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‘Staggering’ CVD rise projected in U.S., especially in minorities
A new analysis projects steep increases by 2060 in the prevalence of cardiovascular (CV) risk factors and disease that will disproportionately affect non-White populations who have limited access to health care.
The study by Reza Mohebi, MD, Massachusetts General Hospital and Harvard Medical School, both in Boston, and colleagues was published in the Journal of the American College of Cardiology.
“Even though several assumptions underlie these projections, the importance of this work cannot be overestimated,” Andreas P. Kalogeropoulos, MD, MPH, PhD, and Javed Butler, MD, MPH, MBA, wrote in an accompanying editorial. “The absolute numbers are staggering.”
From 2025 to 2060, the number of people with any one of four CV risk factors – type 2 diabetes, hypertension, dyslipidemia, and obesity – is projected to increase by 15.4 million, to 34.7 million.
And the number of people with of any one of four CV disease types – ischemic heart disease, heart failure, MI, and stroke – is projected to increase by 3.2 million, to 6.8 million.
Although the model predicts that the prevalence of CV risk factors will gradually decrease among White Americans, the highest prevalence of CV risk factors will be among the White population because of its overall size.
Conversely, the projected prevalence of CV risk factors is expected to increase in Black, Hispanic, Asian, and other race/ethnicity populations.
In parallel, the prevalence of CV disease is projected to decrease in the White population and increase among all other race/ethnicities, particularly in the Black and Hispanic populations.
“Our results project a worrisome increase with a particularly ominous increase in risk factors and disease in our most vulnerable patients, including Blacks and Hispanics,” senior author James L. Januzzi Jr., MD, summarized in a video issued by the society.
“The steep rise in CV risk factors and disease reflects the generally higher prevalence in populations projected to increase in the United States, owing to immigration and growth, including Black or Hispanic individuals,” Dr. Januzzi, also from Massachusetts General and Harvard, said in an interview.
“The disproportionate size of the risk is expected in a sense, as minority populations are disproportionately disadvantaged with respect to their health care,” he said. “But whether it is expected or not, the increase in projected prevalence is, nonetheless, concerning and a call to action.”
This study identifies “areas of opportunity for change in the U.S. health care system,” he continued. “Business as usual will result in us encountering a huge number of individuals with CV risk factors and diseases.”
The results from the current analysis assume there will be no modification in health care policies or changes in access to care for at-risk populations, Dr. Mohebi and colleagues noted.
To “stem the rising tide of CV disease in at-risk individuals,” would require strategies such as “emphasis on education regarding CV risk factors, improving access to quality healthcare, and facilitating lower-cost access to effective therapies for treatment of CV risk factors,” according to the researchers.
“Such advances need to be applied in a more equitable way throughout the United States, however,” they cautioned.
Census plus NHANES data
The researchers used 2020 U.S. census data and projected growth and 2013-2018 U.S. National Health and Nutrition Survey data to estimate the number of people with CV risk factors and CV disease from 2025 to 2060.
The estimates are based on a growing population and a fixed frequency.
The projected changes in CV risk factors and disease over time were similar in men and women.
The researchers acknowledge that study limitations include the assumption that the prevalence patterns for CV risk factors and disease will be stable.
“To the extent the frequency of risk factors and disease are not likely to remain static, that assumption may reduce the accuracy of the projections,” Dr. Januzzi said. “However, we would point out that the goals of our analysis were to set general trends, and not to seek to project exact figures.”
Also, they did not take into account the effect of COVID-19. CV diseases were also based on self-report and CV risk factors could have been underestimated in minority populations that do not access health care.
Changing demographic landscape
It is “striking” that the numbers of non-White individuals with CV risk factors is projected to surpass the number of White individuals over time, and the number of non-White individuals with CV disease will be almost as many as White individuals by the year 2060, the editorialists noted.
“From a policy perspective, this means that unless appropriate, targeted action is taken, disparities in the burden of cardiovascular disease are only going to be exacerbated over time,” wrote Dr. Kalogeropoulos, from Stony Brook (N.Y.) University, and Dr. Butler, from Baylor College of Medicine, Dallas.
“On the positive side,” they continued, “the absolute increase in the percent prevalence of cardiovascular risk factors and conditions is projected to lie within a manageable range,” assuming that specific prevention policies are implemented.
“This is an opportunity for professional societies, including the cardiovascular care community, to re-evaluate priorities and strategies, for both training and practice, to best match the growing demands of a changing demographic landscape in the United States,” Dr. Kalogeropoulos and Dr. Butler concluded.
Dr. Mohebi is supported by the Barry Fellowship. Dr. Januzzi is supported by the Hutter Family Professorship; is a Trustee of the American College of Cardiology; is a board member of Imbria Pharmaceuticals; has received grant support from Abbott Diagnostics, Applied Therapeutics, Innolife, and Novartis; has received consulting income from Abbott Diagnostics, Boehringer Ingelheim, Janssen, Novartis, and Roche Diagnostics; and participates in clinical endpoint committees/data safety monitoring boards for AbbVie, Siemens, Takeda, and Vifor. Dr. Kalogeropoulos has received research funding from the National Heart, Lung, and Blood Institute; the American Heart Association; and the Centers for Disease Control and Prevention. Dr. Butler has been a consultant for numerous pharmaceutical companies.
A version of this article first appeared on Medscape.com.
A new analysis projects steep increases by 2060 in the prevalence of cardiovascular (CV) risk factors and disease that will disproportionately affect non-White populations who have limited access to health care.
The study by Reza Mohebi, MD, Massachusetts General Hospital and Harvard Medical School, both in Boston, and colleagues was published in the Journal of the American College of Cardiology.
“Even though several assumptions underlie these projections, the importance of this work cannot be overestimated,” Andreas P. Kalogeropoulos, MD, MPH, PhD, and Javed Butler, MD, MPH, MBA, wrote in an accompanying editorial. “The absolute numbers are staggering.”
From 2025 to 2060, the number of people with any one of four CV risk factors – type 2 diabetes, hypertension, dyslipidemia, and obesity – is projected to increase by 15.4 million, to 34.7 million.
And the number of people with of any one of four CV disease types – ischemic heart disease, heart failure, MI, and stroke – is projected to increase by 3.2 million, to 6.8 million.
Although the model predicts that the prevalence of CV risk factors will gradually decrease among White Americans, the highest prevalence of CV risk factors will be among the White population because of its overall size.
Conversely, the projected prevalence of CV risk factors is expected to increase in Black, Hispanic, Asian, and other race/ethnicity populations.
In parallel, the prevalence of CV disease is projected to decrease in the White population and increase among all other race/ethnicities, particularly in the Black and Hispanic populations.
“Our results project a worrisome increase with a particularly ominous increase in risk factors and disease in our most vulnerable patients, including Blacks and Hispanics,” senior author James L. Januzzi Jr., MD, summarized in a video issued by the society.
“The steep rise in CV risk factors and disease reflects the generally higher prevalence in populations projected to increase in the United States, owing to immigration and growth, including Black or Hispanic individuals,” Dr. Januzzi, also from Massachusetts General and Harvard, said in an interview.
“The disproportionate size of the risk is expected in a sense, as minority populations are disproportionately disadvantaged with respect to their health care,” he said. “But whether it is expected or not, the increase in projected prevalence is, nonetheless, concerning and a call to action.”
This study identifies “areas of opportunity for change in the U.S. health care system,” he continued. “Business as usual will result in us encountering a huge number of individuals with CV risk factors and diseases.”
The results from the current analysis assume there will be no modification in health care policies or changes in access to care for at-risk populations, Dr. Mohebi and colleagues noted.
To “stem the rising tide of CV disease in at-risk individuals,” would require strategies such as “emphasis on education regarding CV risk factors, improving access to quality healthcare, and facilitating lower-cost access to effective therapies for treatment of CV risk factors,” according to the researchers.
“Such advances need to be applied in a more equitable way throughout the United States, however,” they cautioned.
Census plus NHANES data
The researchers used 2020 U.S. census data and projected growth and 2013-2018 U.S. National Health and Nutrition Survey data to estimate the number of people with CV risk factors and CV disease from 2025 to 2060.
The estimates are based on a growing population and a fixed frequency.
The projected changes in CV risk factors and disease over time were similar in men and women.
The researchers acknowledge that study limitations include the assumption that the prevalence patterns for CV risk factors and disease will be stable.
“To the extent the frequency of risk factors and disease are not likely to remain static, that assumption may reduce the accuracy of the projections,” Dr. Januzzi said. “However, we would point out that the goals of our analysis were to set general trends, and not to seek to project exact figures.”
Also, they did not take into account the effect of COVID-19. CV diseases were also based on self-report and CV risk factors could have been underestimated in minority populations that do not access health care.
Changing demographic landscape
It is “striking” that the numbers of non-White individuals with CV risk factors is projected to surpass the number of White individuals over time, and the number of non-White individuals with CV disease will be almost as many as White individuals by the year 2060, the editorialists noted.
“From a policy perspective, this means that unless appropriate, targeted action is taken, disparities in the burden of cardiovascular disease are only going to be exacerbated over time,” wrote Dr. Kalogeropoulos, from Stony Brook (N.Y.) University, and Dr. Butler, from Baylor College of Medicine, Dallas.
“On the positive side,” they continued, “the absolute increase in the percent prevalence of cardiovascular risk factors and conditions is projected to lie within a manageable range,” assuming that specific prevention policies are implemented.
“This is an opportunity for professional societies, including the cardiovascular care community, to re-evaluate priorities and strategies, for both training and practice, to best match the growing demands of a changing demographic landscape in the United States,” Dr. Kalogeropoulos and Dr. Butler concluded.
Dr. Mohebi is supported by the Barry Fellowship. Dr. Januzzi is supported by the Hutter Family Professorship; is a Trustee of the American College of Cardiology; is a board member of Imbria Pharmaceuticals; has received grant support from Abbott Diagnostics, Applied Therapeutics, Innolife, and Novartis; has received consulting income from Abbott Diagnostics, Boehringer Ingelheim, Janssen, Novartis, and Roche Diagnostics; and participates in clinical endpoint committees/data safety monitoring boards for AbbVie, Siemens, Takeda, and Vifor. Dr. Kalogeropoulos has received research funding from the National Heart, Lung, and Blood Institute; the American Heart Association; and the Centers for Disease Control and Prevention. Dr. Butler has been a consultant for numerous pharmaceutical companies.
A version of this article first appeared on Medscape.com.
A new analysis projects steep increases by 2060 in the prevalence of cardiovascular (CV) risk factors and disease that will disproportionately affect non-White populations who have limited access to health care.
The study by Reza Mohebi, MD, Massachusetts General Hospital and Harvard Medical School, both in Boston, and colleagues was published in the Journal of the American College of Cardiology.
“Even though several assumptions underlie these projections, the importance of this work cannot be overestimated,” Andreas P. Kalogeropoulos, MD, MPH, PhD, and Javed Butler, MD, MPH, MBA, wrote in an accompanying editorial. “The absolute numbers are staggering.”
From 2025 to 2060, the number of people with any one of four CV risk factors – type 2 diabetes, hypertension, dyslipidemia, and obesity – is projected to increase by 15.4 million, to 34.7 million.
And the number of people with of any one of four CV disease types – ischemic heart disease, heart failure, MI, and stroke – is projected to increase by 3.2 million, to 6.8 million.
Although the model predicts that the prevalence of CV risk factors will gradually decrease among White Americans, the highest prevalence of CV risk factors will be among the White population because of its overall size.
Conversely, the projected prevalence of CV risk factors is expected to increase in Black, Hispanic, Asian, and other race/ethnicity populations.
In parallel, the prevalence of CV disease is projected to decrease in the White population and increase among all other race/ethnicities, particularly in the Black and Hispanic populations.
“Our results project a worrisome increase with a particularly ominous increase in risk factors and disease in our most vulnerable patients, including Blacks and Hispanics,” senior author James L. Januzzi Jr., MD, summarized in a video issued by the society.
“The steep rise in CV risk factors and disease reflects the generally higher prevalence in populations projected to increase in the United States, owing to immigration and growth, including Black or Hispanic individuals,” Dr. Januzzi, also from Massachusetts General and Harvard, said in an interview.
“The disproportionate size of the risk is expected in a sense, as minority populations are disproportionately disadvantaged with respect to their health care,” he said. “But whether it is expected or not, the increase in projected prevalence is, nonetheless, concerning and a call to action.”
This study identifies “areas of opportunity for change in the U.S. health care system,” he continued. “Business as usual will result in us encountering a huge number of individuals with CV risk factors and diseases.”
The results from the current analysis assume there will be no modification in health care policies or changes in access to care for at-risk populations, Dr. Mohebi and colleagues noted.
To “stem the rising tide of CV disease in at-risk individuals,” would require strategies such as “emphasis on education regarding CV risk factors, improving access to quality healthcare, and facilitating lower-cost access to effective therapies for treatment of CV risk factors,” according to the researchers.
“Such advances need to be applied in a more equitable way throughout the United States, however,” they cautioned.
Census plus NHANES data
The researchers used 2020 U.S. census data and projected growth and 2013-2018 U.S. National Health and Nutrition Survey data to estimate the number of people with CV risk factors and CV disease from 2025 to 2060.
The estimates are based on a growing population and a fixed frequency.
The projected changes in CV risk factors and disease over time were similar in men and women.
The researchers acknowledge that study limitations include the assumption that the prevalence patterns for CV risk factors and disease will be stable.
“To the extent the frequency of risk factors and disease are not likely to remain static, that assumption may reduce the accuracy of the projections,” Dr. Januzzi said. “However, we would point out that the goals of our analysis were to set general trends, and not to seek to project exact figures.”
Also, they did not take into account the effect of COVID-19. CV diseases were also based on self-report and CV risk factors could have been underestimated in minority populations that do not access health care.
Changing demographic landscape
It is “striking” that the numbers of non-White individuals with CV risk factors is projected to surpass the number of White individuals over time, and the number of non-White individuals with CV disease will be almost as many as White individuals by the year 2060, the editorialists noted.
“From a policy perspective, this means that unless appropriate, targeted action is taken, disparities in the burden of cardiovascular disease are only going to be exacerbated over time,” wrote Dr. Kalogeropoulos, from Stony Brook (N.Y.) University, and Dr. Butler, from Baylor College of Medicine, Dallas.
“On the positive side,” they continued, “the absolute increase in the percent prevalence of cardiovascular risk factors and conditions is projected to lie within a manageable range,” assuming that specific prevention policies are implemented.
“This is an opportunity for professional societies, including the cardiovascular care community, to re-evaluate priorities and strategies, for both training and practice, to best match the growing demands of a changing demographic landscape in the United States,” Dr. Kalogeropoulos and Dr. Butler concluded.
Dr. Mohebi is supported by the Barry Fellowship. Dr. Januzzi is supported by the Hutter Family Professorship; is a Trustee of the American College of Cardiology; is a board member of Imbria Pharmaceuticals; has received grant support from Abbott Diagnostics, Applied Therapeutics, Innolife, and Novartis; has received consulting income from Abbott Diagnostics, Boehringer Ingelheim, Janssen, Novartis, and Roche Diagnostics; and participates in clinical endpoint committees/data safety monitoring boards for AbbVie, Siemens, Takeda, and Vifor. Dr. Kalogeropoulos has received research funding from the National Heart, Lung, and Blood Institute; the American Heart Association; and the Centers for Disease Control and Prevention. Dr. Butler has been a consultant for numerous pharmaceutical companies.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF AMERICAN COLLEGE OF CARDIOLOGY
Topline results for novel drug in ATTR amyloidosis with cardiomyopathy
The RNA interference (RNAi) therapeutic patisiran (Onpattro, Alnylam Pharmaceuticals) led to statistically significant improvement in functional capacity and quality of life in adults with transthyretin-mediated (ATTR) amyloidosis with cardiomyopathy in the phase 3 APOLLO-B study, according to topline results released Aug. 3.
“We are thrilled that APOLLO-B successfully met all its major objectives, which we believe for the first time validates the hypothesis that TTR silencing by an RNAi therapeutic can be an effective approach for treating the cardiomyopathy of ATTR amyloidosis,” Pushkal Garg, MD, Alnylam chief medical officer, said in a news release.
The Food and Drug Administration approved patisiran in 2018 for polyneuropathy caused by hereditary ATTR in adults on the basis of results of the APOLLO phase 3 trial, as reported by this news organization.
APOLLO-B enrolled 360 adults with ATTR amyloidosis (hereditary or wild-type) with cardiomyopathy at 69 centers in 21 countries. Half were randomly allocated to 0.3 mg/kg of patisiran or placebo administered intravenously every 3 weeks for 12 months.
The study met the primary endpoint of a statistically significant improvement from baseline in the 6-minute walk test at 12 months compared with placebo (P = .0162), the company said.
The study also met the first secondary endpoint of a statistically significant improvement from baseline in quality of life compared with placebo, as measured by the Kansas City Cardiomyopathy Questionnaire (P = .0397).
The patisiran and placebo groups had similar frequencies of adverse events (91% and 94%, respectively) and serious adverse events (34% and 35%, respectively).
“ATTR amyloidosis with cardiomyopathy is an increasingly recognized cause of heart failure, affecting greater than 250,000 patients around the world. These patients have limited treatment options, and disease progression is common. As such, we are encouraged to see the potential of patisiran to improve the functional capacity and quality of life of patients living with this fatal, multisystem disease,” Dr. Garg said in the release.
Full results from APOLLO-B will be presented at a late-breaker session at the 18th International Symposium on Amyloidosis in September in Heidelberg, Germany.
Based on these results, the company plans to file a supplementary new drug application (sNDA) for patisiran for this indication with the FDA later this year, the release noted.
A version of this article first appeared on Medscape.com.
The RNA interference (RNAi) therapeutic patisiran (Onpattro, Alnylam Pharmaceuticals) led to statistically significant improvement in functional capacity and quality of life in adults with transthyretin-mediated (ATTR) amyloidosis with cardiomyopathy in the phase 3 APOLLO-B study, according to topline results released Aug. 3.
“We are thrilled that APOLLO-B successfully met all its major objectives, which we believe for the first time validates the hypothesis that TTR silencing by an RNAi therapeutic can be an effective approach for treating the cardiomyopathy of ATTR amyloidosis,” Pushkal Garg, MD, Alnylam chief medical officer, said in a news release.
The Food and Drug Administration approved patisiran in 2018 for polyneuropathy caused by hereditary ATTR in adults on the basis of results of the APOLLO phase 3 trial, as reported by this news organization.
APOLLO-B enrolled 360 adults with ATTR amyloidosis (hereditary or wild-type) with cardiomyopathy at 69 centers in 21 countries. Half were randomly allocated to 0.3 mg/kg of patisiran or placebo administered intravenously every 3 weeks for 12 months.
The study met the primary endpoint of a statistically significant improvement from baseline in the 6-minute walk test at 12 months compared with placebo (P = .0162), the company said.
The study also met the first secondary endpoint of a statistically significant improvement from baseline in quality of life compared with placebo, as measured by the Kansas City Cardiomyopathy Questionnaire (P = .0397).
The patisiran and placebo groups had similar frequencies of adverse events (91% and 94%, respectively) and serious adverse events (34% and 35%, respectively).
“ATTR amyloidosis with cardiomyopathy is an increasingly recognized cause of heart failure, affecting greater than 250,000 patients around the world. These patients have limited treatment options, and disease progression is common. As such, we are encouraged to see the potential of patisiran to improve the functional capacity and quality of life of patients living with this fatal, multisystem disease,” Dr. Garg said in the release.
Full results from APOLLO-B will be presented at a late-breaker session at the 18th International Symposium on Amyloidosis in September in Heidelberg, Germany.
Based on these results, the company plans to file a supplementary new drug application (sNDA) for patisiran for this indication with the FDA later this year, the release noted.
A version of this article first appeared on Medscape.com.
The RNA interference (RNAi) therapeutic patisiran (Onpattro, Alnylam Pharmaceuticals) led to statistically significant improvement in functional capacity and quality of life in adults with transthyretin-mediated (ATTR) amyloidosis with cardiomyopathy in the phase 3 APOLLO-B study, according to topline results released Aug. 3.
“We are thrilled that APOLLO-B successfully met all its major objectives, which we believe for the first time validates the hypothesis that TTR silencing by an RNAi therapeutic can be an effective approach for treating the cardiomyopathy of ATTR amyloidosis,” Pushkal Garg, MD, Alnylam chief medical officer, said in a news release.
The Food and Drug Administration approved patisiran in 2018 for polyneuropathy caused by hereditary ATTR in adults on the basis of results of the APOLLO phase 3 trial, as reported by this news organization.
APOLLO-B enrolled 360 adults with ATTR amyloidosis (hereditary or wild-type) with cardiomyopathy at 69 centers in 21 countries. Half were randomly allocated to 0.3 mg/kg of patisiran or placebo administered intravenously every 3 weeks for 12 months.
The study met the primary endpoint of a statistically significant improvement from baseline in the 6-minute walk test at 12 months compared with placebo (P = .0162), the company said.
The study also met the first secondary endpoint of a statistically significant improvement from baseline in quality of life compared with placebo, as measured by the Kansas City Cardiomyopathy Questionnaire (P = .0397).
The patisiran and placebo groups had similar frequencies of adverse events (91% and 94%, respectively) and serious adverse events (34% and 35%, respectively).
“ATTR amyloidosis with cardiomyopathy is an increasingly recognized cause of heart failure, affecting greater than 250,000 patients around the world. These patients have limited treatment options, and disease progression is common. As such, we are encouraged to see the potential of patisiran to improve the functional capacity and quality of life of patients living with this fatal, multisystem disease,” Dr. Garg said in the release.
Full results from APOLLO-B will be presented at a late-breaker session at the 18th International Symposium on Amyloidosis in September in Heidelberg, Germany.
Based on these results, the company plans to file a supplementary new drug application (sNDA) for patisiran for this indication with the FDA later this year, the release noted.
A version of this article first appeared on Medscape.com.
Why exercise doesn’t help people with long COVID
When Joel Fram woke up on the morning of March 12, 2020, he had a pretty good idea why he felt so lousy.
He lives in New York, where the first wave of the coronavirus was tearing through the city. “I instantly knew,” said the 55-year-old Broadway music director. It was COVID-19.
What started with a general sense of having been hit by a truck soon included a sore throat and such severe fatigue that he once fell asleep in the middle of sending a text to his sister. The final symptoms were chest tightness and trouble breathing.
And then he started to feel better. “By mid-April, my body was feeling essentially back to normal,” he said.
So he did what would have been smart after almost any other illness: He began working out. That didn’t last long. “It felt like someone pulled the carpet out from under me,” he remembered. “I couldn’t walk three blocks without getting breathless and fatigued.”
That was the first indication Mr. Fram had long COVID.
According to the National Center for Health Statistics, at least 7.5% of American adults – close to 20 million people – have symptoms of long COVID.
COVID-19 patients who had the most severe illness will struggle the most with exercise later, according to a review published in June from researchers at the University of California, San Francisco. But even people with mild symptoms can struggle to regain their previous levels of fitness.
“We have participants in our study who had relatively mild acute symptoms and went on to have really profound decreases in their ability to exercise,” said Matthew S. Durstenfeld, MD, a cardiologist at UCSF and principal author of the review.
Most people with long COVID will have lower-than-expected scores on tests of aerobic fitness, as shown by Yale researchers in a study published in August 2021.
“Some amount of that is due to deconditioning,” Dr. Durstenfeld said. “You’re not feeling well, so you’re not exercising to the same degree you might have been before you got infected.”
In a study published in April, people with long COVID told researchers at Britain’s University of Leeds they spent 93% less time in physical activity than they did before their infection.
But multiple studies have found deconditioning is not entirely – or even mostly – to blame.
A 2021 study found that 89% of participants with long COVID had postexertional malaise (PEM), which happens when a patient’s symptoms get worse after they do even minor physical or mental activities. According to the CDC, postexertional malaise can hit as long as 12-48 hours after the activity, and it can take people up to 2 weeks to fully recover.
Unfortunately, the advice patients get from their doctors sometimes makes the problem worse.
How long COVID defies simple solutions
Long COVID is a “dynamic disability” that requires health professionals to go off script when a patient’s symptoms don’t respond in a predictable way to treatment, said David Putrino, PhD, a neuroscientist, physical therapist, and director of rehabilitation innovation for the Mount Sinai Health System in New York.
“We’re not so good at dealing with somebody who, for all intents and purposes, can appear healthy and nondisabled on one day and be completely debilitated the next day,” he said.
Dr. Putrino said more than half of his clinic’s long-COVID patients told his team they had at least one of these persistent problems:
- Fatigue (82%).
- Brain fog (67%).
- Headache (60%).
- Sleep problems (59%).
- Dizziness (54%).
And 86% said exercise worsened their symptoms.
The symptoms are similar to what doctors see with illnesses such as lupus, Lyme disease, and chronic fatigue syndrome – something many experts compare long COVID to. Researchers and medical professionals still don’t know exactly how COVID-19 causes those symptoms. But there are some theories.
Potential causes of long-COVID symptoms
Dr. Putrino said it is possible the virus enters a patient’s cells and hijacks the mitochondria – a part of the cell that provides energy. It can linger there for weeks or months – something known as viral persistence.
“All of a sudden, the body’s getting less energy for itself, even though it’s producing the same amount, or even a little more,” he said. And there is a consequence to this extra stress on the cells. “Creating energy isn’t free. You’re producing more waste products, which puts your body in a state of oxidative stress,” Dr. Putrino said. Oxidative stress damages cells as molecules interact with oxygen in harmful ways.
“The other big mechanism is autonomic dysfunction,” Dr. Putrino said. It’s marked by breathing problems, heart palpitations, and other glitches in areas most healthy people never have to think about. About 70% of long-COVID patients at Mount Sinai’s clinic have some degree of autonomic dysfunction, he said.
For a person with autonomic dysfunction, something as basic as changing posture can trigger a storm of cytokines, a chemical messenger that tells the immune system where and how to respond to challenges like an injury or infection.
“Suddenly, you have this on-off switch,” Dr. Putrino said. “You go straight to ‘fight or flight,’ ” with a surge of adrenaline and a spiking heart rate, “then plunge back to ‘rest or digest.’ You go from fired up to so sleepy, you can’t keep your eyes open.”
A patient with viral persistence and one with autonomic dysfunction may have the same negative reaction to exercise, even though the triggers are completely different.
So how can doctors help long-COVID patients?
The first step, Dr. Putrino said, is to understand the difference between long COVID and a long recovery from COVID-19 infection.
Many of the patients in the latter group still have symptoms 4 weeks after their first infection. “At 4 weeks, yeah, they’re still feeling symptoms, but that’s not long COVID,” he said. “That’s just taking a while to get over a viral infection.”
Fitness advice is simple for those people: Take it easy at first, and gradually increase the amount and intensity of aerobic exercise and strength training.
But that advice would be disastrous for someone who meets Dr. Putrino’s stricter definition of long COVID: “Three to 4 months out from initial infection, they’re experiencing severe fatigue, exertional symptoms, cognitive symptoms, heart palpitations, shortness of breath,” he said.
“Our clinic is extraordinarily cautious with exercise” for those patients, he said.
In Dr. Putrino’s experience, about 20%-30% of patients will make significant progress after 12 weeks. “They’re feeling more or less like they felt pre-COVID,” he said.
The unluckiest 10%-20% won’t make any progress at all. Any type of therapy, even if it’s as simple as moving their legs from a flat position, worsens their symptoms.
The majority – 50%-60% – will have some improvement in their symptoms. But then progress will stop, for reasons researchers are still trying to figure out.
“My sense is that gradually increasing your exercise is still good advice for the vast majority of people,” UCSF’s Dr. Durstenfeld said.
Ideally, that exercise will be supervised by someone trained in cardiac, pulmonary, and/or autonomic rehabilitation – a specialized type of therapy aimed at resyncing the autonomic nervous system that governs breathing and other unconscious functions, he said. But those therapies are rarely covered by insurance, which means most long-COVID patients are on their own.
Dr. Durstenfeld said it’s important that patients keep trying and not give up. “With slow and steady progress, a lot of people can get profoundly better,” he said.
Mr. Fram, who’s worked with careful supervision, says he’s getting closer to something like his pre-COVID-19 life.
But he’s not there yet. Long COVID, he said, “affects my life every single day.”
A version of this article first appeared on WebMD.com.
When Joel Fram woke up on the morning of March 12, 2020, he had a pretty good idea why he felt so lousy.
He lives in New York, where the first wave of the coronavirus was tearing through the city. “I instantly knew,” said the 55-year-old Broadway music director. It was COVID-19.
What started with a general sense of having been hit by a truck soon included a sore throat and such severe fatigue that he once fell asleep in the middle of sending a text to his sister. The final symptoms were chest tightness and trouble breathing.
And then he started to feel better. “By mid-April, my body was feeling essentially back to normal,” he said.
So he did what would have been smart after almost any other illness: He began working out. That didn’t last long. “It felt like someone pulled the carpet out from under me,” he remembered. “I couldn’t walk three blocks without getting breathless and fatigued.”
That was the first indication Mr. Fram had long COVID.
According to the National Center for Health Statistics, at least 7.5% of American adults – close to 20 million people – have symptoms of long COVID.
COVID-19 patients who had the most severe illness will struggle the most with exercise later, according to a review published in June from researchers at the University of California, San Francisco. But even people with mild symptoms can struggle to regain their previous levels of fitness.
“We have participants in our study who had relatively mild acute symptoms and went on to have really profound decreases in their ability to exercise,” said Matthew S. Durstenfeld, MD, a cardiologist at UCSF and principal author of the review.
Most people with long COVID will have lower-than-expected scores on tests of aerobic fitness, as shown by Yale researchers in a study published in August 2021.
“Some amount of that is due to deconditioning,” Dr. Durstenfeld said. “You’re not feeling well, so you’re not exercising to the same degree you might have been before you got infected.”
In a study published in April, people with long COVID told researchers at Britain’s University of Leeds they spent 93% less time in physical activity than they did before their infection.
But multiple studies have found deconditioning is not entirely – or even mostly – to blame.
A 2021 study found that 89% of participants with long COVID had postexertional malaise (PEM), which happens when a patient’s symptoms get worse after they do even minor physical or mental activities. According to the CDC, postexertional malaise can hit as long as 12-48 hours after the activity, and it can take people up to 2 weeks to fully recover.
Unfortunately, the advice patients get from their doctors sometimes makes the problem worse.
How long COVID defies simple solutions
Long COVID is a “dynamic disability” that requires health professionals to go off script when a patient’s symptoms don’t respond in a predictable way to treatment, said David Putrino, PhD, a neuroscientist, physical therapist, and director of rehabilitation innovation for the Mount Sinai Health System in New York.
“We’re not so good at dealing with somebody who, for all intents and purposes, can appear healthy and nondisabled on one day and be completely debilitated the next day,” he said.
Dr. Putrino said more than half of his clinic’s long-COVID patients told his team they had at least one of these persistent problems:
- Fatigue (82%).
- Brain fog (67%).
- Headache (60%).
- Sleep problems (59%).
- Dizziness (54%).
And 86% said exercise worsened their symptoms.
The symptoms are similar to what doctors see with illnesses such as lupus, Lyme disease, and chronic fatigue syndrome – something many experts compare long COVID to. Researchers and medical professionals still don’t know exactly how COVID-19 causes those symptoms. But there are some theories.
Potential causes of long-COVID symptoms
Dr. Putrino said it is possible the virus enters a patient’s cells and hijacks the mitochondria – a part of the cell that provides energy. It can linger there for weeks or months – something known as viral persistence.
“All of a sudden, the body’s getting less energy for itself, even though it’s producing the same amount, or even a little more,” he said. And there is a consequence to this extra stress on the cells. “Creating energy isn’t free. You’re producing more waste products, which puts your body in a state of oxidative stress,” Dr. Putrino said. Oxidative stress damages cells as molecules interact with oxygen in harmful ways.
“The other big mechanism is autonomic dysfunction,” Dr. Putrino said. It’s marked by breathing problems, heart palpitations, and other glitches in areas most healthy people never have to think about. About 70% of long-COVID patients at Mount Sinai’s clinic have some degree of autonomic dysfunction, he said.
For a person with autonomic dysfunction, something as basic as changing posture can trigger a storm of cytokines, a chemical messenger that tells the immune system where and how to respond to challenges like an injury or infection.
“Suddenly, you have this on-off switch,” Dr. Putrino said. “You go straight to ‘fight or flight,’ ” with a surge of adrenaline and a spiking heart rate, “then plunge back to ‘rest or digest.’ You go from fired up to so sleepy, you can’t keep your eyes open.”
A patient with viral persistence and one with autonomic dysfunction may have the same negative reaction to exercise, even though the triggers are completely different.
So how can doctors help long-COVID patients?
The first step, Dr. Putrino said, is to understand the difference between long COVID and a long recovery from COVID-19 infection.
Many of the patients in the latter group still have symptoms 4 weeks after their first infection. “At 4 weeks, yeah, they’re still feeling symptoms, but that’s not long COVID,” he said. “That’s just taking a while to get over a viral infection.”
Fitness advice is simple for those people: Take it easy at first, and gradually increase the amount and intensity of aerobic exercise and strength training.
But that advice would be disastrous for someone who meets Dr. Putrino’s stricter definition of long COVID: “Three to 4 months out from initial infection, they’re experiencing severe fatigue, exertional symptoms, cognitive symptoms, heart palpitations, shortness of breath,” he said.
“Our clinic is extraordinarily cautious with exercise” for those patients, he said.
In Dr. Putrino’s experience, about 20%-30% of patients will make significant progress after 12 weeks. “They’re feeling more or less like they felt pre-COVID,” he said.
The unluckiest 10%-20% won’t make any progress at all. Any type of therapy, even if it’s as simple as moving their legs from a flat position, worsens their symptoms.
The majority – 50%-60% – will have some improvement in their symptoms. But then progress will stop, for reasons researchers are still trying to figure out.
“My sense is that gradually increasing your exercise is still good advice for the vast majority of people,” UCSF’s Dr. Durstenfeld said.
Ideally, that exercise will be supervised by someone trained in cardiac, pulmonary, and/or autonomic rehabilitation – a specialized type of therapy aimed at resyncing the autonomic nervous system that governs breathing and other unconscious functions, he said. But those therapies are rarely covered by insurance, which means most long-COVID patients are on their own.
Dr. Durstenfeld said it’s important that patients keep trying and not give up. “With slow and steady progress, a lot of people can get profoundly better,” he said.
Mr. Fram, who’s worked with careful supervision, says he’s getting closer to something like his pre-COVID-19 life.
But he’s not there yet. Long COVID, he said, “affects my life every single day.”
A version of this article first appeared on WebMD.com.
When Joel Fram woke up on the morning of March 12, 2020, he had a pretty good idea why he felt so lousy.
He lives in New York, where the first wave of the coronavirus was tearing through the city. “I instantly knew,” said the 55-year-old Broadway music director. It was COVID-19.
What started with a general sense of having been hit by a truck soon included a sore throat and such severe fatigue that he once fell asleep in the middle of sending a text to his sister. The final symptoms were chest tightness and trouble breathing.
And then he started to feel better. “By mid-April, my body was feeling essentially back to normal,” he said.
So he did what would have been smart after almost any other illness: He began working out. That didn’t last long. “It felt like someone pulled the carpet out from under me,” he remembered. “I couldn’t walk three blocks without getting breathless and fatigued.”
That was the first indication Mr. Fram had long COVID.
According to the National Center for Health Statistics, at least 7.5% of American adults – close to 20 million people – have symptoms of long COVID.
COVID-19 patients who had the most severe illness will struggle the most with exercise later, according to a review published in June from researchers at the University of California, San Francisco. But even people with mild symptoms can struggle to regain their previous levels of fitness.
“We have participants in our study who had relatively mild acute symptoms and went on to have really profound decreases in their ability to exercise,” said Matthew S. Durstenfeld, MD, a cardiologist at UCSF and principal author of the review.
Most people with long COVID will have lower-than-expected scores on tests of aerobic fitness, as shown by Yale researchers in a study published in August 2021.
“Some amount of that is due to deconditioning,” Dr. Durstenfeld said. “You’re not feeling well, so you’re not exercising to the same degree you might have been before you got infected.”
In a study published in April, people with long COVID told researchers at Britain’s University of Leeds they spent 93% less time in physical activity than they did before their infection.
But multiple studies have found deconditioning is not entirely – or even mostly – to blame.
A 2021 study found that 89% of participants with long COVID had postexertional malaise (PEM), which happens when a patient’s symptoms get worse after they do even minor physical or mental activities. According to the CDC, postexertional malaise can hit as long as 12-48 hours after the activity, and it can take people up to 2 weeks to fully recover.
Unfortunately, the advice patients get from their doctors sometimes makes the problem worse.
How long COVID defies simple solutions
Long COVID is a “dynamic disability” that requires health professionals to go off script when a patient’s symptoms don’t respond in a predictable way to treatment, said David Putrino, PhD, a neuroscientist, physical therapist, and director of rehabilitation innovation for the Mount Sinai Health System in New York.
“We’re not so good at dealing with somebody who, for all intents and purposes, can appear healthy and nondisabled on one day and be completely debilitated the next day,” he said.
Dr. Putrino said more than half of his clinic’s long-COVID patients told his team they had at least one of these persistent problems:
- Fatigue (82%).
- Brain fog (67%).
- Headache (60%).
- Sleep problems (59%).
- Dizziness (54%).
And 86% said exercise worsened their symptoms.
The symptoms are similar to what doctors see with illnesses such as lupus, Lyme disease, and chronic fatigue syndrome – something many experts compare long COVID to. Researchers and medical professionals still don’t know exactly how COVID-19 causes those symptoms. But there are some theories.
Potential causes of long-COVID symptoms
Dr. Putrino said it is possible the virus enters a patient’s cells and hijacks the mitochondria – a part of the cell that provides energy. It can linger there for weeks or months – something known as viral persistence.
“All of a sudden, the body’s getting less energy for itself, even though it’s producing the same amount, or even a little more,” he said. And there is a consequence to this extra stress on the cells. “Creating energy isn’t free. You’re producing more waste products, which puts your body in a state of oxidative stress,” Dr. Putrino said. Oxidative stress damages cells as molecules interact with oxygen in harmful ways.
“The other big mechanism is autonomic dysfunction,” Dr. Putrino said. It’s marked by breathing problems, heart palpitations, and other glitches in areas most healthy people never have to think about. About 70% of long-COVID patients at Mount Sinai’s clinic have some degree of autonomic dysfunction, he said.
For a person with autonomic dysfunction, something as basic as changing posture can trigger a storm of cytokines, a chemical messenger that tells the immune system where and how to respond to challenges like an injury or infection.
“Suddenly, you have this on-off switch,” Dr. Putrino said. “You go straight to ‘fight or flight,’ ” with a surge of adrenaline and a spiking heart rate, “then plunge back to ‘rest or digest.’ You go from fired up to so sleepy, you can’t keep your eyes open.”
A patient with viral persistence and one with autonomic dysfunction may have the same negative reaction to exercise, even though the triggers are completely different.
So how can doctors help long-COVID patients?
The first step, Dr. Putrino said, is to understand the difference between long COVID and a long recovery from COVID-19 infection.
Many of the patients in the latter group still have symptoms 4 weeks after their first infection. “At 4 weeks, yeah, they’re still feeling symptoms, but that’s not long COVID,” he said. “That’s just taking a while to get over a viral infection.”
Fitness advice is simple for those people: Take it easy at first, and gradually increase the amount and intensity of aerobic exercise and strength training.
But that advice would be disastrous for someone who meets Dr. Putrino’s stricter definition of long COVID: “Three to 4 months out from initial infection, they’re experiencing severe fatigue, exertional symptoms, cognitive symptoms, heart palpitations, shortness of breath,” he said.
“Our clinic is extraordinarily cautious with exercise” for those patients, he said.
In Dr. Putrino’s experience, about 20%-30% of patients will make significant progress after 12 weeks. “They’re feeling more or less like they felt pre-COVID,” he said.
The unluckiest 10%-20% won’t make any progress at all. Any type of therapy, even if it’s as simple as moving their legs from a flat position, worsens their symptoms.
The majority – 50%-60% – will have some improvement in their symptoms. But then progress will stop, for reasons researchers are still trying to figure out.
“My sense is that gradually increasing your exercise is still good advice for the vast majority of people,” UCSF’s Dr. Durstenfeld said.
Ideally, that exercise will be supervised by someone trained in cardiac, pulmonary, and/or autonomic rehabilitation – a specialized type of therapy aimed at resyncing the autonomic nervous system that governs breathing and other unconscious functions, he said. But those therapies are rarely covered by insurance, which means most long-COVID patients are on their own.
Dr. Durstenfeld said it’s important that patients keep trying and not give up. “With slow and steady progress, a lot of people can get profoundly better,” he said.
Mr. Fram, who’s worked with careful supervision, says he’s getting closer to something like his pre-COVID-19 life.
But he’s not there yet. Long COVID, he said, “affects my life every single day.”
A version of this article first appeared on WebMD.com.
The gut microbes have spoken: All fiber is good fiber
Finding a fiber of good moral fiber
If you’ve ever wandered into the supplement aisle at your local grocery store, you’ve probably noticed an overabundance of fiber supplements that claim to do this for you and benefit that. Since there’s no Food and Drug Administration regulation on fiber supplements, manufacturers are free to (and do) make whatever wild claims they like. And much like choosing which of 500 shows to watch on Netflix, when you’re spoiled for choice, it can be difficult to pick.
Enter a team of molecular geneticists and microbiologists from Duke University. They can’t tell you what show to watch next, but they can tell you which fiber to choose, thanks to their new study. And the answer? Yes.
Well that’s not very helpful, but let us explain. For their study, a group of 28 received three of the main fiber supplements (inulin, dextrin, and galactooligosaccharides) for a week each, followed by a week off of fibers for their gut to return to baseline until they’d received all three. Those who consumed the least fiber at baseline saw the greatest benefit from fiber supplementation, with no appreciable difference between the three types. It was the same story for study participants who already consumed enough fiber; because their guts already hosted a more-optimal microbiome, the type of supplement didn’t matter. The benefits were the same across the board.
In an additional study, the Duke researchers found that gut microbiomes reacted to new fiber within a day, being primed to consume fiber on the first dose and digesting it more quickly on the second fiber dose.
The results, the researchers pointed out, make sense, since the average American only consumes 20%-40% of their daily recommended supply of fiber. Our digestive systems aren’t picky; they just want more, so go out there and choose whatever fiber you’d like. Do that, and then feel free to eat as many double bacon cheeseburgers as you’d like. That is the pinnacle of diet right there. Dietitians literally could not complain about it.
Jarlsberg vs. Camembert: This time it’s skeletal
Fiber is fabulous, of course, but the road to dietary health and wellness fulfillment takes us to many other, equally wondrous places. Hey, look! This next exit is covered with cheese.
All the cheeses are here, from Abbaye de Belloc to Zwitser, and there, right between the jalapeno cheddar and the Jermi tortes you’ll find Jarlsberg, a mild, semisoft, nutty-flavored cheese that comes from Jarlsberg in eastern Norway. A recent study also suggests that Jarlsberg may help to prevent osteopenia and osteoporosis.
A group of Norwegian investigators gathered together 66 healthy women and gave them a daily portion of either Jarlsberg or Camembert for 6 weeks, at which point the Camembert group was switched to Jarlsberg for another 6 weeks.
The research team choose Camembert because of its similarity to Jarlsberg in fat and protein content. Jarlsberg, however, also is rich in vitamin K2, which is important for bone health, and a substance known as DHNA, which “might combat bone thinning and increase bone tissue formation,” they said in a Eurekalert release.
After the first 6 weeks, blood levels of osteocalcin; vitamin K2; and PINP, a peptide involved in bone turnover, were significantly higher in the Jarlsberg group only. All those measures rose significantly after the switch from Camembert to Jarlsberg, while levels of total and LDL cholesterol “fell significantly in the Camembert group after they switched to Jarlsberg,” the team added.
But wait! There’s more! HbA1c fell significantly among those initially eating the Jarlsberg but rose sharply in those eating Camembert. Do you see where this is going? After the Camembert group made the switch to Jarlsberg, their HbA1c levels fell significantly as well.
So it’s not just a cheese thing: The effects are specific to Jarlsberg. Can you guess what we’re having for lunch? Double bacon and fiber Jarlsbergers. Mmm, Jarlsburgers.
Luck be a lady: The mother of twins
It’s widely believed that women who have twins must be more fertile, giving birth to more than one child at a time. Some studies have supported the idea, but more recent work is refuting that claim. In actuality, it might just be more statistics and luck than fertility after all.
Those earlier studies supporting fertility didn’t specify whether the chances of twin births were based on the ability to produce more than one egg at a time or on the number of births that women had overall. Looking at 100,000 preindustrial European births, before contraception was available, researchers from Norway, Germany, France, and the United Kingdom found that the number of total births, twins included, makes all the difference.
“When a woman gives birth several times, the chances increase that at least one of these births will be a twin birth,” investigator Gine Roll Skjærvø of the Norwegian University of Science and Technology said in a written statement.
Since twins occur in 1%-3% of all births, the more births that a woman has, the better her chances of giving birth to twins. The researchers compared it to playing the lottery. You buy enough tickets, eventually your numbers are going to come up. Despite that, however, they found that women who give birth to twins give birth less often than those who don’t have twins. Which raises the idea of sheer luck.
The researchers said that there’s still a lot to uncover in twin births, noting that “uncritically comparing groups of women with and without twins can trick us into believing the opposite of what is really true. These groupings may either hide the effects of twinning and fertility genes where they exist, or vice versa, create the illusion of these if they do not exist.”
For now, this new research claims that it’s basically a lottery. And women who give birth to twins hit the jackpot.
Those with low wages may be earning future memory loss
Not only are low wages detrimental to our souls, hopes, and dreams, but a new study shows that low wages also are linked to quicker memory decline later in life. Sustained low wages not only cause stress and food insecurity in the lives of many, but they also can cause diseases such as depression, obesity, and high blood pressure, which are risk factors for cognitive aging.
The study was conducted using records from the Health and Retirement Study for the years 1992-2016 and focused on 2,879 adults born between 1936 and 1941. The participants were divided into three groups: those who never earned low wages, those who sometimes did, and those who always did.
The investigators found that workers who earned sustained low wages – defined as an hourly wage lower than two-thirds of the federal median wage for the corresponding year – “experienced significantly faster memory decline in older age” than did those who never earned low wages.
There are signs of inflation everywhere we look these days, but many people are not earning higher wages to compensate for the extra expenses. “Increasing the federal minimum wage, for example to $15 per hour, remains a gridlock issue in Congress,” lead author Katrina Kezios of the Columbia University Mailman School of Public Health, said in a statement released by the university.
If only salaries would rise instead of prices for once.
Finding a fiber of good moral fiber
If you’ve ever wandered into the supplement aisle at your local grocery store, you’ve probably noticed an overabundance of fiber supplements that claim to do this for you and benefit that. Since there’s no Food and Drug Administration regulation on fiber supplements, manufacturers are free to (and do) make whatever wild claims they like. And much like choosing which of 500 shows to watch on Netflix, when you’re spoiled for choice, it can be difficult to pick.
Enter a team of molecular geneticists and microbiologists from Duke University. They can’t tell you what show to watch next, but they can tell you which fiber to choose, thanks to their new study. And the answer? Yes.
Well that’s not very helpful, but let us explain. For their study, a group of 28 received three of the main fiber supplements (inulin, dextrin, and galactooligosaccharides) for a week each, followed by a week off of fibers for their gut to return to baseline until they’d received all three. Those who consumed the least fiber at baseline saw the greatest benefit from fiber supplementation, with no appreciable difference between the three types. It was the same story for study participants who already consumed enough fiber; because their guts already hosted a more-optimal microbiome, the type of supplement didn’t matter. The benefits were the same across the board.
In an additional study, the Duke researchers found that gut microbiomes reacted to new fiber within a day, being primed to consume fiber on the first dose and digesting it more quickly on the second fiber dose.
The results, the researchers pointed out, make sense, since the average American only consumes 20%-40% of their daily recommended supply of fiber. Our digestive systems aren’t picky; they just want more, so go out there and choose whatever fiber you’d like. Do that, and then feel free to eat as many double bacon cheeseburgers as you’d like. That is the pinnacle of diet right there. Dietitians literally could not complain about it.
Jarlsberg vs. Camembert: This time it’s skeletal
Fiber is fabulous, of course, but the road to dietary health and wellness fulfillment takes us to many other, equally wondrous places. Hey, look! This next exit is covered with cheese.
All the cheeses are here, from Abbaye de Belloc to Zwitser, and there, right between the jalapeno cheddar and the Jermi tortes you’ll find Jarlsberg, a mild, semisoft, nutty-flavored cheese that comes from Jarlsberg in eastern Norway. A recent study also suggests that Jarlsberg may help to prevent osteopenia and osteoporosis.
A group of Norwegian investigators gathered together 66 healthy women and gave them a daily portion of either Jarlsberg or Camembert for 6 weeks, at which point the Camembert group was switched to Jarlsberg for another 6 weeks.
The research team choose Camembert because of its similarity to Jarlsberg in fat and protein content. Jarlsberg, however, also is rich in vitamin K2, which is important for bone health, and a substance known as DHNA, which “might combat bone thinning and increase bone tissue formation,” they said in a Eurekalert release.
After the first 6 weeks, blood levels of osteocalcin; vitamin K2; and PINP, a peptide involved in bone turnover, were significantly higher in the Jarlsberg group only. All those measures rose significantly after the switch from Camembert to Jarlsberg, while levels of total and LDL cholesterol “fell significantly in the Camembert group after they switched to Jarlsberg,” the team added.
But wait! There’s more! HbA1c fell significantly among those initially eating the Jarlsberg but rose sharply in those eating Camembert. Do you see where this is going? After the Camembert group made the switch to Jarlsberg, their HbA1c levels fell significantly as well.
So it’s not just a cheese thing: The effects are specific to Jarlsberg. Can you guess what we’re having for lunch? Double bacon and fiber Jarlsbergers. Mmm, Jarlsburgers.
Luck be a lady: The mother of twins
It’s widely believed that women who have twins must be more fertile, giving birth to more than one child at a time. Some studies have supported the idea, but more recent work is refuting that claim. In actuality, it might just be more statistics and luck than fertility after all.
Those earlier studies supporting fertility didn’t specify whether the chances of twin births were based on the ability to produce more than one egg at a time or on the number of births that women had overall. Looking at 100,000 preindustrial European births, before contraception was available, researchers from Norway, Germany, France, and the United Kingdom found that the number of total births, twins included, makes all the difference.
“When a woman gives birth several times, the chances increase that at least one of these births will be a twin birth,” investigator Gine Roll Skjærvø of the Norwegian University of Science and Technology said in a written statement.
Since twins occur in 1%-3% of all births, the more births that a woman has, the better her chances of giving birth to twins. The researchers compared it to playing the lottery. You buy enough tickets, eventually your numbers are going to come up. Despite that, however, they found that women who give birth to twins give birth less often than those who don’t have twins. Which raises the idea of sheer luck.
The researchers said that there’s still a lot to uncover in twin births, noting that “uncritically comparing groups of women with and without twins can trick us into believing the opposite of what is really true. These groupings may either hide the effects of twinning and fertility genes where they exist, or vice versa, create the illusion of these if they do not exist.”
For now, this new research claims that it’s basically a lottery. And women who give birth to twins hit the jackpot.
Those with low wages may be earning future memory loss
Not only are low wages detrimental to our souls, hopes, and dreams, but a new study shows that low wages also are linked to quicker memory decline later in life. Sustained low wages not only cause stress and food insecurity in the lives of many, but they also can cause diseases such as depression, obesity, and high blood pressure, which are risk factors for cognitive aging.
The study was conducted using records from the Health and Retirement Study for the years 1992-2016 and focused on 2,879 adults born between 1936 and 1941. The participants were divided into three groups: those who never earned low wages, those who sometimes did, and those who always did.
The investigators found that workers who earned sustained low wages – defined as an hourly wage lower than two-thirds of the federal median wage for the corresponding year – “experienced significantly faster memory decline in older age” than did those who never earned low wages.
There are signs of inflation everywhere we look these days, but many people are not earning higher wages to compensate for the extra expenses. “Increasing the federal minimum wage, for example to $15 per hour, remains a gridlock issue in Congress,” lead author Katrina Kezios of the Columbia University Mailman School of Public Health, said in a statement released by the university.
If only salaries would rise instead of prices for once.
Finding a fiber of good moral fiber
If you’ve ever wandered into the supplement aisle at your local grocery store, you’ve probably noticed an overabundance of fiber supplements that claim to do this for you and benefit that. Since there’s no Food and Drug Administration regulation on fiber supplements, manufacturers are free to (and do) make whatever wild claims they like. And much like choosing which of 500 shows to watch on Netflix, when you’re spoiled for choice, it can be difficult to pick.
Enter a team of molecular geneticists and microbiologists from Duke University. They can’t tell you what show to watch next, but they can tell you which fiber to choose, thanks to their new study. And the answer? Yes.
Well that’s not very helpful, but let us explain. For their study, a group of 28 received three of the main fiber supplements (inulin, dextrin, and galactooligosaccharides) for a week each, followed by a week off of fibers for their gut to return to baseline until they’d received all three. Those who consumed the least fiber at baseline saw the greatest benefit from fiber supplementation, with no appreciable difference between the three types. It was the same story for study participants who already consumed enough fiber; because their guts already hosted a more-optimal microbiome, the type of supplement didn’t matter. The benefits were the same across the board.
In an additional study, the Duke researchers found that gut microbiomes reacted to new fiber within a day, being primed to consume fiber on the first dose and digesting it more quickly on the second fiber dose.
The results, the researchers pointed out, make sense, since the average American only consumes 20%-40% of their daily recommended supply of fiber. Our digestive systems aren’t picky; they just want more, so go out there and choose whatever fiber you’d like. Do that, and then feel free to eat as many double bacon cheeseburgers as you’d like. That is the pinnacle of diet right there. Dietitians literally could not complain about it.
Jarlsberg vs. Camembert: This time it’s skeletal
Fiber is fabulous, of course, but the road to dietary health and wellness fulfillment takes us to many other, equally wondrous places. Hey, look! This next exit is covered with cheese.
All the cheeses are here, from Abbaye de Belloc to Zwitser, and there, right between the jalapeno cheddar and the Jermi tortes you’ll find Jarlsberg, a mild, semisoft, nutty-flavored cheese that comes from Jarlsberg in eastern Norway. A recent study also suggests that Jarlsberg may help to prevent osteopenia and osteoporosis.
A group of Norwegian investigators gathered together 66 healthy women and gave them a daily portion of either Jarlsberg or Camembert for 6 weeks, at which point the Camembert group was switched to Jarlsberg for another 6 weeks.
The research team choose Camembert because of its similarity to Jarlsberg in fat and protein content. Jarlsberg, however, also is rich in vitamin K2, which is important for bone health, and a substance known as DHNA, which “might combat bone thinning and increase bone tissue formation,” they said in a Eurekalert release.
After the first 6 weeks, blood levels of osteocalcin; vitamin K2; and PINP, a peptide involved in bone turnover, were significantly higher in the Jarlsberg group only. All those measures rose significantly after the switch from Camembert to Jarlsberg, while levels of total and LDL cholesterol “fell significantly in the Camembert group after they switched to Jarlsberg,” the team added.
But wait! There’s more! HbA1c fell significantly among those initially eating the Jarlsberg but rose sharply in those eating Camembert. Do you see where this is going? After the Camembert group made the switch to Jarlsberg, their HbA1c levels fell significantly as well.
So it’s not just a cheese thing: The effects are specific to Jarlsberg. Can you guess what we’re having for lunch? Double bacon and fiber Jarlsbergers. Mmm, Jarlsburgers.
Luck be a lady: The mother of twins
It’s widely believed that women who have twins must be more fertile, giving birth to more than one child at a time. Some studies have supported the idea, but more recent work is refuting that claim. In actuality, it might just be more statistics and luck than fertility after all.
Those earlier studies supporting fertility didn’t specify whether the chances of twin births were based on the ability to produce more than one egg at a time or on the number of births that women had overall. Looking at 100,000 preindustrial European births, before contraception was available, researchers from Norway, Germany, France, and the United Kingdom found that the number of total births, twins included, makes all the difference.
“When a woman gives birth several times, the chances increase that at least one of these births will be a twin birth,” investigator Gine Roll Skjærvø of the Norwegian University of Science and Technology said in a written statement.
Since twins occur in 1%-3% of all births, the more births that a woman has, the better her chances of giving birth to twins. The researchers compared it to playing the lottery. You buy enough tickets, eventually your numbers are going to come up. Despite that, however, they found that women who give birth to twins give birth less often than those who don’t have twins. Which raises the idea of sheer luck.
The researchers said that there’s still a lot to uncover in twin births, noting that “uncritically comparing groups of women with and without twins can trick us into believing the opposite of what is really true. These groupings may either hide the effects of twinning and fertility genes where they exist, or vice versa, create the illusion of these if they do not exist.”
For now, this new research claims that it’s basically a lottery. And women who give birth to twins hit the jackpot.
Those with low wages may be earning future memory loss
Not only are low wages detrimental to our souls, hopes, and dreams, but a new study shows that low wages also are linked to quicker memory decline later in life. Sustained low wages not only cause stress and food insecurity in the lives of many, but they also can cause diseases such as depression, obesity, and high blood pressure, which are risk factors for cognitive aging.
The study was conducted using records from the Health and Retirement Study for the years 1992-2016 and focused on 2,879 adults born between 1936 and 1941. The participants were divided into three groups: those who never earned low wages, those who sometimes did, and those who always did.
The investigators found that workers who earned sustained low wages – defined as an hourly wage lower than two-thirds of the federal median wage for the corresponding year – “experienced significantly faster memory decline in older age” than did those who never earned low wages.
There are signs of inflation everywhere we look these days, but many people are not earning higher wages to compensate for the extra expenses. “Increasing the federal minimum wage, for example to $15 per hour, remains a gridlock issue in Congress,” lead author Katrina Kezios of the Columbia University Mailman School of Public Health, said in a statement released by the university.
If only salaries would rise instead of prices for once.
Haven’t had COVID yet? Wanna bet?
We all have friends or relatives who, somehow, have managed to avoid catching COVID-19, which has infected more than 91.5 million Americans. You may even be one of the lucky ones yourself.
But health experts are saying: Not so fast. because they didn’t have symptoms or had mild cases they mistook for a cold or allergies.
The upshot: These silent COVID-19 cases reflect a hidden side of the pandemic that may be helping to drive new surges and viral variants.
Still, infectious disease experts say there is little doubt that some people have indeed managed to avoid COVID-19 infection altogether, and they are trying to understand why.
Several recent studies have suggested certain genetic and immune system traits may better protect this group of people against the coronavirus, making them less likely than others to be infected or seriously sickened. Researchers around the world are now studying these seemingly super-immune people for clues to what makes them so special, with an eye toward better vaccines, treatments, and prevention strategies.
Infectious disease specialists say both types of cases – those unknowingly infected by COVID-19 and people who’ve avoided the virus altogether – matter greatly to public health, more than 2 years into the pandemic.
“It’s definitely true that some people have had COVID and don’t realize it,” says Stephen Kissler, PhD, an infectious disease researcher with the Harvard T.H. Chan School of Public Health, Boston. “It is potentially good news if there’s more immunity in the population than we realize.”
But he says that being able to identify genetic and other factors that may offer some people protection against COVID-19 is an “exciting prospect” that could help find out who’s most at risk and improve efforts to get the pandemic under control.
Some studies have found a person’s genetic profile, past exposure to other COVID-like viruses, allergies, and even drugs they take for other conditions may all provide some defense – even for people who have not been vaccinated, don’t use masks, or don’t practice social distancing.
A person’s medical history and genetics may help decide their risk from new diseases, meaning “we may be able to help identify people who are at especially high risk from infection,” Dr. Kissler says. “That knowledge could help those people better shield themselves from infection and get quicker access to treatment and vaccines, if necessary. … We don’t yet know, but studies are ongoing for these things.”
Amesh Adalja, MD, an infectious disease specialist with the Johns Hopkins Center for Health Security, Baltimore, agrees that emerging research on people who’ve avoided infection offers the chance of new public health strategies to combat COVID-19.
“I’m sure there is some subset of people who are [COVID] negative,” he says. “So what explains that phenomenon, especially if that person was out there getting significant exposures?”
Have you had COVID without knowing it?
In a media briefing late last month, White House COVID-19 Response Coordinator Ashish Jha, MD, said more than 70% of the U.S. population has had the virus, according to the latest CDC data. That’s up from 33.5% in December.
But the actual number of people in the U.S. who have been infected with SARS-CoV-2, the scientific name for the virus that causes COVID-19, is likely to be much higher due to cases without symptoms that are unreported, experts say.
Since the early days of the pandemic, researchers have tried to put a number on these hidden cases, but that figure has been evolving and a clear consensus has not emerged.
In September 2020, a study published in the Annals of Internal Medicine said “approximately 40% to 45% of those infected with SARS-CoV-2 will remain asymptomatic.”
A follow-up analysis of 95 studies, published last December, reached similar findings, estimating that more than 40% of COVID-19 infections didn’t come with symptoms.
To get a better handle on the issue, CDC officials have been working with the American Red Cross and other blood banks to track COVID-19 antibodies – proteins your body makes after exposure to the virus to fight off an infection – in donors who said they have never had COVID-19.
While that joint effort is still ongoing, early findings say the number of donors with antibodies from COVID-19 infection increased in blood donors from 3.5% in July 2020 to at least 20.2% in May 2021. Since then, those percentages have soared, in part due to the introduction of vaccines, which also make the body produce COVID-19 antibodies.
The most current findings show that 83.3% of donors have combined COVID infection– and vaccine-induced antibodies in their blood. Those findings are based on 1.4 million blood donations.
Health experts say all of these studies are strong evidence that many COVID-19 cases continue to go undetected. In fact, the University of Washington Institute for Health Metrics and Evaluation estimates that only 7% of positive COVID-19 cases in the U.S. are being detected. That means case rates are actually 14.5 times higher than the official count of 131,000 new COVID infections each day, according to the Centers for Disease Control and Prevention, which reports the virus is still killing about 440 Americans daily.
So, why is all this important, in terms of public health?
Experts say people are more likely to be cautious if they know COVID-19 cases are high where they live, work, and play. On the other hand, if they believe case rates in their communities are lower than they actually are, they may be less likely to get vaccinated and boosted, wear masks indoors, avoid crowded indoor spaces, and take other precautions to fend off infection.
How do some avoid infection altogether?
In addition to tracking cases that go unreported and don’t have symptoms, infectious disease experts have also been trying to figure out why some people have managed to avoid getting the highly contagious virus.
Several leading lines of research have produced promising early results – suggesting that a person’s genetic makeup, past exposure to less-lethal coronaviruses, allergies, and even certain drugs they take for other conditions may all provide at least some protection against COVID.
“Our study showed that there are many human genes – hundreds of genes – that can impact SARS-CoV-2 infection,” says Neville Sanjana, PhD, a geneticist at New York University and the New York Genome Center who co-led the study. “With a better understanding of host genetic factors, we can find new kinds of therapies that target these host factors to block infection.”
In addition, he says several studies show some drugs that regulate genes, such as the breast cancer drug tamoxifen, also appear to knock down COVID-19 risk. He suggests such drugs, already approved by the Food and Drug Administration, might be “repurposed” to target the virus.
Studies in other countries show that patients taking tamoxifen before the pandemic were protected against severe COVID-19, Dr. Sanjana says. “That was a really cool thing, highlighting the power of harnessing host genetics. The virus critically depends on our genes to complete key parts of its life cycle.”
The NYU research findings echo other studies that have been published in recent months.
In July, a team of researchers led by the National Cancer Institute identified a genetic factor that appears to determine how severe an infection will be. In a study involving 3,000 people, they found that two gene changes, or mutations, that decrease the expression of a gene called OAS1 boosted the risk of hospitalization from COVID-19. OAS1 is part of the immune system’s response to viral infections.
As a result, developing a genetic therapy designed to increase the OAS1 gene’s expression might reduce the risk of severe disease.
“It’s very natural to get infected once you are exposed. There’s no magic bullet for that. But after you get infected, how you’re going to respond to this infection, that’s what is going to be affected by your genetic variants,” said Ludmila Prokunina-Olsson, PhD, the study’s lead researcher and chief of the National Cancer Institute’s Laboratory of Translational Genomics, Bethesda, Md., in an interview with NBC News.
Benjamin tenOever, PhD, a New York University virologist who co-authored the 2020 research, says the new genetic research is promising, but he believes it’s unlikely scientists will be able to identify a single gene responsible for actually preventing a COVID-19 infection.
“On the flip side, we have identified many genes that makes the disease worse,” he says.
T cells ‘remember’ past viral infections
As Dr. tenOever and Dr. Sanjana suggest, another intriguing line of research has found that prior viral infections may prime the body’s immune system to fight COVID-19.
Four other common coronaviruses – aside from SARS-CoV-2 – infect people worldwide, typically causing mild to moderate upper respiratory illnesses like the common cold, says Alessandro Sette, PhD, an infectious disease expert and vaccine researcher with the La Jolla (Calif.) Institute for Immunology.
In a recent study published in Science, he and his team found past infection with these other coronaviruses may give some protection against SARS-CoV-2.
T cells – white blood cells that act like immunological ninjas to ferret out and fight infections – appear to maintain a kind of “biological memory” of coronaviruses they have seen before and can mount an attack on similar pathogens, such SARS-CoV-2, Dr. Sette says.
The new work builds on a prior research he helped lead that found 40%-60% of people never exposed to SARS-CoV-2 had T cells that reacted to the virus – with their immune systems recognizing fragments of a virus they had never seen before.
Dr. Sette says his research shows that people whose T cells have this “preexisting memory” of past coronavirus exposures also tend to respond better to vaccination for reasons not yet well understood.
“The question is, at which point will there be enough immunity from vaccination, repeated infections from other coronaviruses, but also some of the variants of the SARS-CoV-2 … where infections become less frequent? We’re not there yet,” he says.
In addition to these exciting genetic and T-cell findings, other research has suggested low-grade inflammation from allergies – a key part of the body’s immune response to foreign substances – may also give some people an extra leg up, in terms of avoiding COVID infection.
Last May, a study of 1,400 households published in The Journal of Allergy and Clinical Immunology found that having a food allergy cut the risk of COVID-19 infection in half.
The researchers said it’s unclear why allergies may reduce the risk of infection, but they noted that people with food allergies express fewer ACE2 receptors on the surface of their airway cells, making it harder for the virus to enter cells.
The big picture: Prevention still your best bet
So, what’s the takeaway from all of this emerging research?
New York University’s Dr. tenOever says that while genes, T cells and allergies may offer some protection against COVID, tried-and-true precautions – vaccination, wearing masks, avoiding crowded indoor spaces, and social distancing – are likely to provide a greater defense.
He believes these precautions are likely why he and his family have never contracted COVID-19.
“I was tested weekly, as were my kids at school,” he says. “We definitely never got COVID, despite the fact that we live in New York City and I worked in a hospital every single day of the pandemic.”
Ziyad Al-Aly, MD, an infectious disease specialist and director of clinical epidemiology at Washington University in St. Louis, agrees that the new research on COVID-19 is intriguing but won’t likely result in practical changes in the approach to fighting the virus in the near term.
“Getting a deeper understanding of potential genetic factors or other characteristics – that could really help us understand why the virus just comes and goes without any ill effects in some people, and in other people it produces really serious disease,” he says. “That will really help us eventually to design better vaccines to prevent it or reduce severity or even [treat] people who get severe disease.”
In the meantime, Dr. Al-Aly says, “it’s still best to do everything you can to avoid infection in the first place – even if you’re vaccinated or previously infected, you should really try to avoid reinfection.”
That means sit outside if you can when visiting a restaurant. Wear a mask on a plane, even though it’s not required. And get vaccinated and boosted.
“In the future, there may be more tools to address this pandemic, but that’s really the best advice for now,” Dr. Al-Aly says.
A version of this article first appeared on WebMD.com.
We all have friends or relatives who, somehow, have managed to avoid catching COVID-19, which has infected more than 91.5 million Americans. You may even be one of the lucky ones yourself.
But health experts are saying: Not so fast. because they didn’t have symptoms or had mild cases they mistook for a cold or allergies.
The upshot: These silent COVID-19 cases reflect a hidden side of the pandemic that may be helping to drive new surges and viral variants.
Still, infectious disease experts say there is little doubt that some people have indeed managed to avoid COVID-19 infection altogether, and they are trying to understand why.
Several recent studies have suggested certain genetic and immune system traits may better protect this group of people against the coronavirus, making them less likely than others to be infected or seriously sickened. Researchers around the world are now studying these seemingly super-immune people for clues to what makes them so special, with an eye toward better vaccines, treatments, and prevention strategies.
Infectious disease specialists say both types of cases – those unknowingly infected by COVID-19 and people who’ve avoided the virus altogether – matter greatly to public health, more than 2 years into the pandemic.
“It’s definitely true that some people have had COVID and don’t realize it,” says Stephen Kissler, PhD, an infectious disease researcher with the Harvard T.H. Chan School of Public Health, Boston. “It is potentially good news if there’s more immunity in the population than we realize.”
But he says that being able to identify genetic and other factors that may offer some people protection against COVID-19 is an “exciting prospect” that could help find out who’s most at risk and improve efforts to get the pandemic under control.
Some studies have found a person’s genetic profile, past exposure to other COVID-like viruses, allergies, and even drugs they take for other conditions may all provide some defense – even for people who have not been vaccinated, don’t use masks, or don’t practice social distancing.
A person’s medical history and genetics may help decide their risk from new diseases, meaning “we may be able to help identify people who are at especially high risk from infection,” Dr. Kissler says. “That knowledge could help those people better shield themselves from infection and get quicker access to treatment and vaccines, if necessary. … We don’t yet know, but studies are ongoing for these things.”
Amesh Adalja, MD, an infectious disease specialist with the Johns Hopkins Center for Health Security, Baltimore, agrees that emerging research on people who’ve avoided infection offers the chance of new public health strategies to combat COVID-19.
“I’m sure there is some subset of people who are [COVID] negative,” he says. “So what explains that phenomenon, especially if that person was out there getting significant exposures?”
Have you had COVID without knowing it?
In a media briefing late last month, White House COVID-19 Response Coordinator Ashish Jha, MD, said more than 70% of the U.S. population has had the virus, according to the latest CDC data. That’s up from 33.5% in December.
But the actual number of people in the U.S. who have been infected with SARS-CoV-2, the scientific name for the virus that causes COVID-19, is likely to be much higher due to cases without symptoms that are unreported, experts say.
Since the early days of the pandemic, researchers have tried to put a number on these hidden cases, but that figure has been evolving and a clear consensus has not emerged.
In September 2020, a study published in the Annals of Internal Medicine said “approximately 40% to 45% of those infected with SARS-CoV-2 will remain asymptomatic.”
A follow-up analysis of 95 studies, published last December, reached similar findings, estimating that more than 40% of COVID-19 infections didn’t come with symptoms.
To get a better handle on the issue, CDC officials have been working with the American Red Cross and other blood banks to track COVID-19 antibodies – proteins your body makes after exposure to the virus to fight off an infection – in donors who said they have never had COVID-19.
While that joint effort is still ongoing, early findings say the number of donors with antibodies from COVID-19 infection increased in blood donors from 3.5% in July 2020 to at least 20.2% in May 2021. Since then, those percentages have soared, in part due to the introduction of vaccines, which also make the body produce COVID-19 antibodies.
The most current findings show that 83.3% of donors have combined COVID infection– and vaccine-induced antibodies in their blood. Those findings are based on 1.4 million blood donations.
Health experts say all of these studies are strong evidence that many COVID-19 cases continue to go undetected. In fact, the University of Washington Institute for Health Metrics and Evaluation estimates that only 7% of positive COVID-19 cases in the U.S. are being detected. That means case rates are actually 14.5 times higher than the official count of 131,000 new COVID infections each day, according to the Centers for Disease Control and Prevention, which reports the virus is still killing about 440 Americans daily.
So, why is all this important, in terms of public health?
Experts say people are more likely to be cautious if they know COVID-19 cases are high where they live, work, and play. On the other hand, if they believe case rates in their communities are lower than they actually are, they may be less likely to get vaccinated and boosted, wear masks indoors, avoid crowded indoor spaces, and take other precautions to fend off infection.
How do some avoid infection altogether?
In addition to tracking cases that go unreported and don’t have symptoms, infectious disease experts have also been trying to figure out why some people have managed to avoid getting the highly contagious virus.
Several leading lines of research have produced promising early results – suggesting that a person’s genetic makeup, past exposure to less-lethal coronaviruses, allergies, and even certain drugs they take for other conditions may all provide at least some protection against COVID.
“Our study showed that there are many human genes – hundreds of genes – that can impact SARS-CoV-2 infection,” says Neville Sanjana, PhD, a geneticist at New York University and the New York Genome Center who co-led the study. “With a better understanding of host genetic factors, we can find new kinds of therapies that target these host factors to block infection.”
In addition, he says several studies show some drugs that regulate genes, such as the breast cancer drug tamoxifen, also appear to knock down COVID-19 risk. He suggests such drugs, already approved by the Food and Drug Administration, might be “repurposed” to target the virus.
Studies in other countries show that patients taking tamoxifen before the pandemic were protected against severe COVID-19, Dr. Sanjana says. “That was a really cool thing, highlighting the power of harnessing host genetics. The virus critically depends on our genes to complete key parts of its life cycle.”
The NYU research findings echo other studies that have been published in recent months.
In July, a team of researchers led by the National Cancer Institute identified a genetic factor that appears to determine how severe an infection will be. In a study involving 3,000 people, they found that two gene changes, or mutations, that decrease the expression of a gene called OAS1 boosted the risk of hospitalization from COVID-19. OAS1 is part of the immune system’s response to viral infections.
As a result, developing a genetic therapy designed to increase the OAS1 gene’s expression might reduce the risk of severe disease.
“It’s very natural to get infected once you are exposed. There’s no magic bullet for that. But after you get infected, how you’re going to respond to this infection, that’s what is going to be affected by your genetic variants,” said Ludmila Prokunina-Olsson, PhD, the study’s lead researcher and chief of the National Cancer Institute’s Laboratory of Translational Genomics, Bethesda, Md., in an interview with NBC News.
Benjamin tenOever, PhD, a New York University virologist who co-authored the 2020 research, says the new genetic research is promising, but he believes it’s unlikely scientists will be able to identify a single gene responsible for actually preventing a COVID-19 infection.
“On the flip side, we have identified many genes that makes the disease worse,” he says.
T cells ‘remember’ past viral infections
As Dr. tenOever and Dr. Sanjana suggest, another intriguing line of research has found that prior viral infections may prime the body’s immune system to fight COVID-19.
Four other common coronaviruses – aside from SARS-CoV-2 – infect people worldwide, typically causing mild to moderate upper respiratory illnesses like the common cold, says Alessandro Sette, PhD, an infectious disease expert and vaccine researcher with the La Jolla (Calif.) Institute for Immunology.
In a recent study published in Science, he and his team found past infection with these other coronaviruses may give some protection against SARS-CoV-2.
T cells – white blood cells that act like immunological ninjas to ferret out and fight infections – appear to maintain a kind of “biological memory” of coronaviruses they have seen before and can mount an attack on similar pathogens, such SARS-CoV-2, Dr. Sette says.
The new work builds on a prior research he helped lead that found 40%-60% of people never exposed to SARS-CoV-2 had T cells that reacted to the virus – with their immune systems recognizing fragments of a virus they had never seen before.
Dr. Sette says his research shows that people whose T cells have this “preexisting memory” of past coronavirus exposures also tend to respond better to vaccination for reasons not yet well understood.
“The question is, at which point will there be enough immunity from vaccination, repeated infections from other coronaviruses, but also some of the variants of the SARS-CoV-2 … where infections become less frequent? We’re not there yet,” he says.
In addition to these exciting genetic and T-cell findings, other research has suggested low-grade inflammation from allergies – a key part of the body’s immune response to foreign substances – may also give some people an extra leg up, in terms of avoiding COVID infection.
Last May, a study of 1,400 households published in The Journal of Allergy and Clinical Immunology found that having a food allergy cut the risk of COVID-19 infection in half.
The researchers said it’s unclear why allergies may reduce the risk of infection, but they noted that people with food allergies express fewer ACE2 receptors on the surface of their airway cells, making it harder for the virus to enter cells.
The big picture: Prevention still your best bet
So, what’s the takeaway from all of this emerging research?
New York University’s Dr. tenOever says that while genes, T cells and allergies may offer some protection against COVID, tried-and-true precautions – vaccination, wearing masks, avoiding crowded indoor spaces, and social distancing – are likely to provide a greater defense.
He believes these precautions are likely why he and his family have never contracted COVID-19.
“I was tested weekly, as were my kids at school,” he says. “We definitely never got COVID, despite the fact that we live in New York City and I worked in a hospital every single day of the pandemic.”
Ziyad Al-Aly, MD, an infectious disease specialist and director of clinical epidemiology at Washington University in St. Louis, agrees that the new research on COVID-19 is intriguing but won’t likely result in practical changes in the approach to fighting the virus in the near term.
“Getting a deeper understanding of potential genetic factors or other characteristics – that could really help us understand why the virus just comes and goes without any ill effects in some people, and in other people it produces really serious disease,” he says. “That will really help us eventually to design better vaccines to prevent it or reduce severity or even [treat] people who get severe disease.”
In the meantime, Dr. Al-Aly says, “it’s still best to do everything you can to avoid infection in the first place – even if you’re vaccinated or previously infected, you should really try to avoid reinfection.”
That means sit outside if you can when visiting a restaurant. Wear a mask on a plane, even though it’s not required. And get vaccinated and boosted.
“In the future, there may be more tools to address this pandemic, but that’s really the best advice for now,” Dr. Al-Aly says.
A version of this article first appeared on WebMD.com.
We all have friends or relatives who, somehow, have managed to avoid catching COVID-19, which has infected more than 91.5 million Americans. You may even be one of the lucky ones yourself.
But health experts are saying: Not so fast. because they didn’t have symptoms or had mild cases they mistook for a cold or allergies.
The upshot: These silent COVID-19 cases reflect a hidden side of the pandemic that may be helping to drive new surges and viral variants.
Still, infectious disease experts say there is little doubt that some people have indeed managed to avoid COVID-19 infection altogether, and they are trying to understand why.
Several recent studies have suggested certain genetic and immune system traits may better protect this group of people against the coronavirus, making them less likely than others to be infected or seriously sickened. Researchers around the world are now studying these seemingly super-immune people for clues to what makes them so special, with an eye toward better vaccines, treatments, and prevention strategies.
Infectious disease specialists say both types of cases – those unknowingly infected by COVID-19 and people who’ve avoided the virus altogether – matter greatly to public health, more than 2 years into the pandemic.
“It’s definitely true that some people have had COVID and don’t realize it,” says Stephen Kissler, PhD, an infectious disease researcher with the Harvard T.H. Chan School of Public Health, Boston. “It is potentially good news if there’s more immunity in the population than we realize.”
But he says that being able to identify genetic and other factors that may offer some people protection against COVID-19 is an “exciting prospect” that could help find out who’s most at risk and improve efforts to get the pandemic under control.
Some studies have found a person’s genetic profile, past exposure to other COVID-like viruses, allergies, and even drugs they take for other conditions may all provide some defense – even for people who have not been vaccinated, don’t use masks, or don’t practice social distancing.
A person’s medical history and genetics may help decide their risk from new diseases, meaning “we may be able to help identify people who are at especially high risk from infection,” Dr. Kissler says. “That knowledge could help those people better shield themselves from infection and get quicker access to treatment and vaccines, if necessary. … We don’t yet know, but studies are ongoing for these things.”
Amesh Adalja, MD, an infectious disease specialist with the Johns Hopkins Center for Health Security, Baltimore, agrees that emerging research on people who’ve avoided infection offers the chance of new public health strategies to combat COVID-19.
“I’m sure there is some subset of people who are [COVID] negative,” he says. “So what explains that phenomenon, especially if that person was out there getting significant exposures?”
Have you had COVID without knowing it?
In a media briefing late last month, White House COVID-19 Response Coordinator Ashish Jha, MD, said more than 70% of the U.S. population has had the virus, according to the latest CDC data. That’s up from 33.5% in December.
But the actual number of people in the U.S. who have been infected with SARS-CoV-2, the scientific name for the virus that causes COVID-19, is likely to be much higher due to cases without symptoms that are unreported, experts say.
Since the early days of the pandemic, researchers have tried to put a number on these hidden cases, but that figure has been evolving and a clear consensus has not emerged.
In September 2020, a study published in the Annals of Internal Medicine said “approximately 40% to 45% of those infected with SARS-CoV-2 will remain asymptomatic.”
A follow-up analysis of 95 studies, published last December, reached similar findings, estimating that more than 40% of COVID-19 infections didn’t come with symptoms.
To get a better handle on the issue, CDC officials have been working with the American Red Cross and other blood banks to track COVID-19 antibodies – proteins your body makes after exposure to the virus to fight off an infection – in donors who said they have never had COVID-19.
While that joint effort is still ongoing, early findings say the number of donors with antibodies from COVID-19 infection increased in blood donors from 3.5% in July 2020 to at least 20.2% in May 2021. Since then, those percentages have soared, in part due to the introduction of vaccines, which also make the body produce COVID-19 antibodies.
The most current findings show that 83.3% of donors have combined COVID infection– and vaccine-induced antibodies in their blood. Those findings are based on 1.4 million blood donations.
Health experts say all of these studies are strong evidence that many COVID-19 cases continue to go undetected. In fact, the University of Washington Institute for Health Metrics and Evaluation estimates that only 7% of positive COVID-19 cases in the U.S. are being detected. That means case rates are actually 14.5 times higher than the official count of 131,000 new COVID infections each day, according to the Centers for Disease Control and Prevention, which reports the virus is still killing about 440 Americans daily.
So, why is all this important, in terms of public health?
Experts say people are more likely to be cautious if they know COVID-19 cases are high where they live, work, and play. On the other hand, if they believe case rates in their communities are lower than they actually are, they may be less likely to get vaccinated and boosted, wear masks indoors, avoid crowded indoor spaces, and take other precautions to fend off infection.
How do some avoid infection altogether?
In addition to tracking cases that go unreported and don’t have symptoms, infectious disease experts have also been trying to figure out why some people have managed to avoid getting the highly contagious virus.
Several leading lines of research have produced promising early results – suggesting that a person’s genetic makeup, past exposure to less-lethal coronaviruses, allergies, and even certain drugs they take for other conditions may all provide at least some protection against COVID.
“Our study showed that there are many human genes – hundreds of genes – that can impact SARS-CoV-2 infection,” says Neville Sanjana, PhD, a geneticist at New York University and the New York Genome Center who co-led the study. “With a better understanding of host genetic factors, we can find new kinds of therapies that target these host factors to block infection.”
In addition, he says several studies show some drugs that regulate genes, such as the breast cancer drug tamoxifen, also appear to knock down COVID-19 risk. He suggests such drugs, already approved by the Food and Drug Administration, might be “repurposed” to target the virus.
Studies in other countries show that patients taking tamoxifen before the pandemic were protected against severe COVID-19, Dr. Sanjana says. “That was a really cool thing, highlighting the power of harnessing host genetics. The virus critically depends on our genes to complete key parts of its life cycle.”
The NYU research findings echo other studies that have been published in recent months.
In July, a team of researchers led by the National Cancer Institute identified a genetic factor that appears to determine how severe an infection will be. In a study involving 3,000 people, they found that two gene changes, or mutations, that decrease the expression of a gene called OAS1 boosted the risk of hospitalization from COVID-19. OAS1 is part of the immune system’s response to viral infections.
As a result, developing a genetic therapy designed to increase the OAS1 gene’s expression might reduce the risk of severe disease.
“It’s very natural to get infected once you are exposed. There’s no magic bullet for that. But after you get infected, how you’re going to respond to this infection, that’s what is going to be affected by your genetic variants,” said Ludmila Prokunina-Olsson, PhD, the study’s lead researcher and chief of the National Cancer Institute’s Laboratory of Translational Genomics, Bethesda, Md., in an interview with NBC News.
Benjamin tenOever, PhD, a New York University virologist who co-authored the 2020 research, says the new genetic research is promising, but he believes it’s unlikely scientists will be able to identify a single gene responsible for actually preventing a COVID-19 infection.
“On the flip side, we have identified many genes that makes the disease worse,” he says.
T cells ‘remember’ past viral infections
As Dr. tenOever and Dr. Sanjana suggest, another intriguing line of research has found that prior viral infections may prime the body’s immune system to fight COVID-19.
Four other common coronaviruses – aside from SARS-CoV-2 – infect people worldwide, typically causing mild to moderate upper respiratory illnesses like the common cold, says Alessandro Sette, PhD, an infectious disease expert and vaccine researcher with the La Jolla (Calif.) Institute for Immunology.
In a recent study published in Science, he and his team found past infection with these other coronaviruses may give some protection against SARS-CoV-2.
T cells – white blood cells that act like immunological ninjas to ferret out and fight infections – appear to maintain a kind of “biological memory” of coronaviruses they have seen before and can mount an attack on similar pathogens, such SARS-CoV-2, Dr. Sette says.
The new work builds on a prior research he helped lead that found 40%-60% of people never exposed to SARS-CoV-2 had T cells that reacted to the virus – with their immune systems recognizing fragments of a virus they had never seen before.
Dr. Sette says his research shows that people whose T cells have this “preexisting memory” of past coronavirus exposures also tend to respond better to vaccination for reasons not yet well understood.
“The question is, at which point will there be enough immunity from vaccination, repeated infections from other coronaviruses, but also some of the variants of the SARS-CoV-2 … where infections become less frequent? We’re not there yet,” he says.
In addition to these exciting genetic and T-cell findings, other research has suggested low-grade inflammation from allergies – a key part of the body’s immune response to foreign substances – may also give some people an extra leg up, in terms of avoiding COVID infection.
Last May, a study of 1,400 households published in The Journal of Allergy and Clinical Immunology found that having a food allergy cut the risk of COVID-19 infection in half.
The researchers said it’s unclear why allergies may reduce the risk of infection, but they noted that people with food allergies express fewer ACE2 receptors on the surface of their airway cells, making it harder for the virus to enter cells.
The big picture: Prevention still your best bet
So, what’s the takeaway from all of this emerging research?
New York University’s Dr. tenOever says that while genes, T cells and allergies may offer some protection against COVID, tried-and-true precautions – vaccination, wearing masks, avoiding crowded indoor spaces, and social distancing – are likely to provide a greater defense.
He believes these precautions are likely why he and his family have never contracted COVID-19.
“I was tested weekly, as were my kids at school,” he says. “We definitely never got COVID, despite the fact that we live in New York City and I worked in a hospital every single day of the pandemic.”
Ziyad Al-Aly, MD, an infectious disease specialist and director of clinical epidemiology at Washington University in St. Louis, agrees that the new research on COVID-19 is intriguing but won’t likely result in practical changes in the approach to fighting the virus in the near term.
“Getting a deeper understanding of potential genetic factors or other characteristics – that could really help us understand why the virus just comes and goes without any ill effects in some people, and in other people it produces really serious disease,” he says. “That will really help us eventually to design better vaccines to prevent it or reduce severity or even [treat] people who get severe disease.”
In the meantime, Dr. Al-Aly says, “it’s still best to do everything you can to avoid infection in the first place – even if you’re vaccinated or previously infected, you should really try to avoid reinfection.”
That means sit outside if you can when visiting a restaurant. Wear a mask on a plane, even though it’s not required. And get vaccinated and boosted.
“In the future, there may be more tools to address this pandemic, but that’s really the best advice for now,” Dr. Al-Aly says.
A version of this article first appeared on WebMD.com.
Long COVID comes in three forms: Study
, according to a new preprint study published on MedRxiv that hasn’t yet been peer-reviewed.
Long COVID has been hard to define due to its large number of symptoms, but researchers at King’s College London have identified three distinct profiles – with long-term symptoms focused on neurological, respiratory, or physical conditions. So far, they also found patterns among people infected with the original coronavirus strain, the Alpha variant, and the Delta variant.
“These data show clearly that post-COVID syndrome is not just one condition but appears to have several subtypes,” Claire Steves, PhD, one of the study authors and a senior clinical lecturer in King’s College London’s School of Life Course & Population Sciences, said in a statement.
“Understanding the root causes of these subtypes may help in finding treatment strategies,” she said. “Moreover, these data emphasize the need for long-COVID services to incorporate a personalized approach sensitive to the issues of each individual.”
The research team analyzed ZOE COVID app data for 1,459 people who have had symptoms for more than 84 days, or 12 weeks, according to their definition of long COVID or post-COVID syndrome.
They found that the largest group had a cluster of symptoms in the nervous system, such as fatigue, brain fog, and headaches. It was the most common subtype among the Alpha variant, which was dominant in winter 2020-2021, and the Delta variant, which was dominant in 2021.
The second group had respiratory symptoms, such as chest pain and severe shortness of breath, which could suggest lung damage, the researchers wrote. It was the largest cluster for the original coronavirus strain in spring 2020, when people were unvaccinated.
The third group included people who reported a diverse range of physical symptoms, including heart palpitations, muscle aches and pain, and changes to their skin and hair. This group had some of the “most severe and debilitating multi-organ symptoms,” the researchers wrote.
The researchers found that the subtypes were similar in vaccinated and unvaccinated people based on the variants investigated so far. But the data showed that the risk of long COVID was reduced by vaccination.
In addition, although the three subtypes were present in all the variants, other symptom clusters had subtle differences among the variants, such as symptoms in the stomach and intestines. The differences could be due to other things that changed during the pandemic, such as the time of year, social behaviors, and treatments, the researchers said.
“Machine learning approaches, such as clustering analysis, have made it possible to start exploring and identifying different profiles of post-COVID syndrome,” Marc Modat, PhD, who led the analysis and is a senior lecturer at King’s College London’s School of Biomedical Engineering & Imaging Sciences, said in the statement.
“This opens new avenues of research to better understand COVID-19 and to motivate clinical research that might mitigate the long-term effects of the disease,” he said.
A version of this article first appeared on WebMD.com.
, according to a new preprint study published on MedRxiv that hasn’t yet been peer-reviewed.
Long COVID has been hard to define due to its large number of symptoms, but researchers at King’s College London have identified three distinct profiles – with long-term symptoms focused on neurological, respiratory, or physical conditions. So far, they also found patterns among people infected with the original coronavirus strain, the Alpha variant, and the Delta variant.
“These data show clearly that post-COVID syndrome is not just one condition but appears to have several subtypes,” Claire Steves, PhD, one of the study authors and a senior clinical lecturer in King’s College London’s School of Life Course & Population Sciences, said in a statement.
“Understanding the root causes of these subtypes may help in finding treatment strategies,” she said. “Moreover, these data emphasize the need for long-COVID services to incorporate a personalized approach sensitive to the issues of each individual.”
The research team analyzed ZOE COVID app data for 1,459 people who have had symptoms for more than 84 days, or 12 weeks, according to their definition of long COVID or post-COVID syndrome.
They found that the largest group had a cluster of symptoms in the nervous system, such as fatigue, brain fog, and headaches. It was the most common subtype among the Alpha variant, which was dominant in winter 2020-2021, and the Delta variant, which was dominant in 2021.
The second group had respiratory symptoms, such as chest pain and severe shortness of breath, which could suggest lung damage, the researchers wrote. It was the largest cluster for the original coronavirus strain in spring 2020, when people were unvaccinated.
The third group included people who reported a diverse range of physical symptoms, including heart palpitations, muscle aches and pain, and changes to their skin and hair. This group had some of the “most severe and debilitating multi-organ symptoms,” the researchers wrote.
The researchers found that the subtypes were similar in vaccinated and unvaccinated people based on the variants investigated so far. But the data showed that the risk of long COVID was reduced by vaccination.
In addition, although the three subtypes were present in all the variants, other symptom clusters had subtle differences among the variants, such as symptoms in the stomach and intestines. The differences could be due to other things that changed during the pandemic, such as the time of year, social behaviors, and treatments, the researchers said.
“Machine learning approaches, such as clustering analysis, have made it possible to start exploring and identifying different profiles of post-COVID syndrome,” Marc Modat, PhD, who led the analysis and is a senior lecturer at King’s College London’s School of Biomedical Engineering & Imaging Sciences, said in the statement.
“This opens new avenues of research to better understand COVID-19 and to motivate clinical research that might mitigate the long-term effects of the disease,” he said.
A version of this article first appeared on WebMD.com.
, according to a new preprint study published on MedRxiv that hasn’t yet been peer-reviewed.
Long COVID has been hard to define due to its large number of symptoms, but researchers at King’s College London have identified three distinct profiles – with long-term symptoms focused on neurological, respiratory, or physical conditions. So far, they also found patterns among people infected with the original coronavirus strain, the Alpha variant, and the Delta variant.
“These data show clearly that post-COVID syndrome is not just one condition but appears to have several subtypes,” Claire Steves, PhD, one of the study authors and a senior clinical lecturer in King’s College London’s School of Life Course & Population Sciences, said in a statement.
“Understanding the root causes of these subtypes may help in finding treatment strategies,” she said. “Moreover, these data emphasize the need for long-COVID services to incorporate a personalized approach sensitive to the issues of each individual.”
The research team analyzed ZOE COVID app data for 1,459 people who have had symptoms for more than 84 days, or 12 weeks, according to their definition of long COVID or post-COVID syndrome.
They found that the largest group had a cluster of symptoms in the nervous system, such as fatigue, brain fog, and headaches. It was the most common subtype among the Alpha variant, which was dominant in winter 2020-2021, and the Delta variant, which was dominant in 2021.
The second group had respiratory symptoms, such as chest pain and severe shortness of breath, which could suggest lung damage, the researchers wrote. It was the largest cluster for the original coronavirus strain in spring 2020, when people were unvaccinated.
The third group included people who reported a diverse range of physical symptoms, including heart palpitations, muscle aches and pain, and changes to their skin and hair. This group had some of the “most severe and debilitating multi-organ symptoms,” the researchers wrote.
The researchers found that the subtypes were similar in vaccinated and unvaccinated people based on the variants investigated so far. But the data showed that the risk of long COVID was reduced by vaccination.
In addition, although the three subtypes were present in all the variants, other symptom clusters had subtle differences among the variants, such as symptoms in the stomach and intestines. The differences could be due to other things that changed during the pandemic, such as the time of year, social behaviors, and treatments, the researchers said.
“Machine learning approaches, such as clustering analysis, have made it possible to start exploring and identifying different profiles of post-COVID syndrome,” Marc Modat, PhD, who led the analysis and is a senior lecturer at King’s College London’s School of Biomedical Engineering & Imaging Sciences, said in the statement.
“This opens new avenues of research to better understand COVID-19 and to motivate clinical research that might mitigate the long-term effects of the disease,” he said.
A version of this article first appeared on WebMD.com.
Burnout and stress of today: How do we cope?
Interestingly, the group that seems to be least impacted by this was health care administrators (with 12% of them planning on leaving their jobs).
I couldn’t stop thinking about these percentages.
I am reminded every day of the commitment and excellence of my colleagues in the health care field, and I do not want to lose them. I am hoping the following information and my thoughts on this topic will be helpful for those thinking about leaving health care.
Surgeon general’s burnout report
The surgeon general recently released a report on addressing health care worker burnout.2 It includes several very interesting and appropriate observations. I will summarize the most important ones here:
1. Our health depends on the well-being of our health workforce.
2. Direct harm to health care workers can lead to anxiety, depression, insomnia, and interpersonal and relationship struggles.
3. Health care workers experience exhaustion from providing overwhelming care and empathy.
4. Health care workers spend less time with patients and too much time with EHRs.
5. There are health workforce shortages.
The report is comprehensive, and everything in it is correct. The real issue is how does it go from being a report to true actionable items that we as health care professionals benefit from? I think in regards to exhaustion from overwhelming care responsibilities, and empathy fatigue, we need better boundaries.
Those who go into medicine, and especially those who go into primary care, always put the patients’ needs first. When operating in a broken system, it stays broken when individuals cover for the deficiencies in the system. Adding four extra patients every day because there is no one to refer them to with availability is injurious to the health care provider, and those providers who accept these additional patients will eventually be part of the 23% who want to leave their jobs. It feels awful to say no, but until the system stops accommodating there will not be substantial change.
The empathy drain
One of the unreported stresses of open access for patients through EHR communications is the empathy drain on physicians. When I see a patient in clinic with chronic symptoms or issues, I spend important time making sure we have a plan and an agreed upon time frame.
With the EHR, patients frequently send multiple messages for the same symptoms between visits. It is okay to redirect the patient and share that these issues will be discussed at length at appointments. My reasoning on this is that I think it is better for me to better care for myself and stay as the doctor for my patients, than always say yes to limitless needs and soon be looking for the off ramp.
The following statistic in the surgeon general’s report really hit home. For every hour of direct patient care, physicians currently spend 2 hours on the EHR system. Most practices allow 10%-20% of time for catch up, where with statistics like this it should be 50%. This concept is fully lost on administrators, or ignored.
It is only when we refuse to continue to accept and follow a broken system that it will change. A minority of internal medicine and family doctors (4.5% in 2018) practice in direct primary care models, where these issues are addressed. Unfortunately, this model as it is currently available is not an option for lower income patients.
A major theme in the surgeon general’s report was that administrative burdens need to be reduced by 75% by 2025. When I look at the report, I see the suggestions, I just don’t see how it will be achieved. Despite almost all clinics moving to the EHR, paperwork in the form of faxes and forms has increased.
A sweeping reform would be needed to eliminate daily faxes from PT offices, visiting nurse services, prior authorization, patients reminders from insurance companies, and disability forms from patients. I am glad that there is acknowledgment of the problem, but this change will take more than 3 years.
Takeaways
So what do we do?
Be good to yourself, and your colleagues. The pandemic has isolated us, which accelerates burnout.
Reach out to people you care about.
We are all feeling this. Set boundaries that allow you to care for yourself, and accept that you are doing your best, even if you can’t meet the needs of all your patients all the time.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Sinsky CA et al. Covid-related stress and work intentions in a sample of US health care workers. Mayo Clin Proc Innov Qual Outcomes. 2021 Dec;5(6):1165-73.
2. Addressing health worker burnout. The U.S. Surgeon General’s advisory on building a thriving health workforce.
Interestingly, the group that seems to be least impacted by this was health care administrators (with 12% of them planning on leaving their jobs).
I couldn’t stop thinking about these percentages.
I am reminded every day of the commitment and excellence of my colleagues in the health care field, and I do not want to lose them. I am hoping the following information and my thoughts on this topic will be helpful for those thinking about leaving health care.
Surgeon general’s burnout report
The surgeon general recently released a report on addressing health care worker burnout.2 It includes several very interesting and appropriate observations. I will summarize the most important ones here:
1. Our health depends on the well-being of our health workforce.
2. Direct harm to health care workers can lead to anxiety, depression, insomnia, and interpersonal and relationship struggles.
3. Health care workers experience exhaustion from providing overwhelming care and empathy.
4. Health care workers spend less time with patients and too much time with EHRs.
5. There are health workforce shortages.
The report is comprehensive, and everything in it is correct. The real issue is how does it go from being a report to true actionable items that we as health care professionals benefit from? I think in regards to exhaustion from overwhelming care responsibilities, and empathy fatigue, we need better boundaries.
Those who go into medicine, and especially those who go into primary care, always put the patients’ needs first. When operating in a broken system, it stays broken when individuals cover for the deficiencies in the system. Adding four extra patients every day because there is no one to refer them to with availability is injurious to the health care provider, and those providers who accept these additional patients will eventually be part of the 23% who want to leave their jobs. It feels awful to say no, but until the system stops accommodating there will not be substantial change.
The empathy drain
One of the unreported stresses of open access for patients through EHR communications is the empathy drain on physicians. When I see a patient in clinic with chronic symptoms or issues, I spend important time making sure we have a plan and an agreed upon time frame.
With the EHR, patients frequently send multiple messages for the same symptoms between visits. It is okay to redirect the patient and share that these issues will be discussed at length at appointments. My reasoning on this is that I think it is better for me to better care for myself and stay as the doctor for my patients, than always say yes to limitless needs and soon be looking for the off ramp.
The following statistic in the surgeon general’s report really hit home. For every hour of direct patient care, physicians currently spend 2 hours on the EHR system. Most practices allow 10%-20% of time for catch up, where with statistics like this it should be 50%. This concept is fully lost on administrators, or ignored.
It is only when we refuse to continue to accept and follow a broken system that it will change. A minority of internal medicine and family doctors (4.5% in 2018) practice in direct primary care models, where these issues are addressed. Unfortunately, this model as it is currently available is not an option for lower income patients.
A major theme in the surgeon general’s report was that administrative burdens need to be reduced by 75% by 2025. When I look at the report, I see the suggestions, I just don’t see how it will be achieved. Despite almost all clinics moving to the EHR, paperwork in the form of faxes and forms has increased.
A sweeping reform would be needed to eliminate daily faxes from PT offices, visiting nurse services, prior authorization, patients reminders from insurance companies, and disability forms from patients. I am glad that there is acknowledgment of the problem, but this change will take more than 3 years.
Takeaways
So what do we do?
Be good to yourself, and your colleagues. The pandemic has isolated us, which accelerates burnout.
Reach out to people you care about.
We are all feeling this. Set boundaries that allow you to care for yourself, and accept that you are doing your best, even if you can’t meet the needs of all your patients all the time.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Sinsky CA et al. Covid-related stress and work intentions in a sample of US health care workers. Mayo Clin Proc Innov Qual Outcomes. 2021 Dec;5(6):1165-73.
2. Addressing health worker burnout. The U.S. Surgeon General’s advisory on building a thriving health workforce.
Interestingly, the group that seems to be least impacted by this was health care administrators (with 12% of them planning on leaving their jobs).
I couldn’t stop thinking about these percentages.
I am reminded every day of the commitment and excellence of my colleagues in the health care field, and I do not want to lose them. I am hoping the following information and my thoughts on this topic will be helpful for those thinking about leaving health care.
Surgeon general’s burnout report
The surgeon general recently released a report on addressing health care worker burnout.2 It includes several very interesting and appropriate observations. I will summarize the most important ones here:
1. Our health depends on the well-being of our health workforce.
2. Direct harm to health care workers can lead to anxiety, depression, insomnia, and interpersonal and relationship struggles.
3. Health care workers experience exhaustion from providing overwhelming care and empathy.
4. Health care workers spend less time with patients and too much time with EHRs.
5. There are health workforce shortages.
The report is comprehensive, and everything in it is correct. The real issue is how does it go from being a report to true actionable items that we as health care professionals benefit from? I think in regards to exhaustion from overwhelming care responsibilities, and empathy fatigue, we need better boundaries.
Those who go into medicine, and especially those who go into primary care, always put the patients’ needs first. When operating in a broken system, it stays broken when individuals cover for the deficiencies in the system. Adding four extra patients every day because there is no one to refer them to with availability is injurious to the health care provider, and those providers who accept these additional patients will eventually be part of the 23% who want to leave their jobs. It feels awful to say no, but until the system stops accommodating there will not be substantial change.
The empathy drain
One of the unreported stresses of open access for patients through EHR communications is the empathy drain on physicians. When I see a patient in clinic with chronic symptoms or issues, I spend important time making sure we have a plan and an agreed upon time frame.
With the EHR, patients frequently send multiple messages for the same symptoms between visits. It is okay to redirect the patient and share that these issues will be discussed at length at appointments. My reasoning on this is that I think it is better for me to better care for myself and stay as the doctor for my patients, than always say yes to limitless needs and soon be looking for the off ramp.
The following statistic in the surgeon general’s report really hit home. For every hour of direct patient care, physicians currently spend 2 hours on the EHR system. Most practices allow 10%-20% of time for catch up, where with statistics like this it should be 50%. This concept is fully lost on administrators, or ignored.
It is only when we refuse to continue to accept and follow a broken system that it will change. A minority of internal medicine and family doctors (4.5% in 2018) practice in direct primary care models, where these issues are addressed. Unfortunately, this model as it is currently available is not an option for lower income patients.
A major theme in the surgeon general’s report was that administrative burdens need to be reduced by 75% by 2025. When I look at the report, I see the suggestions, I just don’t see how it will be achieved. Despite almost all clinics moving to the EHR, paperwork in the form of faxes and forms has increased.
A sweeping reform would be needed to eliminate daily faxes from PT offices, visiting nurse services, prior authorization, patients reminders from insurance companies, and disability forms from patients. I am glad that there is acknowledgment of the problem, but this change will take more than 3 years.
Takeaways
So what do we do?
Be good to yourself, and your colleagues. The pandemic has isolated us, which accelerates burnout.
Reach out to people you care about.
We are all feeling this. Set boundaries that allow you to care for yourself, and accept that you are doing your best, even if you can’t meet the needs of all your patients all the time.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Sinsky CA et al. Covid-related stress and work intentions in a sample of US health care workers. Mayo Clin Proc Innov Qual Outcomes. 2021 Dec;5(6):1165-73.
2. Addressing health worker burnout. The U.S. Surgeon General’s advisory on building a thriving health workforce.
Gout flares linked to transient jump in MI, stroke risk
There is evidence that gout and heart disease are mechanistically linked by inflammation and patients with gout are at elevated risk for cardiovascular disease (CVD). But do gout flares, on their own, affect short-term risk for CV events? A new analysis based on records from British medical practices suggests that might be the case.
Risk for myocardial infarction or stroke climbed in the weeks after individual gout flare-ups in the study’s more than 60,000 patients with a recent gout diagnosis. The jump in risk, significant but small in absolute terms, held for about 4 months in the case-control study before going away.
A sensitivity analysis that excluded patients who already had CVD when their gout was diagnosed yielded similar results.
The observational study isn’t able to show that gout flares themselves transiently raise the risk for MI or stroke, but it’s enough to send a cautionary message to physicians who care for patients with gout, rheumatologist Abhishek Abhishek, PhD, Nottingham (England) City Hospital, said in an interview.
In such patients who also have conditions like hypertension, diabetes, or dyslipidemia, or a history of heart disease, he said, it’s important “to manage risk factors really aggressively, knowing that when these patients have a gout flare, there’s a temporary increase in risk of a cardiovascular event.”
Managing their absolute CV risk – whether with drug therapy, lifestyle changes, or other interventions – should help limit the transient jump in risk for MI or stroke following a gout flare, proposed Dr. Abhishek, who is senior author on the study published in JAMA, with lead author Edoardo Cipolletta, MD, also from Nottingham City Hospital.
First robust evidence
The case-control study, which involved more than 60,000 patients with a recent gout diagnosis, some who went on to have MI or stroke, looked at rates of such events at different time intervals after gout flares. Those who experienced such events showed a more than 90% increased likelihood of a gout flare-up in the preceding 60 days, a greater than 50% chance of a flare between 60 and 120 days before the event, but no increased likelihood prior to 120 days before the event.
Such a link between gout flares and CV events “has been suspected but never proven,” observed rheumatologist Hyon K. Choi, MD, Harvard Medical School, Boston, who was not associated with the analysis. “This is the first time it has actually been shown in a robust way,” he said in an interview.
The study suggests a “likely causative relationship” between gout flares and CV events, but – as the published report noted – has limitations like any observational study, said Dr. Choi, who also directs the Gout & Crystal Arthropathy Center at Massachusetts General Hospital, Boston. “Hopefully, this can be replicated in other cohorts.”
The analysis controlled for a number of relevant potential confounders, he noted, but couldn’t account for all issues that could argue against gout flares as a direct cause of the MIs and strokes.
Gout attacks are a complex experience with a range of potential indirect effects on CV risk, Dr. Choi observed. They can immobilize patients, possibly raising their risk for thrombotic events, for example. They can be exceptionally painful, which causes stress and can lead to frequent or chronic use of glucocorticoids or NSAIDs, all of which can exacerbate high blood pressure and possibly worsen CV risk.
A unique insight
The timing of gout flares relative to acute vascular events hasn’t been fully explored, observed an accompanying editorial. The current study’s “unique insight,” it stated, “is that disease activity from gout was associated with an incremental increase in risk for acute vascular events during the time period immediately following the gout flare.”
Although the study is observational, a “large body of evidence from animal and human research, mechanistic insights, and clinical interventions” support an association between flares and vascular events and “make a causal link eminently reasonable,” stated the editorialists, Jeffrey L. Anderson, MD, and Kirk U. Knowlton, MD, both with Intermountain Medical Center, Salt Lake City, Utah.
The findings, they wrote, “should alert clinicians and patients to the increased cardiovascular risk in the weeks beginning after a gout flare and should focus attention on optimizing preventive measures.” Those can include “lifestyle measures and standard risk-factor control including adherence to diet, statins, anti-inflammatory drugs (e.g., aspirin, colchicine), smoking cessation, diabetic and blood pressure control, and antithrombotic medications as indicated.”
Dr. Choi said the current results argue for more liberal use of colchicine, and for preferring colchicine over other anti-inflammatories, in patients with gout and traditional CV risk factors, given multiple randomized trials supporting the drug’s use in such cases. “If you use colchicine, you are covering their heart disease risk as well as their gout. It’s two birds with one stone.”
Nested case-control study
The investigators accessed electronic health records from 96,153 patients with recently diagnosed gout in England from 1997 to 2020; the cohort’s mean age was about 76 years, and 69% of participants were men. They matched 10,475 patients with at least one CV event to 52,099 others who didn’t have such an event by age, sex, and time from gout diagnosis. In each matched set of patients, those not experiencing a CV event were assigned a flare-to-event interval based on their matching with patients who did experience such an event.
Those with CV events, compared with patients without an event, had a greater than 90% increased likelihood of experiencing a gout flare-up in the 60 days preceding the event, a more than 50% greater chance of a flare-up 60-120 days before the CV event, but no increased likelihood more than 120 days before the event.
A self-controlled case series based on the same overall cohort with gout yielded similar results while sidestepping any potential for residual confounding, an inherent concern with any case–control analysis, the report notes. It involved 1,421 patients with one or more gout flare and at least one MI or stroke after the diagnosis of gout.
Among that cohort, the CV-event incidence rate ratio, adjusted for age and season of the year, by time interval after a gout flare, was 1.89 (95% confidence interval, 1.54-2.30) at 0-60 days, 1.64 (95% CI, 1.45-1.86) at 61-120 days, and1.29 (95% CI, 1.02-1.64) at 121-180 days.
Also similar, the report noted, were results of several sensitivity analyses, including one that excluded patients with confirmed CVD before their gout diagnosis; another that left out patients at low to moderate CV risk; and one that considered only gout flares treated with colchicine, corticosteroids, or NSAIDs.
The incremental CV event risks observed after flares in the study were small, which “has implications for both cost effectiveness and clinical relevance,” observed Dr. Anderson and Dr. Knowlton.
“An alternative to universal augmentation of cardiovascular risk prevention with therapies among patients with gout flares,” they wrote, would be “to further stratify risk by defining a group at highest near-term risk.” Such interventions could potentially be guided by markers of CV risk such as, for example, levels of high-sensitivity C-reactive protein or lipoprotein(a), or plaque burden on coronary-artery calcium scans.
Dr. Abhishek, Dr. Cipolletta, and the other authors reported no competing interests. Dr. Choi disclosed research support from Ironwood and Horizon; and consulting fees from Ironwood, Selecta, Horizon, Takeda, Kowa, and Vaxart. Dr. Anderson disclosed receiving grants to his institution from Novartis and Milestone.
A version of this article first appeared on Medscape.com.
There is evidence that gout and heart disease are mechanistically linked by inflammation and patients with gout are at elevated risk for cardiovascular disease (CVD). But do gout flares, on their own, affect short-term risk for CV events? A new analysis based on records from British medical practices suggests that might be the case.
Risk for myocardial infarction or stroke climbed in the weeks after individual gout flare-ups in the study’s more than 60,000 patients with a recent gout diagnosis. The jump in risk, significant but small in absolute terms, held for about 4 months in the case-control study before going away.
A sensitivity analysis that excluded patients who already had CVD when their gout was diagnosed yielded similar results.
The observational study isn’t able to show that gout flares themselves transiently raise the risk for MI or stroke, but it’s enough to send a cautionary message to physicians who care for patients with gout, rheumatologist Abhishek Abhishek, PhD, Nottingham (England) City Hospital, said in an interview.
In such patients who also have conditions like hypertension, diabetes, or dyslipidemia, or a history of heart disease, he said, it’s important “to manage risk factors really aggressively, knowing that when these patients have a gout flare, there’s a temporary increase in risk of a cardiovascular event.”
Managing their absolute CV risk – whether with drug therapy, lifestyle changes, or other interventions – should help limit the transient jump in risk for MI or stroke following a gout flare, proposed Dr. Abhishek, who is senior author on the study published in JAMA, with lead author Edoardo Cipolletta, MD, also from Nottingham City Hospital.
First robust evidence
The case-control study, which involved more than 60,000 patients with a recent gout diagnosis, some who went on to have MI or stroke, looked at rates of such events at different time intervals after gout flares. Those who experienced such events showed a more than 90% increased likelihood of a gout flare-up in the preceding 60 days, a greater than 50% chance of a flare between 60 and 120 days before the event, but no increased likelihood prior to 120 days before the event.
Such a link between gout flares and CV events “has been suspected but never proven,” observed rheumatologist Hyon K. Choi, MD, Harvard Medical School, Boston, who was not associated with the analysis. “This is the first time it has actually been shown in a robust way,” he said in an interview.
The study suggests a “likely causative relationship” between gout flares and CV events, but – as the published report noted – has limitations like any observational study, said Dr. Choi, who also directs the Gout & Crystal Arthropathy Center at Massachusetts General Hospital, Boston. “Hopefully, this can be replicated in other cohorts.”
The analysis controlled for a number of relevant potential confounders, he noted, but couldn’t account for all issues that could argue against gout flares as a direct cause of the MIs and strokes.
Gout attacks are a complex experience with a range of potential indirect effects on CV risk, Dr. Choi observed. They can immobilize patients, possibly raising their risk for thrombotic events, for example. They can be exceptionally painful, which causes stress and can lead to frequent or chronic use of glucocorticoids or NSAIDs, all of which can exacerbate high blood pressure and possibly worsen CV risk.
A unique insight
The timing of gout flares relative to acute vascular events hasn’t been fully explored, observed an accompanying editorial. The current study’s “unique insight,” it stated, “is that disease activity from gout was associated with an incremental increase in risk for acute vascular events during the time period immediately following the gout flare.”
Although the study is observational, a “large body of evidence from animal and human research, mechanistic insights, and clinical interventions” support an association between flares and vascular events and “make a causal link eminently reasonable,” stated the editorialists, Jeffrey L. Anderson, MD, and Kirk U. Knowlton, MD, both with Intermountain Medical Center, Salt Lake City, Utah.
The findings, they wrote, “should alert clinicians and patients to the increased cardiovascular risk in the weeks beginning after a gout flare and should focus attention on optimizing preventive measures.” Those can include “lifestyle measures and standard risk-factor control including adherence to diet, statins, anti-inflammatory drugs (e.g., aspirin, colchicine), smoking cessation, diabetic and blood pressure control, and antithrombotic medications as indicated.”
Dr. Choi said the current results argue for more liberal use of colchicine, and for preferring colchicine over other anti-inflammatories, in patients with gout and traditional CV risk factors, given multiple randomized trials supporting the drug’s use in such cases. “If you use colchicine, you are covering their heart disease risk as well as their gout. It’s two birds with one stone.”
Nested case-control study
The investigators accessed electronic health records from 96,153 patients with recently diagnosed gout in England from 1997 to 2020; the cohort’s mean age was about 76 years, and 69% of participants were men. They matched 10,475 patients with at least one CV event to 52,099 others who didn’t have such an event by age, sex, and time from gout diagnosis. In each matched set of patients, those not experiencing a CV event were assigned a flare-to-event interval based on their matching with patients who did experience such an event.
Those with CV events, compared with patients without an event, had a greater than 90% increased likelihood of experiencing a gout flare-up in the 60 days preceding the event, a more than 50% greater chance of a flare-up 60-120 days before the CV event, but no increased likelihood more than 120 days before the event.
A self-controlled case series based on the same overall cohort with gout yielded similar results while sidestepping any potential for residual confounding, an inherent concern with any case–control analysis, the report notes. It involved 1,421 patients with one or more gout flare and at least one MI or stroke after the diagnosis of gout.
Among that cohort, the CV-event incidence rate ratio, adjusted for age and season of the year, by time interval after a gout flare, was 1.89 (95% confidence interval, 1.54-2.30) at 0-60 days, 1.64 (95% CI, 1.45-1.86) at 61-120 days, and1.29 (95% CI, 1.02-1.64) at 121-180 days.
Also similar, the report noted, were results of several sensitivity analyses, including one that excluded patients with confirmed CVD before their gout diagnosis; another that left out patients at low to moderate CV risk; and one that considered only gout flares treated with colchicine, corticosteroids, or NSAIDs.
The incremental CV event risks observed after flares in the study were small, which “has implications for both cost effectiveness and clinical relevance,” observed Dr. Anderson and Dr. Knowlton.
“An alternative to universal augmentation of cardiovascular risk prevention with therapies among patients with gout flares,” they wrote, would be “to further stratify risk by defining a group at highest near-term risk.” Such interventions could potentially be guided by markers of CV risk such as, for example, levels of high-sensitivity C-reactive protein or lipoprotein(a), or plaque burden on coronary-artery calcium scans.
Dr. Abhishek, Dr. Cipolletta, and the other authors reported no competing interests. Dr. Choi disclosed research support from Ironwood and Horizon; and consulting fees from Ironwood, Selecta, Horizon, Takeda, Kowa, and Vaxart. Dr. Anderson disclosed receiving grants to his institution from Novartis and Milestone.
A version of this article first appeared on Medscape.com.
There is evidence that gout and heart disease are mechanistically linked by inflammation and patients with gout are at elevated risk for cardiovascular disease (CVD). But do gout flares, on their own, affect short-term risk for CV events? A new analysis based on records from British medical practices suggests that might be the case.
Risk for myocardial infarction or stroke climbed in the weeks after individual gout flare-ups in the study’s more than 60,000 patients with a recent gout diagnosis. The jump in risk, significant but small in absolute terms, held for about 4 months in the case-control study before going away.
A sensitivity analysis that excluded patients who already had CVD when their gout was diagnosed yielded similar results.
The observational study isn’t able to show that gout flares themselves transiently raise the risk for MI or stroke, but it’s enough to send a cautionary message to physicians who care for patients with gout, rheumatologist Abhishek Abhishek, PhD, Nottingham (England) City Hospital, said in an interview.
In such patients who also have conditions like hypertension, diabetes, or dyslipidemia, or a history of heart disease, he said, it’s important “to manage risk factors really aggressively, knowing that when these patients have a gout flare, there’s a temporary increase in risk of a cardiovascular event.”
Managing their absolute CV risk – whether with drug therapy, lifestyle changes, or other interventions – should help limit the transient jump in risk for MI or stroke following a gout flare, proposed Dr. Abhishek, who is senior author on the study published in JAMA, with lead author Edoardo Cipolletta, MD, also from Nottingham City Hospital.
First robust evidence
The case-control study, which involved more than 60,000 patients with a recent gout diagnosis, some who went on to have MI or stroke, looked at rates of such events at different time intervals after gout flares. Those who experienced such events showed a more than 90% increased likelihood of a gout flare-up in the preceding 60 days, a greater than 50% chance of a flare between 60 and 120 days before the event, but no increased likelihood prior to 120 days before the event.
Such a link between gout flares and CV events “has been suspected but never proven,” observed rheumatologist Hyon K. Choi, MD, Harvard Medical School, Boston, who was not associated with the analysis. “This is the first time it has actually been shown in a robust way,” he said in an interview.
The study suggests a “likely causative relationship” between gout flares and CV events, but – as the published report noted – has limitations like any observational study, said Dr. Choi, who also directs the Gout & Crystal Arthropathy Center at Massachusetts General Hospital, Boston. “Hopefully, this can be replicated in other cohorts.”
The analysis controlled for a number of relevant potential confounders, he noted, but couldn’t account for all issues that could argue against gout flares as a direct cause of the MIs and strokes.
Gout attacks are a complex experience with a range of potential indirect effects on CV risk, Dr. Choi observed. They can immobilize patients, possibly raising their risk for thrombotic events, for example. They can be exceptionally painful, which causes stress and can lead to frequent or chronic use of glucocorticoids or NSAIDs, all of which can exacerbate high blood pressure and possibly worsen CV risk.
A unique insight
The timing of gout flares relative to acute vascular events hasn’t been fully explored, observed an accompanying editorial. The current study’s “unique insight,” it stated, “is that disease activity from gout was associated with an incremental increase in risk for acute vascular events during the time period immediately following the gout flare.”
Although the study is observational, a “large body of evidence from animal and human research, mechanistic insights, and clinical interventions” support an association between flares and vascular events and “make a causal link eminently reasonable,” stated the editorialists, Jeffrey L. Anderson, MD, and Kirk U. Knowlton, MD, both with Intermountain Medical Center, Salt Lake City, Utah.
The findings, they wrote, “should alert clinicians and patients to the increased cardiovascular risk in the weeks beginning after a gout flare and should focus attention on optimizing preventive measures.” Those can include “lifestyle measures and standard risk-factor control including adherence to diet, statins, anti-inflammatory drugs (e.g., aspirin, colchicine), smoking cessation, diabetic and blood pressure control, and antithrombotic medications as indicated.”
Dr. Choi said the current results argue for more liberal use of colchicine, and for preferring colchicine over other anti-inflammatories, in patients with gout and traditional CV risk factors, given multiple randomized trials supporting the drug’s use in such cases. “If you use colchicine, you are covering their heart disease risk as well as their gout. It’s two birds with one stone.”
Nested case-control study
The investigators accessed electronic health records from 96,153 patients with recently diagnosed gout in England from 1997 to 2020; the cohort’s mean age was about 76 years, and 69% of participants were men. They matched 10,475 patients with at least one CV event to 52,099 others who didn’t have such an event by age, sex, and time from gout diagnosis. In each matched set of patients, those not experiencing a CV event were assigned a flare-to-event interval based on their matching with patients who did experience such an event.
Those with CV events, compared with patients without an event, had a greater than 90% increased likelihood of experiencing a gout flare-up in the 60 days preceding the event, a more than 50% greater chance of a flare-up 60-120 days before the CV event, but no increased likelihood more than 120 days before the event.
A self-controlled case series based on the same overall cohort with gout yielded similar results while sidestepping any potential for residual confounding, an inherent concern with any case–control analysis, the report notes. It involved 1,421 patients with one or more gout flare and at least one MI or stroke after the diagnosis of gout.
Among that cohort, the CV-event incidence rate ratio, adjusted for age and season of the year, by time interval after a gout flare, was 1.89 (95% confidence interval, 1.54-2.30) at 0-60 days, 1.64 (95% CI, 1.45-1.86) at 61-120 days, and1.29 (95% CI, 1.02-1.64) at 121-180 days.
Also similar, the report noted, were results of several sensitivity analyses, including one that excluded patients with confirmed CVD before their gout diagnosis; another that left out patients at low to moderate CV risk; and one that considered only gout flares treated with colchicine, corticosteroids, or NSAIDs.
The incremental CV event risks observed after flares in the study were small, which “has implications for both cost effectiveness and clinical relevance,” observed Dr. Anderson and Dr. Knowlton.
“An alternative to universal augmentation of cardiovascular risk prevention with therapies among patients with gout flares,” they wrote, would be “to further stratify risk by defining a group at highest near-term risk.” Such interventions could potentially be guided by markers of CV risk such as, for example, levels of high-sensitivity C-reactive protein or lipoprotein(a), or plaque burden on coronary-artery calcium scans.
Dr. Abhishek, Dr. Cipolletta, and the other authors reported no competing interests. Dr. Choi disclosed research support from Ironwood and Horizon; and consulting fees from Ironwood, Selecta, Horizon, Takeda, Kowa, and Vaxart. Dr. Anderson disclosed receiving grants to his institution from Novartis and Milestone.
A version of this article first appeared on Medscape.com.
FROM JAMA
Is Lp(a) a marker for aortic calcium onset?
Lipoprotein(a) has long been thought to be a potential marker of aortic valve disease, and the population-based Rotterdam Study in the Netherlands has reported that Lp(a) has a strong association with new-onset aortic valve calcium (AVC), but not necessarily with progression of aortic valve disease.
Reporting in the European Heart Journal, the study authors analyzed data on 922 participants in the Rotterdam Study whose Lp(a) was measured along with a computed tomography scan upon enrollment, followed by CT scan 14 years later. At baseline, 702 participants didn’t have AVC, but the follow-up scan identified new-onset AVC in 415 (59.1%).
The investigators found an association between Lp(a) concentration and baseline AVC, with an odds ratio of 1.43 for each 50 mg/dL higher Lp(a) (95% confidence interval, 1.15-1.79), as well as new-onset AVC, with an OR of 1.30 for each 50 mg/dL increase in Lp(a) (95% CI, 1.02-1.65). However, the study found no association between rising Lp(a) levels and AVC progression; it found only an association between baseline AVC score and progression (P < .001).
‘Trigger’ for calcification but not progression
“This suggests that Lp(a) is an important trigger in the initiation of aortic valve calcification, but once the valve is calcified, disease progression may be primarily driven by other factors such as the baseline calcium burden of the valve and likely other unknown factors,” senior study author Daniel Bos, MD, PhD, said in e-mailed comments.
Dr. Bos and coauthors claim this is the first study to show that even minor AVC progresses independently of Lp(a).
“There are previous studies that showed a possible relationship between Lp(a) [and] progression of aortic valve calcium,” he said. “Our study suggests that the most meaningful benefit of Lp(a) lowering may actually be prior to the onset of aortic valve calcification.”
While no treatments have been approved for lowering Lp(a), the study findings could be meaningful if trials, including the ongoing phase 3 Lp(a) HORIZON trial of the investigational antisense agent pelacarsen (NCT04023552), show promising results, Dr. Bos said. Citing Lp(a) HORIZON, he said, “If the study shows Lp(a) lowering leads to a reduction in incident cardiovascular disease, similar strategies may be applied to prevent, rather than slow down, progression of aortic valve calcification.”
Dr. Bos called the Rotterdam Study results “an important first pointer into that direction.” He added, “We will need randomized trials to provide a definitive answer to the question whether Lp(a) lowering may prevent aortic valve calcium.”
Focus on AVC is study ‘weakness’
The study findings raise a key question for clinical trials of investigative Lp(a)-lowering therapies as well as how to use those therapies to treat aortic valve disease, said Christie Ballantyne, MD, chief of cardiology at Baylor College of Medicine in Houston.
The findings could be “problematic” for these clinical trials, he said. “This study is just looking at calcium progression,” Dr. Ballantyne noted. “What we want to know about clinically is the progression to aortic stenosis, and then in particular to progression from mild disease to moderate or severe disease, because once you get into more severe disease, one has to do an intervention with either surgery or TAVR [transcatheter aortic valve replacement].”
He considered the study’s focus on AVC rather than aortic valve function a weakness and noted that only 14 study participants had TAVR. “We’re going to need much bigger numbers to look into this question of progression, including progression to severe diseases,” he said.
However, the Rotterdam Study showed the importance of CT in evaluating AVC, which can easily be done in other trials to further explore the association between Lp(a) and AVC, Dr. Ballantyne said.
Dr. Bos has no relevant disclosures. Study coauthors disclosed relationships with Amgen, Sanofi, Reservlogix, Athera, Experio, Novartis and Ionis Pharmaceuticals. Dr. Ballantyne disclosed relationships with Amgen and Novartis.
Lipoprotein(a) has long been thought to be a potential marker of aortic valve disease, and the population-based Rotterdam Study in the Netherlands has reported that Lp(a) has a strong association with new-onset aortic valve calcium (AVC), but not necessarily with progression of aortic valve disease.
Reporting in the European Heart Journal, the study authors analyzed data on 922 participants in the Rotterdam Study whose Lp(a) was measured along with a computed tomography scan upon enrollment, followed by CT scan 14 years later. At baseline, 702 participants didn’t have AVC, but the follow-up scan identified new-onset AVC in 415 (59.1%).
The investigators found an association between Lp(a) concentration and baseline AVC, with an odds ratio of 1.43 for each 50 mg/dL higher Lp(a) (95% confidence interval, 1.15-1.79), as well as new-onset AVC, with an OR of 1.30 for each 50 mg/dL increase in Lp(a) (95% CI, 1.02-1.65). However, the study found no association between rising Lp(a) levels and AVC progression; it found only an association between baseline AVC score and progression (P < .001).
‘Trigger’ for calcification but not progression
“This suggests that Lp(a) is an important trigger in the initiation of aortic valve calcification, but once the valve is calcified, disease progression may be primarily driven by other factors such as the baseline calcium burden of the valve and likely other unknown factors,” senior study author Daniel Bos, MD, PhD, said in e-mailed comments.
Dr. Bos and coauthors claim this is the first study to show that even minor AVC progresses independently of Lp(a).
“There are previous studies that showed a possible relationship between Lp(a) [and] progression of aortic valve calcium,” he said. “Our study suggests that the most meaningful benefit of Lp(a) lowering may actually be prior to the onset of aortic valve calcification.”
While no treatments have been approved for lowering Lp(a), the study findings could be meaningful if trials, including the ongoing phase 3 Lp(a) HORIZON trial of the investigational antisense agent pelacarsen (NCT04023552), show promising results, Dr. Bos said. Citing Lp(a) HORIZON, he said, “If the study shows Lp(a) lowering leads to a reduction in incident cardiovascular disease, similar strategies may be applied to prevent, rather than slow down, progression of aortic valve calcification.”
Dr. Bos called the Rotterdam Study results “an important first pointer into that direction.” He added, “We will need randomized trials to provide a definitive answer to the question whether Lp(a) lowering may prevent aortic valve calcium.”
Focus on AVC is study ‘weakness’
The study findings raise a key question for clinical trials of investigative Lp(a)-lowering therapies as well as how to use those therapies to treat aortic valve disease, said Christie Ballantyne, MD, chief of cardiology at Baylor College of Medicine in Houston.
The findings could be “problematic” for these clinical trials, he said. “This study is just looking at calcium progression,” Dr. Ballantyne noted. “What we want to know about clinically is the progression to aortic stenosis, and then in particular to progression from mild disease to moderate or severe disease, because once you get into more severe disease, one has to do an intervention with either surgery or TAVR [transcatheter aortic valve replacement].”
He considered the study’s focus on AVC rather than aortic valve function a weakness and noted that only 14 study participants had TAVR. “We’re going to need much bigger numbers to look into this question of progression, including progression to severe diseases,” he said.
However, the Rotterdam Study showed the importance of CT in evaluating AVC, which can easily be done in other trials to further explore the association between Lp(a) and AVC, Dr. Ballantyne said.
Dr. Bos has no relevant disclosures. Study coauthors disclosed relationships with Amgen, Sanofi, Reservlogix, Athera, Experio, Novartis and Ionis Pharmaceuticals. Dr. Ballantyne disclosed relationships with Amgen and Novartis.
Lipoprotein(a) has long been thought to be a potential marker of aortic valve disease, and the population-based Rotterdam Study in the Netherlands has reported that Lp(a) has a strong association with new-onset aortic valve calcium (AVC), but not necessarily with progression of aortic valve disease.
Reporting in the European Heart Journal, the study authors analyzed data on 922 participants in the Rotterdam Study whose Lp(a) was measured along with a computed tomography scan upon enrollment, followed by CT scan 14 years later. At baseline, 702 participants didn’t have AVC, but the follow-up scan identified new-onset AVC in 415 (59.1%).
The investigators found an association between Lp(a) concentration and baseline AVC, with an odds ratio of 1.43 for each 50 mg/dL higher Lp(a) (95% confidence interval, 1.15-1.79), as well as new-onset AVC, with an OR of 1.30 for each 50 mg/dL increase in Lp(a) (95% CI, 1.02-1.65). However, the study found no association between rising Lp(a) levels and AVC progression; it found only an association between baseline AVC score and progression (P < .001).
‘Trigger’ for calcification but not progression
“This suggests that Lp(a) is an important trigger in the initiation of aortic valve calcification, but once the valve is calcified, disease progression may be primarily driven by other factors such as the baseline calcium burden of the valve and likely other unknown factors,” senior study author Daniel Bos, MD, PhD, said in e-mailed comments.
Dr. Bos and coauthors claim this is the first study to show that even minor AVC progresses independently of Lp(a).
“There are previous studies that showed a possible relationship between Lp(a) [and] progression of aortic valve calcium,” he said. “Our study suggests that the most meaningful benefit of Lp(a) lowering may actually be prior to the onset of aortic valve calcification.”
While no treatments have been approved for lowering Lp(a), the study findings could be meaningful if trials, including the ongoing phase 3 Lp(a) HORIZON trial of the investigational antisense agent pelacarsen (NCT04023552), show promising results, Dr. Bos said. Citing Lp(a) HORIZON, he said, “If the study shows Lp(a) lowering leads to a reduction in incident cardiovascular disease, similar strategies may be applied to prevent, rather than slow down, progression of aortic valve calcification.”
Dr. Bos called the Rotterdam Study results “an important first pointer into that direction.” He added, “We will need randomized trials to provide a definitive answer to the question whether Lp(a) lowering may prevent aortic valve calcium.”
Focus on AVC is study ‘weakness’
The study findings raise a key question for clinical trials of investigative Lp(a)-lowering therapies as well as how to use those therapies to treat aortic valve disease, said Christie Ballantyne, MD, chief of cardiology at Baylor College of Medicine in Houston.
The findings could be “problematic” for these clinical trials, he said. “This study is just looking at calcium progression,” Dr. Ballantyne noted. “What we want to know about clinically is the progression to aortic stenosis, and then in particular to progression from mild disease to moderate or severe disease, because once you get into more severe disease, one has to do an intervention with either surgery or TAVR [transcatheter aortic valve replacement].”
He considered the study’s focus on AVC rather than aortic valve function a weakness and noted that only 14 study participants had TAVR. “We’re going to need much bigger numbers to look into this question of progression, including progression to severe diseases,” he said.
However, the Rotterdam Study showed the importance of CT in evaluating AVC, which can easily be done in other trials to further explore the association between Lp(a) and AVC, Dr. Ballantyne said.
Dr. Bos has no relevant disclosures. Study coauthors disclosed relationships with Amgen, Sanofi, Reservlogix, Athera, Experio, Novartis and Ionis Pharmaceuticals. Dr. Ballantyne disclosed relationships with Amgen and Novartis.
FROM THE EUROPEAN HEART JOURNAL
Six specialties attracting the highest private equity acquisitions
While tracking the extent of physician practice acquisition by private equity firms may be difficult, new research highlights what specialties and U.S. regions are most affected by such purchases.
The study, supported by the National Institute for Health Care Management (NIHCM), examined 97,094 physicians practicing in six specialties, 4,738 of whom worked in private equity–acquired practices. Of these specialties, 
“These specialties offer private equity firms diverse revenue streams. You have a mix of commercially insured individuals with Medicare insurance and self-pay,” said Yashaswini Singh, MPA, a doctoral student at the Johns Hopkins Bloomberg School of Public Health, Baltimore, and coauthor of the study, which was published in JAMA Health Forum as a research letter.
“In dermatology, you have a mix of surgical procedures that are covered under insurance, but also a lot of cosmetic procedures that are most likely to be self-pay procedures. This offers private equity several mechanisms to which they can increase their revenues.”
Ms. Singh’s coauthors were part of a previous study looking at private practice penetration by private equity firms. That research found such deals surged from 59 deals in 2013 representing 843 physicians, to 136 private equity acquisition deals representing 1,882 physicians in 2016.
The most recent study notes limited data and use of nondisclosure agreements during early negotiations as part of the difficulty in truly pinpointing private equity’s presence in health care. Monitoring private equity activity has become necessary across all industries, noted the authors of the study. If continued at this rate, long-term private equity acquisition has a multitude of potential pros and cons.
Ms. Singh explained that such specialties are highly fragmented and they allow for economies of scale and scope. In particular, an aging population increases demand for dermatology, ophthalmology, and gastroenterology services such as skin biopsies, cataracts, and colonoscopies. This makes these specialties very attractive to private equity firms. The same can be said for obstetrics and gynecology, as fertility clinics have attracted many private equity investments.
“This is another area where understanding changes to physician practice patterns and patient outcomes is critical as women continue to delay motherhood,” said Ms. Singh.
Reducing competition, increasing focus on patient care
Researchers found significant geographical trends for private equity penetration, as it varies across the country. It is highest in the Northeast, Florida, and Arizona in hospital referral regions. Researchers are still analyzing the cause of this occurrence.
Geographic concentration of private equity penetration likely reflects strategic selection of investment opportunities by private equity funds as the decision to invest in a practice does not happen at random, Ms. Singh noted.
Ms. Singh said she hopes that by documenting a variation and geographic concentration that the NIHCM is providing the first foundational step to tackle questions related to incentives and regulations that facilitate investment.
“Understanding the regulatory and economic environments that facilitate private equity activity is an interesting and important question to explore further,” she said in an interview. “This can include supply-side factors that can shape the business environment, e.g., taxation environment, regulatory burden to complete acquisitions, as well as demand-side factors that facilitate growth.”
Researchers found that continued growth of private equity penetration may lead to consolidation among independent practices facing financial pressures, as well as reduced competition and increased prices within each local health care market.
“Localized consolidation in certain markets has the potential for competition to reduce, [and] reduced competition has been shown in a variety of settings to be associated with increases in prices and reduced access for patients,” said Ms. Singh.
Conversely, Ms. Singh addressed several benefits of growing private equity presence. Companies can exploit their full potential through the addition of private equity expertise and contacts. Specifically, health care development of technological infrastructure is likely, along with reduced patient wait times and the expansion of business hours. It could also be a way for practices to offload administrative responsibilities and for physicians to focus more on the care delivery process.
A version of this article first appeared on Medscape.com.
While tracking the extent of physician practice acquisition by private equity firms may be difficult, new research highlights what specialties and U.S. regions are most affected by such purchases.
The study, supported by the National Institute for Health Care Management (NIHCM), examined 97,094 physicians practicing in six specialties, 4,738 of whom worked in private equity–acquired practices. Of these specialties,
“These specialties offer private equity firms diverse revenue streams. You have a mix of commercially insured individuals with Medicare insurance and self-pay,” said Yashaswini Singh, MPA, a doctoral student at the Johns Hopkins Bloomberg School of Public Health, Baltimore, and coauthor of the study, which was published in JAMA Health Forum as a research letter.
“In dermatology, you have a mix of surgical procedures that are covered under insurance, but also a lot of cosmetic procedures that are most likely to be self-pay procedures. This offers private equity several mechanisms to which they can increase their revenues.”
Ms. Singh’s coauthors were part of a previous study looking at private practice penetration by private equity firms. That research found such deals surged from 59 deals in 2013 representing 843 physicians, to 136 private equity acquisition deals representing 1,882 physicians in 2016.
The most recent study notes limited data and use of nondisclosure agreements during early negotiations as part of the difficulty in truly pinpointing private equity’s presence in health care. Monitoring private equity activity has become necessary across all industries, noted the authors of the study. If continued at this rate, long-term private equity acquisition has a multitude of potential pros and cons.
Ms. Singh explained that such specialties are highly fragmented and they allow for economies of scale and scope. In particular, an aging population increases demand for dermatology, ophthalmology, and gastroenterology services such as skin biopsies, cataracts, and colonoscopies. This makes these specialties very attractive to private equity firms. The same can be said for obstetrics and gynecology, as fertility clinics have attracted many private equity investments.
“This is another area where understanding changes to physician practice patterns and patient outcomes is critical as women continue to delay motherhood,” said Ms. Singh.
Reducing competition, increasing focus on patient care
Researchers found significant geographical trends for private equity penetration, as it varies across the country. It is highest in the Northeast, Florida, and Arizona in hospital referral regions. Researchers are still analyzing the cause of this occurrence.
Geographic concentration of private equity penetration likely reflects strategic selection of investment opportunities by private equity funds as the decision to invest in a practice does not happen at random, Ms. Singh noted.
Ms. Singh said she hopes that by documenting a variation and geographic concentration that the NIHCM is providing the first foundational step to tackle questions related to incentives and regulations that facilitate investment.
“Understanding the regulatory and economic environments that facilitate private equity activity is an interesting and important question to explore further,” she said in an interview. “This can include supply-side factors that can shape the business environment, e.g., taxation environment, regulatory burden to complete acquisitions, as well as demand-side factors that facilitate growth.”
Researchers found that continued growth of private equity penetration may lead to consolidation among independent practices facing financial pressures, as well as reduced competition and increased prices within each local health care market.
“Localized consolidation in certain markets has the potential for competition to reduce, [and] reduced competition has been shown in a variety of settings to be associated with increases in prices and reduced access for patients,” said Ms. Singh.
Conversely, Ms. Singh addressed several benefits of growing private equity presence. Companies can exploit their full potential through the addition of private equity expertise and contacts. Specifically, health care development of technological infrastructure is likely, along with reduced patient wait times and the expansion of business hours. It could also be a way for practices to offload administrative responsibilities and for physicians to focus more on the care delivery process.
A version of this article first appeared on Medscape.com.
While tracking the extent of physician practice acquisition by private equity firms may be difficult, new research highlights what specialties and U.S. regions are most affected by such purchases.
The study, supported by the National Institute for Health Care Management (NIHCM), examined 97,094 physicians practicing in six specialties, 4,738 of whom worked in private equity–acquired practices. Of these specialties,
“These specialties offer private equity firms diverse revenue streams. You have a mix of commercially insured individuals with Medicare insurance and self-pay,” said Yashaswini Singh, MPA, a doctoral student at the Johns Hopkins Bloomberg School of Public Health, Baltimore, and coauthor of the study, which was published in JAMA Health Forum as a research letter.
“In dermatology, you have a mix of surgical procedures that are covered under insurance, but also a lot of cosmetic procedures that are most likely to be self-pay procedures. This offers private equity several mechanisms to which they can increase their revenues.”
Ms. Singh’s coauthors were part of a previous study looking at private practice penetration by private equity firms. That research found such deals surged from 59 deals in 2013 representing 843 physicians, to 136 private equity acquisition deals representing 1,882 physicians in 2016.
The most recent study notes limited data and use of nondisclosure agreements during early negotiations as part of the difficulty in truly pinpointing private equity’s presence in health care. Monitoring private equity activity has become necessary across all industries, noted the authors of the study. If continued at this rate, long-term private equity acquisition has a multitude of potential pros and cons.
Ms. Singh explained that such specialties are highly fragmented and they allow for economies of scale and scope. In particular, an aging population increases demand for dermatology, ophthalmology, and gastroenterology services such as skin biopsies, cataracts, and colonoscopies. This makes these specialties very attractive to private equity firms. The same can be said for obstetrics and gynecology, as fertility clinics have attracted many private equity investments.
“This is another area where understanding changes to physician practice patterns and patient outcomes is critical as women continue to delay motherhood,” said Ms. Singh.
Reducing competition, increasing focus on patient care
Researchers found significant geographical trends for private equity penetration, as it varies across the country. It is highest in the Northeast, Florida, and Arizona in hospital referral regions. Researchers are still analyzing the cause of this occurrence.
Geographic concentration of private equity penetration likely reflects strategic selection of investment opportunities by private equity funds as the decision to invest in a practice does not happen at random, Ms. Singh noted.
Ms. Singh said she hopes that by documenting a variation and geographic concentration that the NIHCM is providing the first foundational step to tackle questions related to incentives and regulations that facilitate investment.
“Understanding the regulatory and economic environments that facilitate private equity activity is an interesting and important question to explore further,” she said in an interview. “This can include supply-side factors that can shape the business environment, e.g., taxation environment, regulatory burden to complete acquisitions, as well as demand-side factors that facilitate growth.”
Researchers found that continued growth of private equity penetration may lead to consolidation among independent practices facing financial pressures, as well as reduced competition and increased prices within each local health care market.
“Localized consolidation in certain markets has the potential for competition to reduce, [and] reduced competition has been shown in a variety of settings to be associated with increases in prices and reduced access for patients,” said Ms. Singh.
Conversely, Ms. Singh addressed several benefits of growing private equity presence. Companies can exploit their full potential through the addition of private equity expertise and contacts. Specifically, health care development of technological infrastructure is likely, along with reduced patient wait times and the expansion of business hours. It could also be a way for practices to offload administrative responsibilities and for physicians to focus more on the care delivery process.
A version of this article first appeared on Medscape.com.
FROM JAMA HEALTH FORUM