(a), the contribution of Lp(a)-cholesterol to LDL-cholesterol is non-negligible using standard assays, with 13-16 mg/dL lower LDL-cholesterol post-correction.”
Secondly, the editorialists point out that these new findings confirm that the effect of Lp(a) inhibitors is likely to be mostly confined to Lp(a), “as would be expected.”
Finally, “and perhaps more importantly, the authors highlight the need to improve clinical reporting of lipid fractions to properly treat LDL-cholesterol and Lp(a) in high-risk patients,” they note.
“The report paves the way for future studies investigating the clinical utility of these additional measurements to initiate and monitor lipid-lowering therapy,” they conclude.
The clinical trial was funded by Ionis Pharmaceuticals, and the direct Lp(a)-cholesterol measurements were funded by Novartis through a research grant to the University of California, San Diego. Dr. Tsimikas is an employee of Ionis Pharmaceuticals and of the University of California, San Diego, and he is a cofounder of Covicept Therapeutics. He is also a coinventor and receives royalties from patents owned by UCSD on oxidation-specific antibodies and on biomarkers related to oxidized lipoproteins, as well as a cofounder and has equity interest in Oxitope and Kleanthi Diagnostics.
A version of this article first appeared on Medscape.com.
New ACC guidance on cardiovascular consequences of COVID-19
The American College of Cardiology has issued an expert consensus clinical guidance document for the evaluation and management of adults with key cardiovascular consequences of COVID-19.
The document makes recommendations on how to evaluate and manage COVID-associated myocarditis and long COVID and gives advice on resumption of exercise following COVID-19 infection.
The clinical guidance was published online March 16 in the Journal of the American College of Cardiology.
“The best means to diagnose and treat myocarditis and long COVID following SARS-CoV-2 infection continues to evolve,” said Ty Gluckman, MD, MHA, cochair of the expert consensus decision pathway. “This document attempts to provide key recommendations for how to evaluate and manage adults with these conditions, including guidance for safe return to play for both competitive and noncompetitive athletes.”
The authors of the guidance note that COVID-19 can be associated with various abnormalities in cardiac testing and a wide range of cardiovascular complications. For some patients, cardiac symptoms such as chest pain, shortness of breath, fatigue, and palpitations persist, lasting months after the initial illness, and evidence of myocardial injury has also been observed in both symptomatic and asymptomatic individuals, as well as after receipt of the COVID-19 mRNA vaccine.
“For clinicians treating these individuals, a growing number of questions exist related to evaluation and management of these conditions, as well as safe resumption of physical activity,” they say. This report is intended to provide practical guidance on these issues.
Myocarditis
The report states that myocarditis has been recognized as a rare but serious complication of SARS-CoV-2 infection as well as COVID-19 mRNA vaccination.
It defines myocarditis as: 1.cardiac symptoms such as chest pain, dyspnea, palpitations, or syncope; 2. elevated cardiac troponin; and 3. abnormal electrocardiographic, echocardiographic, cardiac MRI, and/or histopathologic findings on biopsy.
The document makes the following recommendations in regard to COVID-related myocarditis:
When there is increased suspicion for cardiac involvement with COVID-19, initial testing should consist of an ECG, measurement of cardiac troponin, and an echocardiogram. Cardiology consultation is recommended for those with a rising cardiac troponin and/or echocardiographic abnormalities. Cardiac MRI is recommended in hemodynamically stable patients with suspected myocarditis.
Hospitalization is recommended for patients with definite myocarditis, ideally at an advanced heart failure center. Patients with fulminant myocarditis should be managed at centers with an expertise in advanced heart failure, mechanical circulatory support, and other advanced therapies.
Patients with myocarditis and COVID-19 pneumonia (with an ongoing need for supplemental oxygen) should be treated with corticosteroids. For patients with suspected pericardial involvement, treatment with NSAIDs, colchicine, and/or prednisone is reasonable. Intravenous corticosteroids may be considered in those with suspected or confirmed COVID-19 myocarditis with hemodynamic compromise or MIS-A (multisystem inflammatory syndrome in adults). Empiric use of corticosteroids may also be considered in those with biopsy evidence of severe myocardial infiltrates or fulminant myocarditis, balanced against infection risk.
As appropriate, guideline-directed medical therapy for heart failure should be initiated and continued after discharge.
The document notes that myocarditis following COVID-19 mRNA vaccination is rare, with highest rates seen in young males after the second vaccine dose. As of May 22, 2021, the U.S. Vaccine Adverse Event Reporting System noted rates of 40.6 cases per million after the second vaccine dose among male individuals aged 12-29 years and 2.4 cases per million among male individuals aged 30 and older. Corresponding rates in female individuals were 4.2 and 1 cases per million, respectively.
But the report says that COVID-19 vaccination is associated with “a very favorable benefit-to-risk ratio” for all age and sex groups evaluated thus far.
In general, vaccine-associated myocarditis should be diagnosed, categorized, and treated in a manner analogous to myocarditis following SARS-CoV-2 infection, the guidance advises.
Long COVID
The document refers to long COVID as postacute sequelae of SARS-CoV-2 infection (PASC), and reports that this condition is experienced by up to 10%-30% of infected individuals. It is defined by a constellation of new, returning, or persistent health problems experienced by individuals 4 or more weeks after COVID-19 infection.
Although individuals with this condition may experience wide-ranging symptoms, the symptoms that draw increased attention to the cardiovascular system include tachycardia, exercise intolerance, chest pain, and shortness of breath.
Nicole Bhave, MD, cochair of the expert consensus decision pathway, says: “There appears to be a ‘downward spiral’ for long-COVID patients. Fatigue and decreased exercise capacity lead to diminished activity and bed rest, in turn leading to worsening symptoms and decreased quality of life.” She adds that “the writing committee recommends a basic cardiopulmonary evaluation performed up front to determine if further specialty care and formalized medical therapy is needed for these patients.”
The authors propose two terms to better understand potential etiologies for those with cardiovascular symptoms:
PASC-CVD, or PASC-cardiovascular disease, refers to a broad group of cardiovascular conditions (including myocarditis) that manifest at least 4 weeks after COVID-19 infection.
PASC-CVS, or PASC-cardiovascular syndrome, includes a wide range of cardiovascular symptoms without objective evidence of cardiovascular disease following standard diagnostic testing.
The document makes the following recommendations for the management of PASC-CVD and PASC-CVS.
For patients with cardiovascular symptoms and suspected PASC, the authors suggest that a reasonable initial testing approach includes basic laboratory testing, including cardiac troponin, an ECG, an echocardiogram, an ambulatory rhythm monitor, chest imaging, and/or pulmonary function tests.
Cardiology consultation is recommended for patients with PASC who have abnormal cardiac test results, known cardiovascular disease with new or worsening symptoms, documented cardiac complications during SARS-CoV-2 infection, and/or persistent cardiopulmonary symptoms that are not otherwise explained.
Recumbent or semirecumbent exercise (for example, rowing, swimming, or cycling) is recommended initially for PASC-CVS patients with tachycardia, exercise/orthostatic intolerance, and/or deconditioning, with transition to upright exercise as orthostatic intolerance improves. Exercise duration should also be short (5-10 minutes/day) initially, with gradual increases as functional capacity improves.
Salt and fluid loading represent nonpharmacologic interventions that may provide symptomatic relief for patients with tachycardia, palpitations, and/or orthostatic hypotension.
Beta-blockers, nondihydropyridine calcium-channel blockers, ivabradine, fludrocortisone, and midodrine may be used empirically as well.
Return to play for athletes
The authors note that concerns about possible cardiac injury after COVID-19 fueled early apprehension regarding the safety of competitive sports for athletes recovering from the infection.
But they say that subsequent data from large registries have demonstrated an overall low prevalence of clinical myocarditis, without a rise in the rate of adverse cardiac events. Based on this, updated guidance is provided with a practical, evidence-based framework to guide resumption of athletics and intense exercise training.
They make the following recommendations:
- For athletes recovering from COVID-19 with ongoing cardiopulmonary symptoms (chest pain, shortness of breath, palpitations, lightheadedness) or those requiring hospitalization with increased suspicion for cardiac involvement, further evaluation with triad testing – an ECG, measurement of cardiac troponin, and an echocardiogram – should be performed.
- For those with abnormal test results, further evaluation with cardiac MRI should be considered. Individuals diagnosed with clinical myocarditis should abstain from exercise for 3-6 months.
- Cardiac testing is not recommended for asymptomatic individuals following COVID-19 infection. Individuals should abstain from training for 3 days to ensure that symptoms do not develop.
- For those with mild or moderate noncardiopulmonary symptoms (fever, lethargy, muscle aches), training may resume after symptom resolution.
- For those with remote infection (≥3 months) without ongoing cardiopulmonary symptoms, a gradual increase in exercise is recommended without the need for cardiac testing.
Based on the low prevalence of myocarditis observed in competitive athletes with COVID-19, the authors note that these recommendations can be reasonably applied to high-school athletes (aged 14 and older) along with adult recreational exercise enthusiasts.
Future study is needed, however, to better understand how long cardiac abnormalities persist following COVID-19 infection and the role of exercise training in long COVID.
The authors conclude that the current guidance is intended to help clinicians understand not only when testing may be warranted, but also when it is not.
“Given that it reflects the current state of knowledge through early 2022, it is anticipated that recommendations will change over time as our understanding evolves,” they say.
The 2022 ACC Expert Consensus Decision Pathway on Cardiovascular Sequelae of COVID-19: Myocarditis, Post-Acute Sequelae of SARS-CoV-2 Infection (PASC), and Return to Play will be discussed in a session at the American College of Cardiology’s annual scientific session meeting in Washington in April.
A version of this article first appeared on Medscape.com.
The American College of Cardiology has issued an expert consensus clinical guidance document for the evaluation and management of adults with key cardiovascular consequences of COVID-19.
The document makes recommendations on how to evaluate and manage COVID-associated myocarditis and long COVID and gives advice on resumption of exercise following COVID-19 infection.
The clinical guidance was published online March 16 in the Journal of the American College of Cardiology.
“The best means to diagnose and treat myocarditis and long COVID following SARS-CoV-2 infection continues to evolve,” said Ty Gluckman, MD, MHA, cochair of the expert consensus decision pathway. “This document attempts to provide key recommendations for how to evaluate and manage adults with these conditions, including guidance for safe return to play for both competitive and noncompetitive athletes.”
The authors of the guidance note that COVID-19 can be associated with various abnormalities in cardiac testing and a wide range of cardiovascular complications. For some patients, cardiac symptoms such as chest pain, shortness of breath, fatigue, and palpitations persist, lasting months after the initial illness, and evidence of myocardial injury has also been observed in both symptomatic and asymptomatic individuals, as well as after receipt of the COVID-19 mRNA vaccine.
“For clinicians treating these individuals, a growing number of questions exist related to evaluation and management of these conditions, as well as safe resumption of physical activity,” they say. This report is intended to provide practical guidance on these issues.
Myocarditis
The report states that myocarditis has been recognized as a rare but serious complication of SARS-CoV-2 infection as well as COVID-19 mRNA vaccination.
It defines myocarditis as: 1.cardiac symptoms such as chest pain, dyspnea, palpitations, or syncope; 2. elevated cardiac troponin; and 3. abnormal electrocardiographic, echocardiographic, cardiac MRI, and/or histopathologic findings on biopsy.
The document makes the following recommendations in regard to COVID-related myocarditis:
When there is increased suspicion for cardiac involvement with COVID-19, initial testing should consist of an ECG, measurement of cardiac troponin, and an echocardiogram. Cardiology consultation is recommended for those with a rising cardiac troponin and/or echocardiographic abnormalities. Cardiac MRI is recommended in hemodynamically stable patients with suspected myocarditis.
Hospitalization is recommended for patients with definite myocarditis, ideally at an advanced heart failure center. Patients with fulminant myocarditis should be managed at centers with an expertise in advanced heart failure, mechanical circulatory support, and other advanced therapies.
Patients with myocarditis and COVID-19 pneumonia (with an ongoing need for supplemental oxygen) should be treated with corticosteroids. For patients with suspected pericardial involvement, treatment with NSAIDs, colchicine, and/or prednisone is reasonable. Intravenous corticosteroids may be considered in those with suspected or confirmed COVID-19 myocarditis with hemodynamic compromise or MIS-A (multisystem inflammatory syndrome in adults). Empiric use of corticosteroids may also be considered in those with biopsy evidence of severe myocardial infiltrates or fulminant myocarditis, balanced against infection risk.
As appropriate, guideline-directed medical therapy for heart failure should be initiated and continued after discharge.
The document notes that myocarditis following COVID-19 mRNA vaccination is rare, with highest rates seen in young males after the second vaccine dose. As of May 22, 2021, the U.S. Vaccine Adverse Event Reporting System noted rates of 40.6 cases per million after the second vaccine dose among male individuals aged 12-29 years and 2.4 cases per million among male individuals aged 30 and older. Corresponding rates in female individuals were 4.2 and 1 cases per million, respectively.
But the report says that COVID-19 vaccination is associated with “a very favorable benefit-to-risk ratio” for all age and sex groups evaluated thus far.
In general, vaccine-associated myocarditis should be diagnosed, categorized, and treated in a manner analogous to myocarditis following SARS-CoV-2 infection, the guidance advises.
Long COVID
The document refers to long COVID as postacute sequelae of SARS-CoV-2 infection (PASC), and reports that this condition is experienced by up to 10%-30% of infected individuals. It is defined by a constellation of new, returning, or persistent health problems experienced by individuals 4 or more weeks after COVID-19 infection.
Although individuals with this condition may experience wide-ranging symptoms, the symptoms that draw increased attention to the cardiovascular system include tachycardia, exercise intolerance, chest pain, and shortness of breath.
Nicole Bhave, MD, cochair of the expert consensus decision pathway, says: “There appears to be a ‘downward spiral’ for long-COVID patients. Fatigue and decreased exercise capacity lead to diminished activity and bed rest, in turn leading to worsening symptoms and decreased quality of life.” She adds that “the writing committee recommends a basic cardiopulmonary evaluation performed up front to determine if further specialty care and formalized medical therapy is needed for these patients.”
The authors propose two terms to better understand potential etiologies for those with cardiovascular symptoms:
PASC-CVD, or PASC-cardiovascular disease, refers to a broad group of cardiovascular conditions (including myocarditis) that manifest at least 4 weeks after COVID-19 infection.
PASC-CVS, or PASC-cardiovascular syndrome, includes a wide range of cardiovascular symptoms without objective evidence of cardiovascular disease following standard diagnostic testing.
The document makes the following recommendations for the management of PASC-CVD and PASC-CVS.
For patients with cardiovascular symptoms and suspected PASC, the authors suggest that a reasonable initial testing approach includes basic laboratory testing, including cardiac troponin, an ECG, an echocardiogram, an ambulatory rhythm monitor, chest imaging, and/or pulmonary function tests.
Cardiology consultation is recommended for patients with PASC who have abnormal cardiac test results, known cardiovascular disease with new or worsening symptoms, documented cardiac complications during SARS-CoV-2 infection, and/or persistent cardiopulmonary symptoms that are not otherwise explained.
Recumbent or semirecumbent exercise (for example, rowing, swimming, or cycling) is recommended initially for PASC-CVS patients with tachycardia, exercise/orthostatic intolerance, and/or deconditioning, with transition to upright exercise as orthostatic intolerance improves. Exercise duration should also be short (5-10 minutes/day) initially, with gradual increases as functional capacity improves.
Salt and fluid loading represent nonpharmacologic interventions that may provide symptomatic relief for patients with tachycardia, palpitations, and/or orthostatic hypotension.
Beta-blockers, nondihydropyridine calcium-channel blockers, ivabradine, fludrocortisone, and midodrine may be used empirically as well.
Return to play for athletes
The authors note that concerns about possible cardiac injury after COVID-19 fueled early apprehension regarding the safety of competitive sports for athletes recovering from the infection.
But they say that subsequent data from large registries have demonstrated an overall low prevalence of clinical myocarditis, without a rise in the rate of adverse cardiac events. Based on this, updated guidance is provided with a practical, evidence-based framework to guide resumption of athletics and intense exercise training.
They make the following recommendations:
- For athletes recovering from COVID-19 with ongoing cardiopulmonary symptoms (chest pain, shortness of breath, palpitations, lightheadedness) or those requiring hospitalization with increased suspicion for cardiac involvement, further evaluation with triad testing – an ECG, measurement of cardiac troponin, and an echocardiogram – should be performed.
- For those with abnormal test results, further evaluation with cardiac MRI should be considered. Individuals diagnosed with clinical myocarditis should abstain from exercise for 3-6 months.
- Cardiac testing is not recommended for asymptomatic individuals following COVID-19 infection. Individuals should abstain from training for 3 days to ensure that symptoms do not develop.
- For those with mild or moderate noncardiopulmonary symptoms (fever, lethargy, muscle aches), training may resume after symptom resolution.
- For those with remote infection (≥3 months) without ongoing cardiopulmonary symptoms, a gradual increase in exercise is recommended without the need for cardiac testing.
Based on the low prevalence of myocarditis observed in competitive athletes with COVID-19, the authors note that these recommendations can be reasonably applied to high-school athletes (aged 14 and older) along with adult recreational exercise enthusiasts.
Future study is needed, however, to better understand how long cardiac abnormalities persist following COVID-19 infection and the role of exercise training in long COVID.
The authors conclude that the current guidance is intended to help clinicians understand not only when testing may be warranted, but also when it is not.
“Given that it reflects the current state of knowledge through early 2022, it is anticipated that recommendations will change over time as our understanding evolves,” they say.
The 2022 ACC Expert Consensus Decision Pathway on Cardiovascular Sequelae of COVID-19: Myocarditis, Post-Acute Sequelae of SARS-CoV-2 Infection (PASC), and Return to Play will be discussed in a session at the American College of Cardiology’s annual scientific session meeting in Washington in April.
A version of this article first appeared on Medscape.com.
The American College of Cardiology has issued an expert consensus clinical guidance document for the evaluation and management of adults with key cardiovascular consequences of COVID-19.
The document makes recommendations on how to evaluate and manage COVID-associated myocarditis and long COVID and gives advice on resumption of exercise following COVID-19 infection.
The clinical guidance was published online March 16 in the Journal of the American College of Cardiology.
“The best means to diagnose and treat myocarditis and long COVID following SARS-CoV-2 infection continues to evolve,” said Ty Gluckman, MD, MHA, cochair of the expert consensus decision pathway. “This document attempts to provide key recommendations for how to evaluate and manage adults with these conditions, including guidance for safe return to play for both competitive and noncompetitive athletes.”
The authors of the guidance note that COVID-19 can be associated with various abnormalities in cardiac testing and a wide range of cardiovascular complications. For some patients, cardiac symptoms such as chest pain, shortness of breath, fatigue, and palpitations persist, lasting months after the initial illness, and evidence of myocardial injury has also been observed in both symptomatic and asymptomatic individuals, as well as after receipt of the COVID-19 mRNA vaccine.
“For clinicians treating these individuals, a growing number of questions exist related to evaluation and management of these conditions, as well as safe resumption of physical activity,” they say. This report is intended to provide practical guidance on these issues.
Myocarditis
The report states that myocarditis has been recognized as a rare but serious complication of SARS-CoV-2 infection as well as COVID-19 mRNA vaccination.
It defines myocarditis as: 1.cardiac symptoms such as chest pain, dyspnea, palpitations, or syncope; 2. elevated cardiac troponin; and 3. abnormal electrocardiographic, echocardiographic, cardiac MRI, and/or histopathologic findings on biopsy.
The document makes the following recommendations in regard to COVID-related myocarditis:
When there is increased suspicion for cardiac involvement with COVID-19, initial testing should consist of an ECG, measurement of cardiac troponin, and an echocardiogram. Cardiology consultation is recommended for those with a rising cardiac troponin and/or echocardiographic abnormalities. Cardiac MRI is recommended in hemodynamically stable patients with suspected myocarditis.
Hospitalization is recommended for patients with definite myocarditis, ideally at an advanced heart failure center. Patients with fulminant myocarditis should be managed at centers with an expertise in advanced heart failure, mechanical circulatory support, and other advanced therapies.
Patients with myocarditis and COVID-19 pneumonia (with an ongoing need for supplemental oxygen) should be treated with corticosteroids. For patients with suspected pericardial involvement, treatment with NSAIDs, colchicine, and/or prednisone is reasonable. Intravenous corticosteroids may be considered in those with suspected or confirmed COVID-19 myocarditis with hemodynamic compromise or MIS-A (multisystem inflammatory syndrome in adults). Empiric use of corticosteroids may also be considered in those with biopsy evidence of severe myocardial infiltrates or fulminant myocarditis, balanced against infection risk.
As appropriate, guideline-directed medical therapy for heart failure should be initiated and continued after discharge.
The document notes that myocarditis following COVID-19 mRNA vaccination is rare, with highest rates seen in young males after the second vaccine dose. As of May 22, 2021, the U.S. Vaccine Adverse Event Reporting System noted rates of 40.6 cases per million after the second vaccine dose among male individuals aged 12-29 years and 2.4 cases per million among male individuals aged 30 and older. Corresponding rates in female individuals were 4.2 and 1 cases per million, respectively.
But the report says that COVID-19 vaccination is associated with “a very favorable benefit-to-risk ratio” for all age and sex groups evaluated thus far.
In general, vaccine-associated myocarditis should be diagnosed, categorized, and treated in a manner analogous to myocarditis following SARS-CoV-2 infection, the guidance advises.
Long COVID
The document refers to long COVID as postacute sequelae of SARS-CoV-2 infection (PASC), and reports that this condition is experienced by up to 10%-30% of infected individuals. It is defined by a constellation of new, returning, or persistent health problems experienced by individuals 4 or more weeks after COVID-19 infection.
Although individuals with this condition may experience wide-ranging symptoms, the symptoms that draw increased attention to the cardiovascular system include tachycardia, exercise intolerance, chest pain, and shortness of breath.
Nicole Bhave, MD, cochair of the expert consensus decision pathway, says: “There appears to be a ‘downward spiral’ for long-COVID patients. Fatigue and decreased exercise capacity lead to diminished activity and bed rest, in turn leading to worsening symptoms and decreased quality of life.” She adds that “the writing committee recommends a basic cardiopulmonary evaluation performed up front to determine if further specialty care and formalized medical therapy is needed for these patients.”
The authors propose two terms to better understand potential etiologies for those with cardiovascular symptoms:
PASC-CVD, or PASC-cardiovascular disease, refers to a broad group of cardiovascular conditions (including myocarditis) that manifest at least 4 weeks after COVID-19 infection.
PASC-CVS, or PASC-cardiovascular syndrome, includes a wide range of cardiovascular symptoms without objective evidence of cardiovascular disease following standard diagnostic testing.
The document makes the following recommendations for the management of PASC-CVD and PASC-CVS.
For patients with cardiovascular symptoms and suspected PASC, the authors suggest that a reasonable initial testing approach includes basic laboratory testing, including cardiac troponin, an ECG, an echocardiogram, an ambulatory rhythm monitor, chest imaging, and/or pulmonary function tests.
Cardiology consultation is recommended for patients with PASC who have abnormal cardiac test results, known cardiovascular disease with new or worsening symptoms, documented cardiac complications during SARS-CoV-2 infection, and/or persistent cardiopulmonary symptoms that are not otherwise explained.
Recumbent or semirecumbent exercise (for example, rowing, swimming, or cycling) is recommended initially for PASC-CVS patients with tachycardia, exercise/orthostatic intolerance, and/or deconditioning, with transition to upright exercise as orthostatic intolerance improves. Exercise duration should also be short (5-10 minutes/day) initially, with gradual increases as functional capacity improves.
Salt and fluid loading represent nonpharmacologic interventions that may provide symptomatic relief for patients with tachycardia, palpitations, and/or orthostatic hypotension.
Beta-blockers, nondihydropyridine calcium-channel blockers, ivabradine, fludrocortisone, and midodrine may be used empirically as well.
Return to play for athletes
The authors note that concerns about possible cardiac injury after COVID-19 fueled early apprehension regarding the safety of competitive sports for athletes recovering from the infection.
But they say that subsequent data from large registries have demonstrated an overall low prevalence of clinical myocarditis, without a rise in the rate of adverse cardiac events. Based on this, updated guidance is provided with a practical, evidence-based framework to guide resumption of athletics and intense exercise training.
They make the following recommendations:
- For athletes recovering from COVID-19 with ongoing cardiopulmonary symptoms (chest pain, shortness of breath, palpitations, lightheadedness) or those requiring hospitalization with increased suspicion for cardiac involvement, further evaluation with triad testing – an ECG, measurement of cardiac troponin, and an echocardiogram – should be performed.
- For those with abnormal test results, further evaluation with cardiac MRI should be considered. Individuals diagnosed with clinical myocarditis should abstain from exercise for 3-6 months.
- Cardiac testing is not recommended for asymptomatic individuals following COVID-19 infection. Individuals should abstain from training for 3 days to ensure that symptoms do not develop.
- For those with mild or moderate noncardiopulmonary symptoms (fever, lethargy, muscle aches), training may resume after symptom resolution.
- For those with remote infection (≥3 months) without ongoing cardiopulmonary symptoms, a gradual increase in exercise is recommended without the need for cardiac testing.
Based on the low prevalence of myocarditis observed in competitive athletes with COVID-19, the authors note that these recommendations can be reasonably applied to high-school athletes (aged 14 and older) along with adult recreational exercise enthusiasts.
Future study is needed, however, to better understand how long cardiac abnormalities persist following COVID-19 infection and the role of exercise training in long COVID.
The authors conclude that the current guidance is intended to help clinicians understand not only when testing may be warranted, but also when it is not.
“Given that it reflects the current state of knowledge through early 2022, it is anticipated that recommendations will change over time as our understanding evolves,” they say.
The 2022 ACC Expert Consensus Decision Pathway on Cardiovascular Sequelae of COVID-19: Myocarditis, Post-Acute Sequelae of SARS-CoV-2 Infection (PASC), and Return to Play will be discussed in a session at the American College of Cardiology’s annual scientific session meeting in Washington in April.
A version of this article first appeared on Medscape.com.
High-intensity exercise vs. omega-3s for heart failure risk reduction
A year of high-intensity interval training seemed to benefit obese middle-aged adults at a high risk of heart failure, but omega-3 fatty acid supplementation didn’t have any effect on cardiac biomarkers measured in a small, single-center, prospective study.
“One year of HIIT training reduces adiposity but had no consistent effect on myocardial triglyceride content or visceral adiposity,” wrote lead author Christopher M. Hearon Jr., PhD, and colleagues in JACC: Heart Failure. “However, long-duration HIIT improves fitness and induces favorable cardiac remodeling.” Omega-3 supplementation, however, had “no independent or additive effect.” Dr. Hearon is an instructor of applied clinical research at University of Texas Southwestern Medical Center in Dallas.
Investigators there and at the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital Dallas studied 80 patients aged 40-55 years classified as high risk for HF and obese, randomizing them to a year of high-intensity interval training (HIIT) with supplementation of either 1.6 g omega-3 FA or placebo daily; or to a control group split between supplementation or placebo. Fifty-six patients completed the 1-year study, with a compliance rate of 90% in the HIIT group and 92% in those assigned omega-3 FA supplementation.
Carl J. “Chip” Lavie, MD, of the John Ochsner Heart and Vascular Institute in New Orleans, commented that, although the study was “extremely well done from an excellent research group,” it was limited by its small population and relatively short follow-up. Future research should evaluate HIIT and moderate exercise on clinical events over a longer term as well as different doses of omega-3 “There is tremendous potential for omega-3 in heart failure prevention and treatment.”
HIIT boosts exercise capacity, more
In the study, the HIIT group showed improvement in a number of cardiac markers: around a 22% improvement in exercise capacity as measured by absolute peak and relative peak oxygen uptake (VO2), even without significant weight loss. They improved an average of 0.43 L/min (0.32-0.53; P < .0001) and 4.46 mL/kg per minute (3.18-5.56; P < .0001), respectively.
The researchers attributed the increase in peak VO2 to an increase in peak cardiac output averaging 2.15 L/min (95% confidence interval, 0.90-3.39; P = .001) and stroke volume averaging 9.46 mL (95% CI, 0.65-18.27; P = .04). A year of exercise training also resulted in changes in cardiac remodeling, including increases in left ventricle mass and LV end diastolic volume, averaging 9.4 g (95% CI, 4.36-14.44; P < .001) and 12.33 mL (95% CI, 5.61-19.05; P < .001), respectively.
The study also found that neither intervention had any appreciable impact on body weight, body mass index, body surface area or lean mass, or markers of arterial or local carotid stiffness. The exercise group had a modest decrease in fat mass, averaging 2.63 kg (95% CI,–4.81 to –0.46; P = .02), but without any effect from omega-3 supplementation.
The study acknowledged that high-dose omega-3 supplements have been found to lower triglyceride levels in people with severe hypertriglyceridemia, and hypothesized that HIIT alone or with omega-3 supplementation would improve fitness and biomarkers in people with stage A HF. “Contrary to our hypothesis, we found that one year of n-3FA [omega-3 FA] supplementation had no detectable effect on any parameter related to cardiopulmonary fitness, cardiovascular remodeling/stiffness, visceral adiposity, or myocardial triglyceride content,” Dr. Hearon and colleagues wrote.
The study “shows that obese middle-aged patients with heart failure with preserved ejection fraction [HFpEF] can markedly improve their fitness with HIIT and, generally, fitness is one of the strongest if not the strongest predictor of prognosis and survival,” said Dr. Lavie.
“Studies are needed on exercise that improves fitness in both HF with reduced ejection fraction and HFpEF, but especially HFpEF,” he said.
The study received funding from the American Heart Association Strategically Focused Research Network. Dr. Hearon and coauthors have no relevant disclosures. Dr. Lavie is a speaker and consultant for PAI Health, the Global Organization for EPA and DHA Omega-3s and DSM Nutritional Products.
A year of high-intensity interval training seemed to benefit obese middle-aged adults at a high risk of heart failure, but omega-3 fatty acid supplementation didn’t have any effect on cardiac biomarkers measured in a small, single-center, prospective study.
“One year of HIIT training reduces adiposity but had no consistent effect on myocardial triglyceride content or visceral adiposity,” wrote lead author Christopher M. Hearon Jr., PhD, and colleagues in JACC: Heart Failure. “However, long-duration HIIT improves fitness and induces favorable cardiac remodeling.” Omega-3 supplementation, however, had “no independent or additive effect.” Dr. Hearon is an instructor of applied clinical research at University of Texas Southwestern Medical Center in Dallas.
Investigators there and at the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital Dallas studied 80 patients aged 40-55 years classified as high risk for HF and obese, randomizing them to a year of high-intensity interval training (HIIT) with supplementation of either 1.6 g omega-3 FA or placebo daily; or to a control group split between supplementation or placebo. Fifty-six patients completed the 1-year study, with a compliance rate of 90% in the HIIT group and 92% in those assigned omega-3 FA supplementation.
Carl J. “Chip” Lavie, MD, of the John Ochsner Heart and Vascular Institute in New Orleans, commented that, although the study was “extremely well done from an excellent research group,” it was limited by its small population and relatively short follow-up. Future research should evaluate HIIT and moderate exercise on clinical events over a longer term as well as different doses of omega-3 “There is tremendous potential for omega-3 in heart failure prevention and treatment.”
HIIT boosts exercise capacity, more
In the study, the HIIT group showed improvement in a number of cardiac markers: around a 22% improvement in exercise capacity as measured by absolute peak and relative peak oxygen uptake (VO2), even without significant weight loss. They improved an average of 0.43 L/min (0.32-0.53; P < .0001) and 4.46 mL/kg per minute (3.18-5.56; P < .0001), respectively.
The researchers attributed the increase in peak VO2 to an increase in peak cardiac output averaging 2.15 L/min (95% confidence interval, 0.90-3.39; P = .001) and stroke volume averaging 9.46 mL (95% CI, 0.65-18.27; P = .04). A year of exercise training also resulted in changes in cardiac remodeling, including increases in left ventricle mass and LV end diastolic volume, averaging 9.4 g (95% CI, 4.36-14.44; P < .001) and 12.33 mL (95% CI, 5.61-19.05; P < .001), respectively.
The study also found that neither intervention had any appreciable impact on body weight, body mass index, body surface area or lean mass, or markers of arterial or local carotid stiffness. The exercise group had a modest decrease in fat mass, averaging 2.63 kg (95% CI,–4.81 to –0.46; P = .02), but without any effect from omega-3 supplementation.
The study acknowledged that high-dose omega-3 supplements have been found to lower triglyceride levels in people with severe hypertriglyceridemia, and hypothesized that HIIT alone or with omega-3 supplementation would improve fitness and biomarkers in people with stage A HF. “Contrary to our hypothesis, we found that one year of n-3FA [omega-3 FA] supplementation had no detectable effect on any parameter related to cardiopulmonary fitness, cardiovascular remodeling/stiffness, visceral adiposity, or myocardial triglyceride content,” Dr. Hearon and colleagues wrote.
The study “shows that obese middle-aged patients with heart failure with preserved ejection fraction [HFpEF] can markedly improve their fitness with HIIT and, generally, fitness is one of the strongest if not the strongest predictor of prognosis and survival,” said Dr. Lavie.
“Studies are needed on exercise that improves fitness in both HF with reduced ejection fraction and HFpEF, but especially HFpEF,” he said.
The study received funding from the American Heart Association Strategically Focused Research Network. Dr. Hearon and coauthors have no relevant disclosures. Dr. Lavie is a speaker and consultant for PAI Health, the Global Organization for EPA and DHA Omega-3s and DSM Nutritional Products.
A year of high-intensity interval training seemed to benefit obese middle-aged adults at a high risk of heart failure, but omega-3 fatty acid supplementation didn’t have any effect on cardiac biomarkers measured in a small, single-center, prospective study.
“One year of HIIT training reduces adiposity but had no consistent effect on myocardial triglyceride content or visceral adiposity,” wrote lead author Christopher M. Hearon Jr., PhD, and colleagues in JACC: Heart Failure. “However, long-duration HIIT improves fitness and induces favorable cardiac remodeling.” Omega-3 supplementation, however, had “no independent or additive effect.” Dr. Hearon is an instructor of applied clinical research at University of Texas Southwestern Medical Center in Dallas.
Investigators there and at the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital Dallas studied 80 patients aged 40-55 years classified as high risk for HF and obese, randomizing them to a year of high-intensity interval training (HIIT) with supplementation of either 1.6 g omega-3 FA or placebo daily; or to a control group split between supplementation or placebo. Fifty-six patients completed the 1-year study, with a compliance rate of 90% in the HIIT group and 92% in those assigned omega-3 FA supplementation.
Carl J. “Chip” Lavie, MD, of the John Ochsner Heart and Vascular Institute in New Orleans, commented that, although the study was “extremely well done from an excellent research group,” it was limited by its small population and relatively short follow-up. Future research should evaluate HIIT and moderate exercise on clinical events over a longer term as well as different doses of omega-3 “There is tremendous potential for omega-3 in heart failure prevention and treatment.”
HIIT boosts exercise capacity, more
In the study, the HIIT group showed improvement in a number of cardiac markers: around a 22% improvement in exercise capacity as measured by absolute peak and relative peak oxygen uptake (VO2), even without significant weight loss. They improved an average of 0.43 L/min (0.32-0.53; P < .0001) and 4.46 mL/kg per minute (3.18-5.56; P < .0001), respectively.
The researchers attributed the increase in peak VO2 to an increase in peak cardiac output averaging 2.15 L/min (95% confidence interval, 0.90-3.39; P = .001) and stroke volume averaging 9.46 mL (95% CI, 0.65-18.27; P = .04). A year of exercise training also resulted in changes in cardiac remodeling, including increases in left ventricle mass and LV end diastolic volume, averaging 9.4 g (95% CI, 4.36-14.44; P < .001) and 12.33 mL (95% CI, 5.61-19.05; P < .001), respectively.
The study also found that neither intervention had any appreciable impact on body weight, body mass index, body surface area or lean mass, or markers of arterial or local carotid stiffness. The exercise group had a modest decrease in fat mass, averaging 2.63 kg (95% CI,–4.81 to –0.46; P = .02), but without any effect from omega-3 supplementation.
The study acknowledged that high-dose omega-3 supplements have been found to lower triglyceride levels in people with severe hypertriglyceridemia, and hypothesized that HIIT alone or with omega-3 supplementation would improve fitness and biomarkers in people with stage A HF. “Contrary to our hypothesis, we found that one year of n-3FA [omega-3 FA] supplementation had no detectable effect on any parameter related to cardiopulmonary fitness, cardiovascular remodeling/stiffness, visceral adiposity, or myocardial triglyceride content,” Dr. Hearon and colleagues wrote.
The study “shows that obese middle-aged patients with heart failure with preserved ejection fraction [HFpEF] can markedly improve their fitness with HIIT and, generally, fitness is one of the strongest if not the strongest predictor of prognosis and survival,” said Dr. Lavie.
“Studies are needed on exercise that improves fitness in both HF with reduced ejection fraction and HFpEF, but especially HFpEF,” he said.
The study received funding from the American Heart Association Strategically Focused Research Network. Dr. Hearon and coauthors have no relevant disclosures. Dr. Lavie is a speaker and consultant for PAI Health, the Global Organization for EPA and DHA Omega-3s and DSM Nutritional Products.
FROM JACC: HEART FAILURE
Food insecurity linked to metabolic syndrome in Hispanic/Latino youth
Severe food insecurity was associated with metabolic syndrome and unfavorable cardiometabolic markers in Hispanic/Latino youth, researchers report.
The findings, published March 16 in Pediatrics, highlight the need to investigate interventions that address food insecurity among Hispanic/Latino youth, a segment of the U.S. population at high risk of cardiometabolic complications.
“Among Hispanic/Latino youth, no study, to our knowledge has evaluated food insecurity’s role in metabolic syndrome and metabolic syndrome–relevant cardiometabolic markers in this population,” lead author Luis E. Maldonado, PhD, of the University of North Carolina at Chapel Hill, and colleagues explained.
The researchers conducted a cross-sectional study to evaluate the associations between lower household and child food security and metabolic syndrome, as well as clinically measured cardiometabolic markers, including fasting plasma glucose, waist circumference, triglycerides, systolic and diastolic blood pressure, and high-density lipoprotein cholesterol (HDL-C).
Household food security (high, marginal, low, very low) and child food security (high, marginal, low/very low) measures were evaluated separately, and were adjusted for participant age, sex, site, parental education, and poverty-income ratio.
Data were obtained from the Hispanic Community Children’s Health Study/Study of Latino Youth, a study of offspring of adults enrolled in the Hispanic Community Health Survey/Study of Latinos.
Results
The study cohort included 1,325 Hispanic/Latino youth aged 8-16 years. For both household food security and child food security, youth in the lowest food security category had significantly lower HDL-C compared with youth with high food security (household food security, –3.17; 95% confidence interval, –5.65 to –0.70; child food security, –1.81; 95% CI, –3.54 to –0.09).
In addition, low/very low compared with high child food security was associated with higher triglycerides (beta, 8.68; 95% CI, 1.75-15.61), higher fasting plasma glucose (beta, 1.37; 95% CI, 0.08-2.65), and metabolic syndrome composite variable expected log counts (beta, 2.12; 95% CI, 0.02-0.45).
Furthermore, the researchers found statistically significant interactions between each of the two food security measures and receipt of any food assistance in the previous year in models of triglycerides (P for interactions: household food security, .03 and child food security, .005) and HDL-C (P for interactions: household food security, .01 and child food security, .04).
After evaluating the effect of parental place of birth, they found a statistically significant association for triglycerides only (P for interactions: household food security, .05 and child food security, .008).
“Our study is among the first to document adverse associations between household and child food security measures with a metabolic syndrome score variable and several metabolic syndrome–relevant cardiometabolic markers among US Hispanic/Latino youth,” the researchers wrote.
The researchers acknowledged that the cross-sectional nature of the study was a key limitation; thus, causality could not be inferred.
“In the future, we plan to conduct more qualitative work to better understand how Hispanic/Latino families respond to food insecurity, which may identify the factors that shape their response,” study author Sandra S. Albrecht, PhD, of Columbia University, New York, NY, said in an interview.
Recommendations for pediatricians
Food insecurity researcher Yankun Wang, PhD candidate at Indiana University, Bloomington, commented: “I would recommend pediatricians pay more attention to children from low-income households since they are more likely to have mental and physical health issues due to food insecurity.
“It can be very helpful if pediatricians could help families obtain SNAP benefits, enroll youth in the school breakfast and lunch programs, and promote nutrition education in schools,” Mr. Wang added.
This study was supported by grant funding from the National Heart, Lung, and Blood Institute. The authors reported no relevant disclosures.
Severe food insecurity was associated with metabolic syndrome and unfavorable cardiometabolic markers in Hispanic/Latino youth, researchers report.
The findings, published March 16 in Pediatrics, highlight the need to investigate interventions that address food insecurity among Hispanic/Latino youth, a segment of the U.S. population at high risk of cardiometabolic complications.
“Among Hispanic/Latino youth, no study, to our knowledge has evaluated food insecurity’s role in metabolic syndrome and metabolic syndrome–relevant cardiometabolic markers in this population,” lead author Luis E. Maldonado, PhD, of the University of North Carolina at Chapel Hill, and colleagues explained.
The researchers conducted a cross-sectional study to evaluate the associations between lower household and child food security and metabolic syndrome, as well as clinically measured cardiometabolic markers, including fasting plasma glucose, waist circumference, triglycerides, systolic and diastolic blood pressure, and high-density lipoprotein cholesterol (HDL-C).
Household food security (high, marginal, low, very low) and child food security (high, marginal, low/very low) measures were evaluated separately, and were adjusted for participant age, sex, site, parental education, and poverty-income ratio.
Data were obtained from the Hispanic Community Children’s Health Study/Study of Latino Youth, a study of offspring of adults enrolled in the Hispanic Community Health Survey/Study of Latinos.
Results
The study cohort included 1,325 Hispanic/Latino youth aged 8-16 years. For both household food security and child food security, youth in the lowest food security category had significantly lower HDL-C compared with youth with high food security (household food security, –3.17; 95% confidence interval, –5.65 to –0.70; child food security, –1.81; 95% CI, –3.54 to –0.09).
In addition, low/very low compared with high child food security was associated with higher triglycerides (beta, 8.68; 95% CI, 1.75-15.61), higher fasting plasma glucose (beta, 1.37; 95% CI, 0.08-2.65), and metabolic syndrome composite variable expected log counts (beta, 2.12; 95% CI, 0.02-0.45).
Furthermore, the researchers found statistically significant interactions between each of the two food security measures and receipt of any food assistance in the previous year in models of triglycerides (P for interactions: household food security, .03 and child food security, .005) and HDL-C (P for interactions: household food security, .01 and child food security, .04).
After evaluating the effect of parental place of birth, they found a statistically significant association for triglycerides only (P for interactions: household food security, .05 and child food security, .008).
“Our study is among the first to document adverse associations between household and child food security measures with a metabolic syndrome score variable and several metabolic syndrome–relevant cardiometabolic markers among US Hispanic/Latino youth,” the researchers wrote.
The researchers acknowledged that the cross-sectional nature of the study was a key limitation; thus, causality could not be inferred.
“In the future, we plan to conduct more qualitative work to better understand how Hispanic/Latino families respond to food insecurity, which may identify the factors that shape their response,” study author Sandra S. Albrecht, PhD, of Columbia University, New York, NY, said in an interview.
Recommendations for pediatricians
Food insecurity researcher Yankun Wang, PhD candidate at Indiana University, Bloomington, commented: “I would recommend pediatricians pay more attention to children from low-income households since they are more likely to have mental and physical health issues due to food insecurity.
“It can be very helpful if pediatricians could help families obtain SNAP benefits, enroll youth in the school breakfast and lunch programs, and promote nutrition education in schools,” Mr. Wang added.
This study was supported by grant funding from the National Heart, Lung, and Blood Institute. The authors reported no relevant disclosures.
Severe food insecurity was associated with metabolic syndrome and unfavorable cardiometabolic markers in Hispanic/Latino youth, researchers report.
The findings, published March 16 in Pediatrics, highlight the need to investigate interventions that address food insecurity among Hispanic/Latino youth, a segment of the U.S. population at high risk of cardiometabolic complications.
“Among Hispanic/Latino youth, no study, to our knowledge has evaluated food insecurity’s role in metabolic syndrome and metabolic syndrome–relevant cardiometabolic markers in this population,” lead author Luis E. Maldonado, PhD, of the University of North Carolina at Chapel Hill, and colleagues explained.
The researchers conducted a cross-sectional study to evaluate the associations between lower household and child food security and metabolic syndrome, as well as clinically measured cardiometabolic markers, including fasting plasma glucose, waist circumference, triglycerides, systolic and diastolic blood pressure, and high-density lipoprotein cholesterol (HDL-C).
Household food security (high, marginal, low, very low) and child food security (high, marginal, low/very low) measures were evaluated separately, and were adjusted for participant age, sex, site, parental education, and poverty-income ratio.
Data were obtained from the Hispanic Community Children’s Health Study/Study of Latino Youth, a study of offspring of adults enrolled in the Hispanic Community Health Survey/Study of Latinos.
Results
The study cohort included 1,325 Hispanic/Latino youth aged 8-16 years. For both household food security and child food security, youth in the lowest food security category had significantly lower HDL-C compared with youth with high food security (household food security, –3.17; 95% confidence interval, –5.65 to –0.70; child food security, –1.81; 95% CI, –3.54 to –0.09).
In addition, low/very low compared with high child food security was associated with higher triglycerides (beta, 8.68; 95% CI, 1.75-15.61), higher fasting plasma glucose (beta, 1.37; 95% CI, 0.08-2.65), and metabolic syndrome composite variable expected log counts (beta, 2.12; 95% CI, 0.02-0.45).
Furthermore, the researchers found statistically significant interactions between each of the two food security measures and receipt of any food assistance in the previous year in models of triglycerides (P for interactions: household food security, .03 and child food security, .005) and HDL-C (P for interactions: household food security, .01 and child food security, .04).
After evaluating the effect of parental place of birth, they found a statistically significant association for triglycerides only (P for interactions: household food security, .05 and child food security, .008).
“Our study is among the first to document adverse associations between household and child food security measures with a metabolic syndrome score variable and several metabolic syndrome–relevant cardiometabolic markers among US Hispanic/Latino youth,” the researchers wrote.
The researchers acknowledged that the cross-sectional nature of the study was a key limitation; thus, causality could not be inferred.
“In the future, we plan to conduct more qualitative work to better understand how Hispanic/Latino families respond to food insecurity, which may identify the factors that shape their response,” study author Sandra S. Albrecht, PhD, of Columbia University, New York, NY, said in an interview.
Recommendations for pediatricians
Food insecurity researcher Yankun Wang, PhD candidate at Indiana University, Bloomington, commented: “I would recommend pediatricians pay more attention to children from low-income households since they are more likely to have mental and physical health issues due to food insecurity.
“It can be very helpful if pediatricians could help families obtain SNAP benefits, enroll youth in the school breakfast and lunch programs, and promote nutrition education in schools,” Mr. Wang added.
This study was supported by grant funding from the National Heart, Lung, and Blood Institute. The authors reported no relevant disclosures.
FROM PEDIATRICS
CPAP has only small effect on metabolic syndrome
Continuous positive airway pressure (CPAP) may be only modestly effective for ameliorating metabolic syndrome in patients with moderate to severe obstructive sleep apnea (OSA).
That conclusion comes from investigators in a randomized controlled, trial, who found that, among 100 patients with OSA and a recent diagnosis of metabolic syndrome (MS), 18% of those assigned to use CPAP at night had a reversal of MS at 6 months of follow-up, compared with 4% of controls who were assigned to use nasal strips at night (P = .04).
The majority of patients assigned to CPAP still retained their MS diagnoses at 6 months, and CPAP did not significantly reduce individual components of the syndrome. Use of CPAP was, however, associated with small reductions in visceral fat and improvement in endothelial function, reported Sara Q.C. Giampa, PhD, from the University of São Paulo, and colleagues.
“Despite a significant rate of MS reversibility after CPAP therapy, most of the patients maintained the MS diagnosis. The modest effects of CPAP on MS reversibility underscore the need for combined therapy with CPAP, aiming to maximize metabolic syndrome recovery in parallel with improvements in OSA severity and related symptoms,” according to their study, reported in the journal CHEST®.
Asked whether he still recommends CPAP to patients with OSA and the metabolic syndrome, given the findings, corresponding author Luciano F. Drager, MD, PhD, replied “yes, definitely.”
“Despite the modest rate in reversing metabolic syndrome after CPAP, the rate was 5-fold higher than non-effective treatment (18% vs. 4%),” he said in an interview.
Dr. Drager noted that studies of other single interventions such as physical exercise to reverse MS in patients with OSA also had modest results.
A researcher who studies the relationship between sleep, circadian rhythms, and metabolism commented that, although the patients in the CPAP group were compliant with the assigned equipment and had both reductions in apneic events and improvement in oxygen saturation, the effect of CPAP on the metabolic syndrome was rather small.
“The CPAP was doing what we thought it was supposed to do, but it didn’t have the magnitude of effect on the metabolic syndrome as I expected or I think as the authors expected,” said Deanna Arble, PhD, assistant professor of biological science at Marquette University, Milwaukee.
She noted that the study also failed to detect a significant improvement in the blood pressure component of metabolic syndrome.
“In my experience and my review of the literature, blood pressure tends to be the one that’s improved most dramatically with CPAP,” she said.
Dr. Arble was not involved in the study.
Study details
In the trial, titled TREATOSA-MS, the investigators enrolled 100 patients with a recent diagnosis of metabolic syndrome and moderate to severe OSA, defined as 15 or more apnea-hypopnea index events per hour. The patients were stratified by body mass index and then randomized to undergo therapeutic CPAP or to use nasal strips for 6 months.
At baseline and at the end of each intervention investigators measured anthropometric variables, blood pressure, glucose, and lipid profiles. They also leptin and adiponectin, body composition, food intake, physical activity, subcutaneous and abdominal fat (visceral and hepatic), and endothelial function to control for potential confounders.
As noted previously, they found that after 6 months “most patients with OSA randomized to CPAP retained the MS diagnosis, but the rate of MS reversibility was higher than observed in the placebo group.” The difference in metabolic syndrome reversal, 18% with CPAP versus 4% with nasal strips, translated into a hazard ratio favoring CPAP of 5.27 (P = .04).
Also as noted, in analyses adjusted for baseline values, CPAP did not significantly improve either weight, liver fat, lip profiles, or the adiposity biomarkers leptin and adiponectin, but did have “very modest” influence on reducing visceral fat and improving endothelial function.
Rigorous study
Dr. Arble said that most studies of the association between OSA and metabolic syndrome have focused on only one or two of the parameters that were included in the TREATOSA-MS study, giving the findings additional weight.
“This could potentially be a very good, carefully controlled first insight into how obstructive sleep apnea is related to the metabolic syndrome,” she said.
The study was funded by grants Fundação de Amparo Q22 à Pesquisa do Estado de São Paulo and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior. The authors and Dr. Arble reported having no conflicts of interest to disclose.
Continuous positive airway pressure (CPAP) may be only modestly effective for ameliorating metabolic syndrome in patients with moderate to severe obstructive sleep apnea (OSA).
That conclusion comes from investigators in a randomized controlled, trial, who found that, among 100 patients with OSA and a recent diagnosis of metabolic syndrome (MS), 18% of those assigned to use CPAP at night had a reversal of MS at 6 months of follow-up, compared with 4% of controls who were assigned to use nasal strips at night (P = .04).
The majority of patients assigned to CPAP still retained their MS diagnoses at 6 months, and CPAP did not significantly reduce individual components of the syndrome. Use of CPAP was, however, associated with small reductions in visceral fat and improvement in endothelial function, reported Sara Q.C. Giampa, PhD, from the University of São Paulo, and colleagues.
“Despite a significant rate of MS reversibility after CPAP therapy, most of the patients maintained the MS diagnosis. The modest effects of CPAP on MS reversibility underscore the need for combined therapy with CPAP, aiming to maximize metabolic syndrome recovery in parallel with improvements in OSA severity and related symptoms,” according to their study, reported in the journal CHEST®.
Asked whether he still recommends CPAP to patients with OSA and the metabolic syndrome, given the findings, corresponding author Luciano F. Drager, MD, PhD, replied “yes, definitely.”
“Despite the modest rate in reversing metabolic syndrome after CPAP, the rate was 5-fold higher than non-effective treatment (18% vs. 4%),” he said in an interview.
Dr. Drager noted that studies of other single interventions such as physical exercise to reverse MS in patients with OSA also had modest results.
A researcher who studies the relationship between sleep, circadian rhythms, and metabolism commented that, although the patients in the CPAP group were compliant with the assigned equipment and had both reductions in apneic events and improvement in oxygen saturation, the effect of CPAP on the metabolic syndrome was rather small.
“The CPAP was doing what we thought it was supposed to do, but it didn’t have the magnitude of effect on the metabolic syndrome as I expected or I think as the authors expected,” said Deanna Arble, PhD, assistant professor of biological science at Marquette University, Milwaukee.
She noted that the study also failed to detect a significant improvement in the blood pressure component of metabolic syndrome.
“In my experience and my review of the literature, blood pressure tends to be the one that’s improved most dramatically with CPAP,” she said.
Dr. Arble was not involved in the study.
Study details
In the trial, titled TREATOSA-MS, the investigators enrolled 100 patients with a recent diagnosis of metabolic syndrome and moderate to severe OSA, defined as 15 or more apnea-hypopnea index events per hour. The patients were stratified by body mass index and then randomized to undergo therapeutic CPAP or to use nasal strips for 6 months.
At baseline and at the end of each intervention investigators measured anthropometric variables, blood pressure, glucose, and lipid profiles. They also leptin and adiponectin, body composition, food intake, physical activity, subcutaneous and abdominal fat (visceral and hepatic), and endothelial function to control for potential confounders.
As noted previously, they found that after 6 months “most patients with OSA randomized to CPAP retained the MS diagnosis, but the rate of MS reversibility was higher than observed in the placebo group.” The difference in metabolic syndrome reversal, 18% with CPAP versus 4% with nasal strips, translated into a hazard ratio favoring CPAP of 5.27 (P = .04).
Also as noted, in analyses adjusted for baseline values, CPAP did not significantly improve either weight, liver fat, lip profiles, or the adiposity biomarkers leptin and adiponectin, but did have “very modest” influence on reducing visceral fat and improving endothelial function.
Rigorous study
Dr. Arble said that most studies of the association between OSA and metabolic syndrome have focused on only one or two of the parameters that were included in the TREATOSA-MS study, giving the findings additional weight.
“This could potentially be a very good, carefully controlled first insight into how obstructive sleep apnea is related to the metabolic syndrome,” she said.
The study was funded by grants Fundação de Amparo Q22 à Pesquisa do Estado de São Paulo and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior. The authors and Dr. Arble reported having no conflicts of interest to disclose.
Continuous positive airway pressure (CPAP) may be only modestly effective for ameliorating metabolic syndrome in patients with moderate to severe obstructive sleep apnea (OSA).
That conclusion comes from investigators in a randomized controlled, trial, who found that, among 100 patients with OSA and a recent diagnosis of metabolic syndrome (MS), 18% of those assigned to use CPAP at night had a reversal of MS at 6 months of follow-up, compared with 4% of controls who were assigned to use nasal strips at night (P = .04).
The majority of patients assigned to CPAP still retained their MS diagnoses at 6 months, and CPAP did not significantly reduce individual components of the syndrome. Use of CPAP was, however, associated with small reductions in visceral fat and improvement in endothelial function, reported Sara Q.C. Giampa, PhD, from the University of São Paulo, and colleagues.
“Despite a significant rate of MS reversibility after CPAP therapy, most of the patients maintained the MS diagnosis. The modest effects of CPAP on MS reversibility underscore the need for combined therapy with CPAP, aiming to maximize metabolic syndrome recovery in parallel with improvements in OSA severity and related symptoms,” according to their study, reported in the journal CHEST®.
Asked whether he still recommends CPAP to patients with OSA and the metabolic syndrome, given the findings, corresponding author Luciano F. Drager, MD, PhD, replied “yes, definitely.”
“Despite the modest rate in reversing metabolic syndrome after CPAP, the rate was 5-fold higher than non-effective treatment (18% vs. 4%),” he said in an interview.
Dr. Drager noted that studies of other single interventions such as physical exercise to reverse MS in patients with OSA also had modest results.
A researcher who studies the relationship between sleep, circadian rhythms, and metabolism commented that, although the patients in the CPAP group were compliant with the assigned equipment and had both reductions in apneic events and improvement in oxygen saturation, the effect of CPAP on the metabolic syndrome was rather small.
“The CPAP was doing what we thought it was supposed to do, but it didn’t have the magnitude of effect on the metabolic syndrome as I expected or I think as the authors expected,” said Deanna Arble, PhD, assistant professor of biological science at Marquette University, Milwaukee.
She noted that the study also failed to detect a significant improvement in the blood pressure component of metabolic syndrome.
“In my experience and my review of the literature, blood pressure tends to be the one that’s improved most dramatically with CPAP,” she said.
Dr. Arble was not involved in the study.
Study details
In the trial, titled TREATOSA-MS, the investigators enrolled 100 patients with a recent diagnosis of metabolic syndrome and moderate to severe OSA, defined as 15 or more apnea-hypopnea index events per hour. The patients were stratified by body mass index and then randomized to undergo therapeutic CPAP or to use nasal strips for 6 months.
At baseline and at the end of each intervention investigators measured anthropometric variables, blood pressure, glucose, and lipid profiles. They also leptin and adiponectin, body composition, food intake, physical activity, subcutaneous and abdominal fat (visceral and hepatic), and endothelial function to control for potential confounders.
As noted previously, they found that after 6 months “most patients with OSA randomized to CPAP retained the MS diagnosis, but the rate of MS reversibility was higher than observed in the placebo group.” The difference in metabolic syndrome reversal, 18% with CPAP versus 4% with nasal strips, translated into a hazard ratio favoring CPAP of 5.27 (P = .04).
Also as noted, in analyses adjusted for baseline values, CPAP did not significantly improve either weight, liver fat, lip profiles, or the adiposity biomarkers leptin and adiponectin, but did have “very modest” influence on reducing visceral fat and improving endothelial function.
Rigorous study
Dr. Arble said that most studies of the association between OSA and metabolic syndrome have focused on only one or two of the parameters that were included in the TREATOSA-MS study, giving the findings additional weight.
“This could potentially be a very good, carefully controlled first insight into how obstructive sleep apnea is related to the metabolic syndrome,” she said.
The study was funded by grants Fundação de Amparo Q22 à Pesquisa do Estado de São Paulo and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior. The authors and Dr. Arble reported having no conflicts of interest to disclose.
FROM CHEST
Guidance seeks to improve statin treatment adherence
International experts have created recommendations on ways to improve adherence to statin therapy by offering doctors guidance on how to distinguish between true side effects of statins and those arising due to patients’ expectations of side effects.
A position paper from the International Lipid Expert Panel (ILEP), a group of over 70 experts worldwide, provides a step-by-step approach to diagnosing and managing symptoms, such as muscle aches, and encourages patients to continue the statin therapy they have been prescribed.
The authors described in their paper, published in the Journal of Cachexia, Sarcopenia, and Muscle, how statins are among the most commonly prescribed drugs globally, with “strong and unambiguous evidence” that statin treatment makes a significant difference in preventing cardiovascular disease and dying from it.
They said how, although a recent meta-analysis showed the prevalence of statin intolerance is less than 10%, “as many as 1 in 2 patients stop taking statins, reduce the dose, or take them irregularly because they believe they are responsible for side effects.”
In addition to misattribution of aches and pains, a substantial proportion of statin-associated muscle symptoms (SAMS) result from the action of taking medicines and the expectation that medicines cause side effects. A systematic review of trials estimated that between 38% and 78% of SAMS-related statin intolerance could be attributed to expectation alone.
Nocebo/drucebo effect
President of the ILEP, Professor Maciej Banach, of the Medical University of Lodz and the University of Zielona Góra, both in Poland, who originated these recommendations, said: “There is an enormous worldwide problem with diagnosing statin intolerance correctly. In addition, we know that most diagnosed statin side effects should not, in fact, be attributed to statin therapy.”
He highlighted how as much as 70% of statin side effect symptoms may be due to a psychological phenomenon called the “nocebo” or “drucebo” effect.
“The ‘nocebo/drucebo’ effect is when patients’ expectations that they will experience side effects from the statins result in them actually experiencing these symptoms,” Professor Banach explained. Knowledge gained from the internet, leaflets, friends and family, and other sources, for example, about the most common side effects – muscle pain and liver complaints – can “result in them discontinuing their therapy and, therefore, increasing their risk of heart problems, stroke, and death,” he cautioned.
First author of the paper, Dr. Peter Penson, a reader in Cardiovascular Pharmacology at Liverpool John Moores University, England, said “the benefits of statins are not seen immediately by patients, whilst the associated adverse effects are more tangible, and so many patients stop taking statins, thereby putting themselves at risk of serious illness or death.”
A practical evidence-based guide
The authors expressed hope that their recommendations would help doctors improve patient-centered care for those patients at risk of cardiovascular disease and help these patients understand the reason for their treatment, the benefits, including that statins may prolong their lives, and the potential harms, thus enabling the patient to “make a fully informed decision about commencing and continuing therapy.”
The recommendations include:
- That health care professionals should consider the nocebo/drucebo effect when they first prescribe statins and provide information to patients about the rationale and benefits of the therapy
- The Personalized Lipid Intervention Plan (PLIP) should be used to help this process. It estimates the patient’s 10-year risk of cardiovascular disease with and without statin therapy, as well as providing clear information on adverse side effects, including that muscle symptoms are common but rarely caused by statins
- How to effectively diagnose statin intolerance and exclude nocebo/drucebo effect
- Routine follow-up to check the safety and efficacy of the therapy is recommended, and strategies for managing patients with complete statin intolerance are provided, within the recommendations. Also offered is advice about improving adherence to statin therapy and suggestions for the identification and management of the “relatively small number of patients who have true statin intolerance.”
Dr. Penson emphasized how this was the first paper to deal explicitly with the nocebo/drucebo effect and offers “practical and evidence-based suggestions” to help support individuals who are at risk of cardiovascular disease but who experience adverse effects attributable to their medicines. He added how the PLIP summarizes important lifestyle advice to help patients reduce their risk of heart attacks and strokes and also discusses the evidence for non-statin drugs that can be used to lower cholesterol.
Dr. Penson pointed out how “the vast majority of patients can take statins safely and that the benefits greatly outweigh the potential risk of side effects” and, therefore, an individual’s risk of heart problems, stroke, and death, can be reduced.
A version of this article first appeared on Medscape.com.
International experts have created recommendations on ways to improve adherence to statin therapy by offering doctors guidance on how to distinguish between true side effects of statins and those arising due to patients’ expectations of side effects.
A position paper from the International Lipid Expert Panel (ILEP), a group of over 70 experts worldwide, provides a step-by-step approach to diagnosing and managing symptoms, such as muscle aches, and encourages patients to continue the statin therapy they have been prescribed.
The authors described in their paper, published in the Journal of Cachexia, Sarcopenia, and Muscle, how statins are among the most commonly prescribed drugs globally, with “strong and unambiguous evidence” that statin treatment makes a significant difference in preventing cardiovascular disease and dying from it.
They said how, although a recent meta-analysis showed the prevalence of statin intolerance is less than 10%, “as many as 1 in 2 patients stop taking statins, reduce the dose, or take them irregularly because they believe they are responsible for side effects.”
In addition to misattribution of aches and pains, a substantial proportion of statin-associated muscle symptoms (SAMS) result from the action of taking medicines and the expectation that medicines cause side effects. A systematic review of trials estimated that between 38% and 78% of SAMS-related statin intolerance could be attributed to expectation alone.
Nocebo/drucebo effect
President of the ILEP, Professor Maciej Banach, of the Medical University of Lodz and the University of Zielona Góra, both in Poland, who originated these recommendations, said: “There is an enormous worldwide problem with diagnosing statin intolerance correctly. In addition, we know that most diagnosed statin side effects should not, in fact, be attributed to statin therapy.”
He highlighted how as much as 70% of statin side effect symptoms may be due to a psychological phenomenon called the “nocebo” or “drucebo” effect.
“The ‘nocebo/drucebo’ effect is when patients’ expectations that they will experience side effects from the statins result in them actually experiencing these symptoms,” Professor Banach explained. Knowledge gained from the internet, leaflets, friends and family, and other sources, for example, about the most common side effects – muscle pain and liver complaints – can “result in them discontinuing their therapy and, therefore, increasing their risk of heart problems, stroke, and death,” he cautioned.
First author of the paper, Dr. Peter Penson, a reader in Cardiovascular Pharmacology at Liverpool John Moores University, England, said “the benefits of statins are not seen immediately by patients, whilst the associated adverse effects are more tangible, and so many patients stop taking statins, thereby putting themselves at risk of serious illness or death.”
A practical evidence-based guide
The authors expressed hope that their recommendations would help doctors improve patient-centered care for those patients at risk of cardiovascular disease and help these patients understand the reason for their treatment, the benefits, including that statins may prolong their lives, and the potential harms, thus enabling the patient to “make a fully informed decision about commencing and continuing therapy.”
The recommendations include:
- That health care professionals should consider the nocebo/drucebo effect when they first prescribe statins and provide information to patients about the rationale and benefits of the therapy
- The Personalized Lipid Intervention Plan (PLIP) should be used to help this process. It estimates the patient’s 10-year risk of cardiovascular disease with and without statin therapy, as well as providing clear information on adverse side effects, including that muscle symptoms are common but rarely caused by statins
- How to effectively diagnose statin intolerance and exclude nocebo/drucebo effect
- Routine follow-up to check the safety and efficacy of the therapy is recommended, and strategies for managing patients with complete statin intolerance are provided, within the recommendations. Also offered is advice about improving adherence to statin therapy and suggestions for the identification and management of the “relatively small number of patients who have true statin intolerance.”
Dr. Penson emphasized how this was the first paper to deal explicitly with the nocebo/drucebo effect and offers “practical and evidence-based suggestions” to help support individuals who are at risk of cardiovascular disease but who experience adverse effects attributable to their medicines. He added how the PLIP summarizes important lifestyle advice to help patients reduce their risk of heart attacks and strokes and also discusses the evidence for non-statin drugs that can be used to lower cholesterol.
Dr. Penson pointed out how “the vast majority of patients can take statins safely and that the benefits greatly outweigh the potential risk of side effects” and, therefore, an individual’s risk of heart problems, stroke, and death, can be reduced.
A version of this article first appeared on Medscape.com.
International experts have created recommendations on ways to improve adherence to statin therapy by offering doctors guidance on how to distinguish between true side effects of statins and those arising due to patients’ expectations of side effects.
A position paper from the International Lipid Expert Panel (ILEP), a group of over 70 experts worldwide, provides a step-by-step approach to diagnosing and managing symptoms, such as muscle aches, and encourages patients to continue the statin therapy they have been prescribed.
The authors described in their paper, published in the Journal of Cachexia, Sarcopenia, and Muscle, how statins are among the most commonly prescribed drugs globally, with “strong and unambiguous evidence” that statin treatment makes a significant difference in preventing cardiovascular disease and dying from it.
They said how, although a recent meta-analysis showed the prevalence of statin intolerance is less than 10%, “as many as 1 in 2 patients stop taking statins, reduce the dose, or take them irregularly because they believe they are responsible for side effects.”
In addition to misattribution of aches and pains, a substantial proportion of statin-associated muscle symptoms (SAMS) result from the action of taking medicines and the expectation that medicines cause side effects. A systematic review of trials estimated that between 38% and 78% of SAMS-related statin intolerance could be attributed to expectation alone.
Nocebo/drucebo effect
President of the ILEP, Professor Maciej Banach, of the Medical University of Lodz and the University of Zielona Góra, both in Poland, who originated these recommendations, said: “There is an enormous worldwide problem with diagnosing statin intolerance correctly. In addition, we know that most diagnosed statin side effects should not, in fact, be attributed to statin therapy.”
He highlighted how as much as 70% of statin side effect symptoms may be due to a psychological phenomenon called the “nocebo” or “drucebo” effect.
“The ‘nocebo/drucebo’ effect is when patients’ expectations that they will experience side effects from the statins result in them actually experiencing these symptoms,” Professor Banach explained. Knowledge gained from the internet, leaflets, friends and family, and other sources, for example, about the most common side effects – muscle pain and liver complaints – can “result in them discontinuing their therapy and, therefore, increasing their risk of heart problems, stroke, and death,” he cautioned.
First author of the paper, Dr. Peter Penson, a reader in Cardiovascular Pharmacology at Liverpool John Moores University, England, said “the benefits of statins are not seen immediately by patients, whilst the associated adverse effects are more tangible, and so many patients stop taking statins, thereby putting themselves at risk of serious illness or death.”
A practical evidence-based guide
The authors expressed hope that their recommendations would help doctors improve patient-centered care for those patients at risk of cardiovascular disease and help these patients understand the reason for their treatment, the benefits, including that statins may prolong their lives, and the potential harms, thus enabling the patient to “make a fully informed decision about commencing and continuing therapy.”
The recommendations include:
- That health care professionals should consider the nocebo/drucebo effect when they first prescribe statins and provide information to patients about the rationale and benefits of the therapy
- The Personalized Lipid Intervention Plan (PLIP) should be used to help this process. It estimates the patient’s 10-year risk of cardiovascular disease with and without statin therapy, as well as providing clear information on adverse side effects, including that muscle symptoms are common but rarely caused by statins
- How to effectively diagnose statin intolerance and exclude nocebo/drucebo effect
- Routine follow-up to check the safety and efficacy of the therapy is recommended, and strategies for managing patients with complete statin intolerance are provided, within the recommendations. Also offered is advice about improving adherence to statin therapy and suggestions for the identification and management of the “relatively small number of patients who have true statin intolerance.”
Dr. Penson emphasized how this was the first paper to deal explicitly with the nocebo/drucebo effect and offers “practical and evidence-based suggestions” to help support individuals who are at risk of cardiovascular disease but who experience adverse effects attributable to their medicines. He added how the PLIP summarizes important lifestyle advice to help patients reduce their risk of heart attacks and strokes and also discusses the evidence for non-statin drugs that can be used to lower cholesterol.
Dr. Penson pointed out how “the vast majority of patients can take statins safely and that the benefits greatly outweigh the potential risk of side effects” and, therefore, an individual’s risk of heart problems, stroke, and death, can be reduced.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF CACHEXIA, SARCOPENIA, AND MUSCLE
Resistance exercise may be best workout for a good night’s sleep
CHICAGO – A randomized trial suggests resistance exercise promotes better sleep than other workouts among inactive adults, particularly those who are poor sleepers.
“We thought resistance exercise would be somewhere in the same neighborhood as aerobic exercise or that maybe combined exercise would be a little bit better but, no, it was consistently resistance exercise, on its own, that seemed to show the most benefits across the board,” Angelique Brellenthin, PhD, told this news organization.
The results were presented at the recent Epidemiology, Prevention/Lifestyle & Cardiometabolic Health meeting sponsored by the American Heart Association.
Even before the pandemic and bedtime “doom scrolling” took hold, research showed that a third of Americans regularly get less than 7 hours of sleep. The AHA recommends aerobic exercise to improve sleep and promote cardiovascular health, yet little is known on how it compares with other types of exercise in the general population, she said.
Dr. Brellenthin and coinvestigator Duck-chul Lee, PhD, both of Iowa State University in Ames, recruited 406 inactive adults, aged 35-70 years, who had obesity or overweight (mean body mass index, 31.2 kg/m2) and had elevated or stage 1 hypertension and randomly assigned them to no exercise or 60 minutes of supervised aerobic, resistance, or combination exercise three times per week for 12 months.
The aerobic exercise group could choose among treadmills, upright or recumbent bikes, and ellipticals, and the participants had their heart rate monitored to ensure they were continuously getting moderate- to vigorous-intensity exercise.
The resistance exercise group performed three sets of 8-16 repetitions at 50%-80% of their one-rep maximum on 12 resistance machines: a leg press, chest press, lat pulldown, leg curl, leg extension, biceps curl, triceps pushdown, shoulder press, abdominal crunch, lower back extension, torso rotation, and hip abduction.
The combination group did 30 minutes of aerobic exercise at moderate to vigorous intensity, and then two sets of 8-16 repetitions of resistance exercise on 9 machines instead of 12.
Exercise adherence over the year was 84%, 77%, and 85%, respectively.
Participants also completed the Pittsburgh Sleep Quality Index (PSQI) at baseline and 12 months. Among the 386 participants (53% women) with evaluable data, 35% had poor-quality sleep, as indicated by a global PSQI score of more than 5, and 42% regularly slept less than 7 hours per night.
In adjusted analyses, sleep duration at 12 months, on average, increased by 13 minutes in the resistance-exercise group (P = .009), decreased by 0.6 minute in the aerobic-exercise group, and increased by 2 minutes in the combined-exercise group and by 4 minutes in the control group.
Among participants who got less than 7 hours of sleep at baseline, however, sleep duration increased by 40 minutes (P < .0001), compared with increases of 23 minutes in the aerobic group, 17 minutes in the combined group, and 15 minutes in the control group.
Overall sleep efficiency, or the ratio of total sleep time to time in bed, improved in the resistance (P = .0005) and combined (P = .03) exercise groups, but not in the aerobic or control groups.
Sleep latency, or the time needed to fall asleep, decreased by 3 minutes in the resistance-exercise group, with no notable changes in the other groups.
Sleep quality and the number of sleep disturbances improved in all groups, including the control group. This could be due to simply being part of a health intervention, which included a month of lifestyle education classes, Dr. Brellenthin suggested.
It’s unclear why the aerobic-exercise group didn’t show greater gains, given the wealth of research showing it improves sleep, she said, but it had fewer poor sleepers at baseline than the resistance group (33% vs. 42%). “So it may be that people who were already getting good sleep didn’t have much room to improve.”
Among the poor-quality sleepers at baseline, resistance exercise significantly improved sleep quality (-2.4 vs. -1.0 points; P = .009) and duration (+36 vs. +3 minutes; P = .02), compared with the control group. It also improved sleep efficiency by 9.0%, compared with 0.9% in the control group (P = .002) and 8.0% for the combined-exercise group (P = .01).
“For a lot of people who know their sleep could be a bit better, this could be a place to start without resorting to medications, if they wanted to focus on a lifestyle intervention,” Dr. Brellenthin said.
It’s not fully understood how resistance exercise improves sleep, but it might contribute to better overall mental health and it might enhance the synthesis and release of certain hormones, such as testosterone and human growth hormone, which are associated with better sleep, Dr. Brellenthin said. Another hypothesis is that it causes direct microscopic damage to muscle tissue, forcing that tissue to adapt and grow over time. “So potentially that microscopic damage could provide that extra signal boost to the brain to replenish and repair, and get this person sleep.”
The study was limited by the use of self-reported sleep outcomes and a lack of detailed information on sleep medications, although 81% of participants reported taking no such medications.
The research was supported by a National Institutes of Health/National Heart, Lung, and Blood Institute grant to Dr. Lee. Dr. Brellenthin reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
CHICAGO – A randomized trial suggests resistance exercise promotes better sleep than other workouts among inactive adults, particularly those who are poor sleepers.
“We thought resistance exercise would be somewhere in the same neighborhood as aerobic exercise or that maybe combined exercise would be a little bit better but, no, it was consistently resistance exercise, on its own, that seemed to show the most benefits across the board,” Angelique Brellenthin, PhD, told this news organization.
The results were presented at the recent Epidemiology, Prevention/Lifestyle & Cardiometabolic Health meeting sponsored by the American Heart Association.
Even before the pandemic and bedtime “doom scrolling” took hold, research showed that a third of Americans regularly get less than 7 hours of sleep. The AHA recommends aerobic exercise to improve sleep and promote cardiovascular health, yet little is known on how it compares with other types of exercise in the general population, she said.
Dr. Brellenthin and coinvestigator Duck-chul Lee, PhD, both of Iowa State University in Ames, recruited 406 inactive adults, aged 35-70 years, who had obesity or overweight (mean body mass index, 31.2 kg/m2) and had elevated or stage 1 hypertension and randomly assigned them to no exercise or 60 minutes of supervised aerobic, resistance, or combination exercise three times per week for 12 months.
The aerobic exercise group could choose among treadmills, upright or recumbent bikes, and ellipticals, and the participants had their heart rate monitored to ensure they were continuously getting moderate- to vigorous-intensity exercise.
The resistance exercise group performed three sets of 8-16 repetitions at 50%-80% of their one-rep maximum on 12 resistance machines: a leg press, chest press, lat pulldown, leg curl, leg extension, biceps curl, triceps pushdown, shoulder press, abdominal crunch, lower back extension, torso rotation, and hip abduction.
The combination group did 30 minutes of aerobic exercise at moderate to vigorous intensity, and then two sets of 8-16 repetitions of resistance exercise on 9 machines instead of 12.
Exercise adherence over the year was 84%, 77%, and 85%, respectively.
Participants also completed the Pittsburgh Sleep Quality Index (PSQI) at baseline and 12 months. Among the 386 participants (53% women) with evaluable data, 35% had poor-quality sleep, as indicated by a global PSQI score of more than 5, and 42% regularly slept less than 7 hours per night.
In adjusted analyses, sleep duration at 12 months, on average, increased by 13 minutes in the resistance-exercise group (P = .009), decreased by 0.6 minute in the aerobic-exercise group, and increased by 2 minutes in the combined-exercise group and by 4 minutes in the control group.
Among participants who got less than 7 hours of sleep at baseline, however, sleep duration increased by 40 minutes (P < .0001), compared with increases of 23 minutes in the aerobic group, 17 minutes in the combined group, and 15 minutes in the control group.
Overall sleep efficiency, or the ratio of total sleep time to time in bed, improved in the resistance (P = .0005) and combined (P = .03) exercise groups, but not in the aerobic or control groups.
Sleep latency, or the time needed to fall asleep, decreased by 3 minutes in the resistance-exercise group, with no notable changes in the other groups.
Sleep quality and the number of sleep disturbances improved in all groups, including the control group. This could be due to simply being part of a health intervention, which included a month of lifestyle education classes, Dr. Brellenthin suggested.
It’s unclear why the aerobic-exercise group didn’t show greater gains, given the wealth of research showing it improves sleep, she said, but it had fewer poor sleepers at baseline than the resistance group (33% vs. 42%). “So it may be that people who were already getting good sleep didn’t have much room to improve.”
Among the poor-quality sleepers at baseline, resistance exercise significantly improved sleep quality (-2.4 vs. -1.0 points; P = .009) and duration (+36 vs. +3 minutes; P = .02), compared with the control group. It also improved sleep efficiency by 9.0%, compared with 0.9% in the control group (P = .002) and 8.0% for the combined-exercise group (P = .01).
“For a lot of people who know their sleep could be a bit better, this could be a place to start without resorting to medications, if they wanted to focus on a lifestyle intervention,” Dr. Brellenthin said.
It’s not fully understood how resistance exercise improves sleep, but it might contribute to better overall mental health and it might enhance the synthesis and release of certain hormones, such as testosterone and human growth hormone, which are associated with better sleep, Dr. Brellenthin said. Another hypothesis is that it causes direct microscopic damage to muscle tissue, forcing that tissue to adapt and grow over time. “So potentially that microscopic damage could provide that extra signal boost to the brain to replenish and repair, and get this person sleep.”
The study was limited by the use of self-reported sleep outcomes and a lack of detailed information on sleep medications, although 81% of participants reported taking no such medications.
The research was supported by a National Institutes of Health/National Heart, Lung, and Blood Institute grant to Dr. Lee. Dr. Brellenthin reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
CHICAGO – A randomized trial suggests resistance exercise promotes better sleep than other workouts among inactive adults, particularly those who are poor sleepers.
“We thought resistance exercise would be somewhere in the same neighborhood as aerobic exercise or that maybe combined exercise would be a little bit better but, no, it was consistently resistance exercise, on its own, that seemed to show the most benefits across the board,” Angelique Brellenthin, PhD, told this news organization.
The results were presented at the recent Epidemiology, Prevention/Lifestyle & Cardiometabolic Health meeting sponsored by the American Heart Association.
Even before the pandemic and bedtime “doom scrolling” took hold, research showed that a third of Americans regularly get less than 7 hours of sleep. The AHA recommends aerobic exercise to improve sleep and promote cardiovascular health, yet little is known on how it compares with other types of exercise in the general population, she said.
Dr. Brellenthin and coinvestigator Duck-chul Lee, PhD, both of Iowa State University in Ames, recruited 406 inactive adults, aged 35-70 years, who had obesity or overweight (mean body mass index, 31.2 kg/m2) and had elevated or stage 1 hypertension and randomly assigned them to no exercise or 60 minutes of supervised aerobic, resistance, or combination exercise three times per week for 12 months.
The aerobic exercise group could choose among treadmills, upright or recumbent bikes, and ellipticals, and the participants had their heart rate monitored to ensure they were continuously getting moderate- to vigorous-intensity exercise.
The resistance exercise group performed three sets of 8-16 repetitions at 50%-80% of their one-rep maximum on 12 resistance machines: a leg press, chest press, lat pulldown, leg curl, leg extension, biceps curl, triceps pushdown, shoulder press, abdominal crunch, lower back extension, torso rotation, and hip abduction.
The combination group did 30 minutes of aerobic exercise at moderate to vigorous intensity, and then two sets of 8-16 repetitions of resistance exercise on 9 machines instead of 12.
Exercise adherence over the year was 84%, 77%, and 85%, respectively.
Participants also completed the Pittsburgh Sleep Quality Index (PSQI) at baseline and 12 months. Among the 386 participants (53% women) with evaluable data, 35% had poor-quality sleep, as indicated by a global PSQI score of more than 5, and 42% regularly slept less than 7 hours per night.
In adjusted analyses, sleep duration at 12 months, on average, increased by 13 minutes in the resistance-exercise group (P = .009), decreased by 0.6 minute in the aerobic-exercise group, and increased by 2 minutes in the combined-exercise group and by 4 minutes in the control group.
Among participants who got less than 7 hours of sleep at baseline, however, sleep duration increased by 40 minutes (P < .0001), compared with increases of 23 minutes in the aerobic group, 17 minutes in the combined group, and 15 minutes in the control group.
Overall sleep efficiency, or the ratio of total sleep time to time in bed, improved in the resistance (P = .0005) and combined (P = .03) exercise groups, but not in the aerobic or control groups.
Sleep latency, or the time needed to fall asleep, decreased by 3 minutes in the resistance-exercise group, with no notable changes in the other groups.
Sleep quality and the number of sleep disturbances improved in all groups, including the control group. This could be due to simply being part of a health intervention, which included a month of lifestyle education classes, Dr. Brellenthin suggested.
It’s unclear why the aerobic-exercise group didn’t show greater gains, given the wealth of research showing it improves sleep, she said, but it had fewer poor sleepers at baseline than the resistance group (33% vs. 42%). “So it may be that people who were already getting good sleep didn’t have much room to improve.”
Among the poor-quality sleepers at baseline, resistance exercise significantly improved sleep quality (-2.4 vs. -1.0 points; P = .009) and duration (+36 vs. +3 minutes; P = .02), compared with the control group. It also improved sleep efficiency by 9.0%, compared with 0.9% in the control group (P = .002) and 8.0% for the combined-exercise group (P = .01).
“For a lot of people who know their sleep could be a bit better, this could be a place to start without resorting to medications, if they wanted to focus on a lifestyle intervention,” Dr. Brellenthin said.
It’s not fully understood how resistance exercise improves sleep, but it might contribute to better overall mental health and it might enhance the synthesis and release of certain hormones, such as testosterone and human growth hormone, which are associated with better sleep, Dr. Brellenthin said. Another hypothesis is that it causes direct microscopic damage to muscle tissue, forcing that tissue to adapt and grow over time. “So potentially that microscopic damage could provide that extra signal boost to the brain to replenish and repair, and get this person sleep.”
The study was limited by the use of self-reported sleep outcomes and a lack of detailed information on sleep medications, although 81% of participants reported taking no such medications.
The research was supported by a National Institutes of Health/National Heart, Lung, and Blood Institute grant to Dr. Lee. Dr. Brellenthin reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
REPORTING FROM EPI/LIFESTYLE 2022
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.
Boosting daily exercise after age 70 tied to lower CVD risk
Increasingly active patterns of physical activity were linked with reduced rates of overall mortality and cardiovascular disease (CVD), but early rather than later in late life, in a 20-year follow-up cohort study.
In this population of people older than 65 years, researchers found that physical activity overall was associated with lower rates of incident CVD, particularly among men, and the association was strongest in people 70 to 75 years of age, rather than in older age groups.
They also looked at “trajectories,” or changes in activity over time, and found that a stable-high trajectory of activity was associated with a significantly lower risk for cardiovascular outcomes in men than in those with a stable-low trajectory. For women, more physical activity was consistently associated with lower CVD outcomes, although not statistically significantly so, except for overall mortality, which did reach significance.
Notably, the greatest reduction in cardiovascular risk was reported in people who did more than 20 minutes of physical exercise each day, and it was more pronounced in those 70 years of age.
Physical activity was also associated with a lower incidence of heart failure and coronary heart disease in older people, again especially early on in late life, reported Claudio Barbiellini Amidei, MD, University of Padua, Italy, and colleagues.
The data suggest that physical activity is more effective in preventing CVD onset when implemented early rather than later in life, noted Dr. Amidei in an email.
“The findings of our study are suggestive of a protective effect of physical activity in late-life on cardiovascular health. WHO recommendations for adults and older adults are to practice at least 20 minutes of moderate to vigorous physical activity per day. I believe this is a realistic target, and policy makers should raise awareness on the importance of achieving this goal at all ages, including in late-life,” Dr. Amidei said.
The study was published online Feb. 14 in Heart.
Previous research has demonstrated that the most benefit of high physical activity, compared with low, begins at about 60 years of age, and that is because younger people are at much lower risk, noted Carl “Chip” Lavie MD, FACC, medical director of cardiac rehabilitation and prevention, Ochsner Clinical School–The University of Queensland School of Medicine, New Orleans, who was not involved in the study.
“At quite old ages, for example over age 80, resistance exercise or weight training and balance training may be even more important than aerobic training,” he added.
Activity ‘trajectories’
The benefits of physical activity on cardiovascular risk are well established, the researchers note. Less clear is the role that trajectories of activity over time play, although research to date suggests a reduction in risk with increasing activity from mid-life to early old age, they write.
For the current analysis, the researchers assessed 3,099 Italian participants. Mean age was about 75 years, and baseline data were collected from 1995 to 1997.
Follow-up visits were conducted after 4 years and again after 7 years. Using hospital medical records and mortality data, the researchers were able to collect surveillance data through 2018. Hospital records, surveys, and clinical assessments helped them identify incident and prevalent cardiovascular diseases, such as stroke, coronary heart disease, and heart failure.
Participants’ physical activity patterns were classified as stable-high, low-increasing, high-decreasing, and stable-low. Exposure was evaluated at 70, 75, 80, and 85 years of age.
“In our analyses, we focused on moderate to vigorous physical activity, and these include a broad range of exercises, such as walking very briskly, playing tennis, [and] jogging, but comprise also other activities, such as gardening or doing household chores,” said Dr. Amidei.
Patterns of stable-low physical activity were linked to a significantly greater risk for cardiovascular outcomes in men than patterns of stable-high physical activity (hazard ratio, 0.48; 95% confidence interval, 0.27-0.86; P for trend = .002).
No significant relation was found between physical activity and stroke, the researchers note.
“The benefits of physical activity seem to lessen above the age of 75 years and seem more important in men,” noted Dr. Lavie. “This may be partly due to the higher risk of CVD in men. Women typically lag 13 to 15 years behind men for CVD but start catching up in older years.”
Limitations of the study include lack of information regarding physical activity during mid-life, the limited number of stroke events, the relatively few participants older than 85 years, and potential recall bias, the researchers note.
Another limitation was that the physical activity data were based on patient surveys collected 3 years apart and did not involve the use of an accelerometer, the researchers add.
“Future observational studies are required to confirm our findings and pathophysiological studies are warranted to examine the underlying biological mechanisms. Physical activity is likely to be beneficial at any age, but to summarize our findings, we could say that when it comes to being physically active, the sooner the better,” concluded Dr. Amidei.
Dr. Amidei reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Increasingly active patterns of physical activity were linked with reduced rates of overall mortality and cardiovascular disease (CVD), but early rather than later in late life, in a 20-year follow-up cohort study.
In this population of people older than 65 years, researchers found that physical activity overall was associated with lower rates of incident CVD, particularly among men, and the association was strongest in people 70 to 75 years of age, rather than in older age groups.
They also looked at “trajectories,” or changes in activity over time, and found that a stable-high trajectory of activity was associated with a significantly lower risk for cardiovascular outcomes in men than in those with a stable-low trajectory. For women, more physical activity was consistently associated with lower CVD outcomes, although not statistically significantly so, except for overall mortality, which did reach significance.
Notably, the greatest reduction in cardiovascular risk was reported in people who did more than 20 minutes of physical exercise each day, and it was more pronounced in those 70 years of age.
Physical activity was also associated with a lower incidence of heart failure and coronary heart disease in older people, again especially early on in late life, reported Claudio Barbiellini Amidei, MD, University of Padua, Italy, and colleagues.
The data suggest that physical activity is more effective in preventing CVD onset when implemented early rather than later in life, noted Dr. Amidei in an email.
“The findings of our study are suggestive of a protective effect of physical activity in late-life on cardiovascular health. WHO recommendations for adults and older adults are to practice at least 20 minutes of moderate to vigorous physical activity per day. I believe this is a realistic target, and policy makers should raise awareness on the importance of achieving this goal at all ages, including in late-life,” Dr. Amidei said.
The study was published online Feb. 14 in Heart.
Previous research has demonstrated that the most benefit of high physical activity, compared with low, begins at about 60 years of age, and that is because younger people are at much lower risk, noted Carl “Chip” Lavie MD, FACC, medical director of cardiac rehabilitation and prevention, Ochsner Clinical School–The University of Queensland School of Medicine, New Orleans, who was not involved in the study.
“At quite old ages, for example over age 80, resistance exercise or weight training and balance training may be even more important than aerobic training,” he added.
Activity ‘trajectories’
The benefits of physical activity on cardiovascular risk are well established, the researchers note. Less clear is the role that trajectories of activity over time play, although research to date suggests a reduction in risk with increasing activity from mid-life to early old age, they write.
For the current analysis, the researchers assessed 3,099 Italian participants. Mean age was about 75 years, and baseline data were collected from 1995 to 1997.
Follow-up visits were conducted after 4 years and again after 7 years. Using hospital medical records and mortality data, the researchers were able to collect surveillance data through 2018. Hospital records, surveys, and clinical assessments helped them identify incident and prevalent cardiovascular diseases, such as stroke, coronary heart disease, and heart failure.
Participants’ physical activity patterns were classified as stable-high, low-increasing, high-decreasing, and stable-low. Exposure was evaluated at 70, 75, 80, and 85 years of age.
“In our analyses, we focused on moderate to vigorous physical activity, and these include a broad range of exercises, such as walking very briskly, playing tennis, [and] jogging, but comprise also other activities, such as gardening or doing household chores,” said Dr. Amidei.
Patterns of stable-low physical activity were linked to a significantly greater risk for cardiovascular outcomes in men than patterns of stable-high physical activity (hazard ratio, 0.48; 95% confidence interval, 0.27-0.86; P for trend = .002).
No significant relation was found between physical activity and stroke, the researchers note.
“The benefits of physical activity seem to lessen above the age of 75 years and seem more important in men,” noted Dr. Lavie. “This may be partly due to the higher risk of CVD in men. Women typically lag 13 to 15 years behind men for CVD but start catching up in older years.”
Limitations of the study include lack of information regarding physical activity during mid-life, the limited number of stroke events, the relatively few participants older than 85 years, and potential recall bias, the researchers note.
Another limitation was that the physical activity data were based on patient surveys collected 3 years apart and did not involve the use of an accelerometer, the researchers add.
“Future observational studies are required to confirm our findings and pathophysiological studies are warranted to examine the underlying biological mechanisms. Physical activity is likely to be beneficial at any age, but to summarize our findings, we could say that when it comes to being physically active, the sooner the better,” concluded Dr. Amidei.
Dr. Amidei reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Increasingly active patterns of physical activity were linked with reduced rates of overall mortality and cardiovascular disease (CVD), but early rather than later in late life, in a 20-year follow-up cohort study.
In this population of people older than 65 years, researchers found that physical activity overall was associated with lower rates of incident CVD, particularly among men, and the association was strongest in people 70 to 75 years of age, rather than in older age groups.
They also looked at “trajectories,” or changes in activity over time, and found that a stable-high trajectory of activity was associated with a significantly lower risk for cardiovascular outcomes in men than in those with a stable-low trajectory. For women, more physical activity was consistently associated with lower CVD outcomes, although not statistically significantly so, except for overall mortality, which did reach significance.
Notably, the greatest reduction in cardiovascular risk was reported in people who did more than 20 minutes of physical exercise each day, and it was more pronounced in those 70 years of age.
Physical activity was also associated with a lower incidence of heart failure and coronary heart disease in older people, again especially early on in late life, reported Claudio Barbiellini Amidei, MD, University of Padua, Italy, and colleagues.
The data suggest that physical activity is more effective in preventing CVD onset when implemented early rather than later in life, noted Dr. Amidei in an email.
“The findings of our study are suggestive of a protective effect of physical activity in late-life on cardiovascular health. WHO recommendations for adults and older adults are to practice at least 20 minutes of moderate to vigorous physical activity per day. I believe this is a realistic target, and policy makers should raise awareness on the importance of achieving this goal at all ages, including in late-life,” Dr. Amidei said.
The study was published online Feb. 14 in Heart.
Previous research has demonstrated that the most benefit of high physical activity, compared with low, begins at about 60 years of age, and that is because younger people are at much lower risk, noted Carl “Chip” Lavie MD, FACC, medical director of cardiac rehabilitation and prevention, Ochsner Clinical School–The University of Queensland School of Medicine, New Orleans, who was not involved in the study.
“At quite old ages, for example over age 80, resistance exercise or weight training and balance training may be even more important than aerobic training,” he added.
Activity ‘trajectories’
The benefits of physical activity on cardiovascular risk are well established, the researchers note. Less clear is the role that trajectories of activity over time play, although research to date suggests a reduction in risk with increasing activity from mid-life to early old age, they write.
For the current analysis, the researchers assessed 3,099 Italian participants. Mean age was about 75 years, and baseline data were collected from 1995 to 1997.
Follow-up visits were conducted after 4 years and again after 7 years. Using hospital medical records and mortality data, the researchers were able to collect surveillance data through 2018. Hospital records, surveys, and clinical assessments helped them identify incident and prevalent cardiovascular diseases, such as stroke, coronary heart disease, and heart failure.
Participants’ physical activity patterns were classified as stable-high, low-increasing, high-decreasing, and stable-low. Exposure was evaluated at 70, 75, 80, and 85 years of age.
“In our analyses, we focused on moderate to vigorous physical activity, and these include a broad range of exercises, such as walking very briskly, playing tennis, [and] jogging, but comprise also other activities, such as gardening or doing household chores,” said Dr. Amidei.
Patterns of stable-low physical activity were linked to a significantly greater risk for cardiovascular outcomes in men than patterns of stable-high physical activity (hazard ratio, 0.48; 95% confidence interval, 0.27-0.86; P for trend = .002).
No significant relation was found between physical activity and stroke, the researchers note.
“The benefits of physical activity seem to lessen above the age of 75 years and seem more important in men,” noted Dr. Lavie. “This may be partly due to the higher risk of CVD in men. Women typically lag 13 to 15 years behind men for CVD but start catching up in older years.”
Limitations of the study include lack of information regarding physical activity during mid-life, the limited number of stroke events, the relatively few participants older than 85 years, and potential recall bias, the researchers note.
Another limitation was that the physical activity data were based on patient surveys collected 3 years apart and did not involve the use of an accelerometer, the researchers add.
“Future observational studies are required to confirm our findings and pathophysiological studies are warranted to examine the underlying biological mechanisms. Physical activity is likely to be beneficial at any age, but to summarize our findings, we could say that when it comes to being physically active, the sooner the better,” concluded Dr. Amidei.
Dr. Amidei reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.