MDedge Cardiology

Americans gained nearly 2 pounds per month under COVID-19 shelter-in-place orders in 2020, according to a new study published March 22, 2021, in JAMA Network Open.

Those who kept the same lockdown habits could have gained 20 pounds during the past year, the study authors said.

“We know that weight gain is a public health problem in the U.S. already, so anything making it worse is definitely concerning, and shelter-in-place orders are so ubiquitous that the sheer number of people affected by this makes it extremely relevant,” Gregory Marcus, MD, the senior author and a cardiologist at the University of California, San Francisco, told the New York Times.

Dr. Marcus and colleagues analyzed more than 7,000 weight measurements from 269 people in 37 states who used Bluetooth-connected scales from Feb. 1 to June 1, 2020. Among the participants, about 52% were women, 77% were White, and they had an average age of 52 years.

The research team found that participants had a steady weight gain of more than half a pound every 10 days. That equals about 1.5-2 pounds per month.

Many of the participants were losing weight before the shelter-in-place orders went into effect, Dr. Marcus said. The lockdown effects could be even greater for those who weren’t losing weight before.

“It’s reasonable to assume these individuals are more engaged with their health in general, and more disciplined and on top of things,” he said. “That suggests we could be underestimating – that this is the tip of the iceberg.”

The small study doesn’t represent all of the nation and can’t be generalized to the U.S. population, the study authors noted, but it’s an indicator of what happened during the pandemic. The participants’ weight increased regardless of their location and chronic medical conditions.

Overall, people don’t move around as much during lockdowns, the UCSF researchers reported in another study published in Annals of Internal Medicine in November 2020. According to smartphone data, daily step counts decreased by 27% in March 2020. The step counts increased again throughout the summer but still remained lower than before the COVID-19 pandemic.

“The detrimental health outcomes suggested by these data demonstrate a need to identify concurrent strategies to mitigate weight gain,” the authors wrote in the JAMA Network Open study, “such as encouraging healthy diets and exploring ways to enhance physical activity, as local governments consider new constraints in response to SARS-CoV-2 and potential future pandemics.”

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

Americans gained nearly 2 pounds per month under COVID-19 shelter-in-place orders in 2020, according to a new study published March 22, 2021, in JAMA Network Open.

Those who kept the same lockdown habits could have gained 20 pounds during the past year, the study authors said.

“We know that weight gain is a public health problem in the U.S. already, so anything making it worse is definitely concerning, and shelter-in-place orders are so ubiquitous that the sheer number of people affected by this makes it extremely relevant,” Gregory Marcus, MD, the senior author and a cardiologist at the University of California, San Francisco, told the New York Times.

Dr. Marcus and colleagues analyzed more than 7,000 weight measurements from 269 people in 37 states who used Bluetooth-connected scales from Feb. 1 to June 1, 2020. Among the participants, about 52% were women, 77% were White, and they had an average age of 52 years.

The research team found that participants had a steady weight gain of more than half a pound every 10 days. That equals about 1.5-2 pounds per month.

Many of the participants were losing weight before the shelter-in-place orders went into effect, Dr. Marcus said. The lockdown effects could be even greater for those who weren’t losing weight before.

“It’s reasonable to assume these individuals are more engaged with their health in general, and more disciplined and on top of things,” he said. “That suggests we could be underestimating – that this is the tip of the iceberg.”

The small study doesn’t represent all of the nation and can’t be generalized to the U.S. population, the study authors noted, but it’s an indicator of what happened during the pandemic. The participants’ weight increased regardless of their location and chronic medical conditions.

Overall, people don’t move around as much during lockdowns, the UCSF researchers reported in another study published in Annals of Internal Medicine in November 2020. According to smartphone data, daily step counts decreased by 27% in March 2020. The step counts increased again throughout the summer but still remained lower than before the COVID-19 pandemic.

“The detrimental health outcomes suggested by these data demonstrate a need to identify concurrent strategies to mitigate weight gain,” the authors wrote in the JAMA Network Open study, “such as encouraging healthy diets and exploring ways to enhance physical activity, as local governments consider new constraints in response to SARS-CoV-2 and potential future pandemics.”

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

Americans gained nearly 2 pounds per month under COVID-19 shelter-in-place orders in 2020, according to a new study published March 22, 2021, in JAMA Network Open.

Those who kept the same lockdown habits could have gained 20 pounds during the past year, the study authors said.

“We know that weight gain is a public health problem in the U.S. already, so anything making it worse is definitely concerning, and shelter-in-place orders are so ubiquitous that the sheer number of people affected by this makes it extremely relevant,” Gregory Marcus, MD, the senior author and a cardiologist at the University of California, San Francisco, told the New York Times.

Dr. Marcus and colleagues analyzed more than 7,000 weight measurements from 269 people in 37 states who used Bluetooth-connected scales from Feb. 1 to June 1, 2020. Among the participants, about 52% were women, 77% were White, and they had an average age of 52 years.

The research team found that participants had a steady weight gain of more than half a pound every 10 days. That equals about 1.5-2 pounds per month.

Many of the participants were losing weight before the shelter-in-place orders went into effect, Dr. Marcus said. The lockdown effects could be even greater for those who weren’t losing weight before.

“It’s reasonable to assume these individuals are more engaged with their health in general, and more disciplined and on top of things,” he said. “That suggests we could be underestimating – that this is the tip of the iceberg.”

The small study doesn’t represent all of the nation and can’t be generalized to the U.S. population, the study authors noted, but it’s an indicator of what happened during the pandemic. The participants’ weight increased regardless of their location and chronic medical conditions.

Overall, people don’t move around as much during lockdowns, the UCSF researchers reported in another study published in Annals of Internal Medicine in November 2020. According to smartphone data, daily step counts decreased by 27% in March 2020. The step counts increased again throughout the summer but still remained lower than before the COVID-19 pandemic.

“The detrimental health outcomes suggested by these data demonstrate a need to identify concurrent strategies to mitigate weight gain,” the authors wrote in the JAMA Network Open study, “such as encouraging healthy diets and exploring ways to enhance physical activity, as local governments consider new constraints in response to SARS-CoV-2 and potential future pandemics.”

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

Higher levels of vitamin D than traditionally considered sufficient may help prevent COVID-19 infection – particularly in Black patients, shows a new single-center, retrospective study looking at the role of vitamin D in prevention of infection.

The study, published recently in JAMA Network Open, noted that expert opinion varies as to what “sufficient” levels of vitamin D are, some define this as 30 ng/mL, while others cite 40 ng/mL or greater.

In their discussion, the authors also noted that their results showed the “risk of positive COVID-19 test results decreased significantly with increased vitamin D level of 30 ng/mL or greater when measured as a continuous variable.”

“These new results tell us that having vitamin D levels above those normally considered sufficient is associated with decreased risk of testing positive for COVID-19, at least in Black individuals,” lead author, David Meltzer, MD, chief of hospital medicine at the University of Chicago, said in a press release from his institution.

“These findings suggest that randomized clinical trials to determine whether increasing vitamin D levels to greater than 30-40 ng/mL affect COVID-19 risk are warranted, especially in Black individuals,” he and his coauthors said.
 

Vitamin D at time of testing most strongly associated with COVID risk

An earlier study by the same researchers found that vitamin D deficiency (less than 20 ng/mL) may raise the risk of testing positive for COVID-19 in people from various ethnicities, as reported by this news organization.

Data for this latest study were drawn from electronic health records for 4,638 individuals at the University of Chicago Medicine and were used to examine whether the likelihood of a positive COVID-19 test was associated with a person’s most recent vitamin D level (within the previous year), and whether there was any effect of ethnicity on this outcome.

Mean age was 52.8 years, 69% were women, 49% were Black, 43% White, and 8% were another race/ethnicity. A total of 27% of the individuals were deficient in vitamin D (less than 20 ng/mL), 27% had insufficient levels (20-30 ng/mL), 22% had sufficient levels (30-40 ng/mL), and the remaining 24% had levels of 40 ng/mL or greater.

In total, 333 (7%) of people tested positive for COVID-19, including 102 (5%) Whites and 211 (9%) Blacks. And 36% of Black individuals who tested positive for COVID-19 were classified as vitamin D deficient, compared with 16% of Whites.

A positive test result for COVID-19 was not significantly associated with vitamin D levels in white individuals but was in Black individuals.

In Black people, compared with levels of at least 40 ng/mL, vitamin D levels of 30-40 ng/mL were associated with an incidence rate ratio of 2.64 for COVID-19 positivity (P = .01). For levels of 20-30 ng/mL, the IRR was 1.69 (P = 0.21); and for less than 20 ng/mL the IRR was 2.55 (P = .009).

The researchers also found that the risk of positive test results with lower vitamin D levels increased when those levels were lower just prior to the positive COVID-19 test, lending “support [to] the idea that vitamin D level at the time of testing is most strongly associated with COVID-19 risk,” they wrote.
 

Try upping vitamin D levels to 40 ng/mL or greater to prevent COVID?

In their discussion, the authors noted that significant association of vitamin D levels with COVID-19 risk in Blacks but not in Whites, “could reflect their higher COVID-19 risk, to which socioeconomic factors and structural inequities clearly contribute.

“Biological susceptibility to vitamin D deficiency may also be less frequent in White than Black individuals, since lighter skin increases vitamin D production in response to sunlight, and vitamin D binding proteins may vary by race and affect vitamin D bioavailability.”

Given less than 10% of U.S. adults have a vitamin D level greater than 40 ng/mL, the study findings increase the urgency to consider whether increased sun exposure or supplementation could reduce COVID-19 risk, according to the authors.

“When increased sun exposure is impractical, achieving vitamin D levels of 40 ng/mL or greater typically requires greater supplementation than currently recommended for most individuals of 600-800 IU/d vitamin D3,” they added.

However, Dr. Meltzer also acknowledged that “this is an observational study. We can see that there’s an association between vitamin D levels and likelihood of a COVID-19 diagnosis, but we don’t know exactly why that is, or whether these results are due to the vitamin D directly or other related biological factors.”

All in all, the authors suggested that randomized clinical trials are needed to understand if vitamin D can reduce COVID-19 risk, and as such they should include doses of supplements likely to increase vitamin D to at least 40 ng/mL, and perhaps even higher, although they pointed out that the latter must be achieved safely.

“Studies should also consider the role of vitamin D testing, loading doses, dose adjustments for individuals who are obese or overweight, risks for hypercalcemia, and strategies to monitor for and mitigate hypercalcemia, and that non-White populations, such as Black individuals, may have greater needs for supplementation,” they outlined.

They are now recruiting participants for two separate clinical trials testing the efficacy of vitamin D supplements for preventing COVID-19.

The authors disclosed no relevant financial relationships.

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

Higher levels of vitamin D than traditionally considered sufficient may help prevent COVID-19 infection – particularly in Black patients, shows a new single-center, retrospective study looking at the role of vitamin D in prevention of infection.

The study, published recently in JAMA Network Open, noted that expert opinion varies as to what “sufficient” levels of vitamin D are, some define this as 30 ng/mL, while others cite 40 ng/mL or greater.

In their discussion, the authors also noted that their results showed the “risk of positive COVID-19 test results decreased significantly with increased vitamin D level of 30 ng/mL or greater when measured as a continuous variable.”

“These new results tell us that having vitamin D levels above those normally considered sufficient is associated with decreased risk of testing positive for COVID-19, at least in Black individuals,” lead author, David Meltzer, MD, chief of hospital medicine at the University of Chicago, said in a press release from his institution.

“These findings suggest that randomized clinical trials to determine whether increasing vitamin D levels to greater than 30-40 ng/mL affect COVID-19 risk are warranted, especially in Black individuals,” he and his coauthors said.
 

Vitamin D at time of testing most strongly associated with COVID risk

An earlier study by the same researchers found that vitamin D deficiency (less than 20 ng/mL) may raise the risk of testing positive for COVID-19 in people from various ethnicities, as reported by this news organization.

Data for this latest study were drawn from electronic health records for 4,638 individuals at the University of Chicago Medicine and were used to examine whether the likelihood of a positive COVID-19 test was associated with a person’s most recent vitamin D level (within the previous year), and whether there was any effect of ethnicity on this outcome.

Mean age was 52.8 years, 69% were women, 49% were Black, 43% White, and 8% were another race/ethnicity. A total of 27% of the individuals were deficient in vitamin D (less than 20 ng/mL), 27% had insufficient levels (20-30 ng/mL), 22% had sufficient levels (30-40 ng/mL), and the remaining 24% had levels of 40 ng/mL or greater.

In total, 333 (7%) of people tested positive for COVID-19, including 102 (5%) Whites and 211 (9%) Blacks. And 36% of Black individuals who tested positive for COVID-19 were classified as vitamin D deficient, compared with 16% of Whites.

A positive test result for COVID-19 was not significantly associated with vitamin D levels in white individuals but was in Black individuals.

In Black people, compared with levels of at least 40 ng/mL, vitamin D levels of 30-40 ng/mL were associated with an incidence rate ratio of 2.64 for COVID-19 positivity (P = .01). For levels of 20-30 ng/mL, the IRR was 1.69 (P = 0.21); and for less than 20 ng/mL the IRR was 2.55 (P = .009).

The researchers also found that the risk of positive test results with lower vitamin D levels increased when those levels were lower just prior to the positive COVID-19 test, lending “support [to] the idea that vitamin D level at the time of testing is most strongly associated with COVID-19 risk,” they wrote.
 

Try upping vitamin D levels to 40 ng/mL or greater to prevent COVID?

In their discussion, the authors noted that significant association of vitamin D levels with COVID-19 risk in Blacks but not in Whites, “could reflect their higher COVID-19 risk, to which socioeconomic factors and structural inequities clearly contribute.

“Biological susceptibility to vitamin D deficiency may also be less frequent in White than Black individuals, since lighter skin increases vitamin D production in response to sunlight, and vitamin D binding proteins may vary by race and affect vitamin D bioavailability.”

Given less than 10% of U.S. adults have a vitamin D level greater than 40 ng/mL, the study findings increase the urgency to consider whether increased sun exposure or supplementation could reduce COVID-19 risk, according to the authors.

“When increased sun exposure is impractical, achieving vitamin D levels of 40 ng/mL or greater typically requires greater supplementation than currently recommended for most individuals of 600-800 IU/d vitamin D3,” they added.

However, Dr. Meltzer also acknowledged that “this is an observational study. We can see that there’s an association between vitamin D levels and likelihood of a COVID-19 diagnosis, but we don’t know exactly why that is, or whether these results are due to the vitamin D directly or other related biological factors.”

All in all, the authors suggested that randomized clinical trials are needed to understand if vitamin D can reduce COVID-19 risk, and as such they should include doses of supplements likely to increase vitamin D to at least 40 ng/mL, and perhaps even higher, although they pointed out that the latter must be achieved safely.

“Studies should also consider the role of vitamin D testing, loading doses, dose adjustments for individuals who are obese or overweight, risks for hypercalcemia, and strategies to monitor for and mitigate hypercalcemia, and that non-White populations, such as Black individuals, may have greater needs for supplementation,” they outlined.

They are now recruiting participants for two separate clinical trials testing the efficacy of vitamin D supplements for preventing COVID-19.

The authors disclosed no relevant financial relationships.

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

Higher levels of vitamin D than traditionally considered sufficient may help prevent COVID-19 infection – particularly in Black patients, shows a new single-center, retrospective study looking at the role of vitamin D in prevention of infection.

The study, published recently in JAMA Network Open, noted that expert opinion varies as to what “sufficient” levels of vitamin D are, some define this as 30 ng/mL, while others cite 40 ng/mL or greater.

In their discussion, the authors also noted that their results showed the “risk of positive COVID-19 test results decreased significantly with increased vitamin D level of 30 ng/mL or greater when measured as a continuous variable.”

“These new results tell us that having vitamin D levels above those normally considered sufficient is associated with decreased risk of testing positive for COVID-19, at least in Black individuals,” lead author, David Meltzer, MD, chief of hospital medicine at the University of Chicago, said in a press release from his institution.

“These findings suggest that randomized clinical trials to determine whether increasing vitamin D levels to greater than 30-40 ng/mL affect COVID-19 risk are warranted, especially in Black individuals,” he and his coauthors said.
 

Vitamin D at time of testing most strongly associated with COVID risk

An earlier study by the same researchers found that vitamin D deficiency (less than 20 ng/mL) may raise the risk of testing positive for COVID-19 in people from various ethnicities, as reported by this news organization.

Data for this latest study were drawn from electronic health records for 4,638 individuals at the University of Chicago Medicine and were used to examine whether the likelihood of a positive COVID-19 test was associated with a person’s most recent vitamin D level (within the previous year), and whether there was any effect of ethnicity on this outcome.

Mean age was 52.8 years, 69% were women, 49% were Black, 43% White, and 8% were another race/ethnicity. A total of 27% of the individuals were deficient in vitamin D (less than 20 ng/mL), 27% had insufficient levels (20-30 ng/mL), 22% had sufficient levels (30-40 ng/mL), and the remaining 24% had levels of 40 ng/mL or greater.

In total, 333 (7%) of people tested positive for COVID-19, including 102 (5%) Whites and 211 (9%) Blacks. And 36% of Black individuals who tested positive for COVID-19 were classified as vitamin D deficient, compared with 16% of Whites.

A positive test result for COVID-19 was not significantly associated with vitamin D levels in white individuals but was in Black individuals.

In Black people, compared with levels of at least 40 ng/mL, vitamin D levels of 30-40 ng/mL were associated with an incidence rate ratio of 2.64 for COVID-19 positivity (P = .01). For levels of 20-30 ng/mL, the IRR was 1.69 (P = 0.21); and for less than 20 ng/mL the IRR was 2.55 (P = .009).

The researchers also found that the risk of positive test results with lower vitamin D levels increased when those levels were lower just prior to the positive COVID-19 test, lending “support [to] the idea that vitamin D level at the time of testing is most strongly associated with COVID-19 risk,” they wrote.
 

Try upping vitamin D levels to 40 ng/mL or greater to prevent COVID?

In their discussion, the authors noted that significant association of vitamin D levels with COVID-19 risk in Blacks but not in Whites, “could reflect their higher COVID-19 risk, to which socioeconomic factors and structural inequities clearly contribute.

“Biological susceptibility to vitamin D deficiency may also be less frequent in White than Black individuals, since lighter skin increases vitamin D production in response to sunlight, and vitamin D binding proteins may vary by race and affect vitamin D bioavailability.”

Given less than 10% of U.S. adults have a vitamin D level greater than 40 ng/mL, the study findings increase the urgency to consider whether increased sun exposure or supplementation could reduce COVID-19 risk, according to the authors.

“When increased sun exposure is impractical, achieving vitamin D levels of 40 ng/mL or greater typically requires greater supplementation than currently recommended for most individuals of 600-800 IU/d vitamin D3,” they added.

However, Dr. Meltzer also acknowledged that “this is an observational study. We can see that there’s an association between vitamin D levels and likelihood of a COVID-19 diagnosis, but we don’t know exactly why that is, or whether these results are due to the vitamin D directly or other related biological factors.”

All in all, the authors suggested that randomized clinical trials are needed to understand if vitamin D can reduce COVID-19 risk, and as such they should include doses of supplements likely to increase vitamin D to at least 40 ng/mL, and perhaps even higher, although they pointed out that the latter must be achieved safely.

“Studies should also consider the role of vitamin D testing, loading doses, dose adjustments for individuals who are obese or overweight, risks for hypercalcemia, and strategies to monitor for and mitigate hypercalcemia, and that non-White populations, such as Black individuals, may have greater needs for supplementation,” they outlined.

They are now recruiting participants for two separate clinical trials testing the efficacy of vitamin D supplements for preventing COVID-19.

The authors disclosed no relevant financial relationships.

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

Recently, we had the opportunity to take part in a major EHR conversion project. During this “go-live,” 5 hospitals and approximately 300 ambulatory service and physician practice locations made the transition, consolidating over 100 disparate electronic systems and dozens of interfaces into one world-class medical record.

If you’ve ever been part of such an event, you know it is anything but simple. On the contrary, it requires an enormous financial investment along with years of planning, hours of meetings, and months of training. No matter how much preparation goes into it, there are sure to be bumps along the way. It is a traumatic and stressful time for all involved, but the end result is well worth the effort. Still, there are lessons to be learned and wisdom to be gleaned, and this month we’d like to share a few that we found most important. We believe that many of these are useful lessons even to those who will never live through a go-live.
 

Safety always comes first

Patient safety is a term so often used that it has a tendency to be taken for granted. Health systems build processes and procedures to ensure safety – some even win awards and recognition for their efforts. But the best (and safest) health care institutions build patient safety into their cultures. More than just being taught to use checklists or buzzwords, the staff at these institutions are encouraged to put the welfare of patients first, making all other activities secondary to this pursuit. We had the opportunity to witness the benefits of such a culture during this go-live and were incredibly impressed with the results.

To be successful in an EHR transition of any magnitude, an organization needs to hold patient safety as a core value and provide its employees with the tools to execute on that value. This enables staff to prepare adequately and to identify risks and opportunities before the conversion takes place. Once go-live occurs, staff also must feel empowered to speak up when they identify problem areas that might jeopardize patients’ care. They also must be given a clear escalation path to ensure their voices can be heard. Most importantly, everyone must understand that the electronic health record itself is just one piece of a major operational change.

As workflows are modified to adapt to the new technology, unsafe processes should be called out and fixed quickly. While the EHR may offer the latest in decision support and system integration, no advancement in technology can make up for bad outcomes, nor justify processes that lead to patient harm.
 

Training is no substitute for good support

It takes a long time to train thousands of employees, especially when that training must occur during the era of social distancing in the midst of a pandemic. Still, even in the best of times, education should be married to hands-on experience in order to have a real impact. Unfortunately, this is extremely challenging.

Trainees forget much of what they’ve learned in the weeks or months between education and go-live, so they must be given immediately accessible support to bridge the gap. This is known as “at-the-elbow” (ATE) support, and as the name implies, it consists of individuals who are familiar with the new system and are always available to end users, answering their questions and helping them navigate. Since health care never sleeps, this support needs to be offered 24/7, and it should also be flexible and plentiful.

There are many areas that will require more support than anticipated to accommodate the number of clinical and other staff who will use the system, so support staff must be nimble and available for redeployment. In addition, ensuring high-quality support is essential. As many ATE experts are hired contractors, their knowledge base and communications skills can vary widely. Accountability is key, and end users should feel empowered to identify gaps in coverage and deficits in knowledge base in the ATE.

As employees become more familiar with the new system, the need for ATE will wane, but there will still be questions that arise for many weeks to months, and new EHR users will also be added all the time. A good after–go-live support system should remain available so clinical and clerical employees can get just-in-time assistance whenever they need it.
 

Users should be given clear expectations

Clinicians going through an EHR conversion may be frustrated to discover that the data transferred from their old system into the new one is not quite what they expected. While structured elements such as allergies and immunizations may transfer, unstructured patient histories may not come over at all.

There may be gaps in data, or the opposite may even be true: an overabundance of useless information may transfer over, leaving doctors with dozens of meaningless data points to sift through and eliminate to clean up the chart. This can be extremely time-consuming and discouraging and may jeopardize the success of the go-live.

Providers deserve clear expectations prior to conversion. They should be told what will and will not transfer and be informed that there will be extra work required for documentation at the outset. They may also want the option to preemptively reduce patient volumes to accommodate the additional effort involved in preparing charts. No matter what, this will be a heavy lift, and physicians should understand the implications long before go-live to prepare accordingly.
 

Old habits die hard

One of the most common complaints we’ve heard following EHR conversions is that “things just worked better in the old system.” We always respond with a question: “Were things better, or just different?” The truth may lie somewhere in the middle, but there is no question that muscle memory develops over many years, and change is difficult no matter how much better the new system is. Still, appropriate expectations, access to just-in-time support, and a continual focus on safety will ensure that the long-term benefits of a patient-centered and integrated electronic record will far outweigh the initial challenges of go-live.

Dr. Notte is a family physician and chief medical officer of Abington (Pa.) Hospital–Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health. They have no conflicts related to the content of this piece.

Recently, we had the opportunity to take part in a major EHR conversion project. During this “go-live,” 5 hospitals and approximately 300 ambulatory service and physician practice locations made the transition, consolidating over 100 disparate electronic systems and dozens of interfaces into one world-class medical record.

If you’ve ever been part of such an event, you know it is anything but simple. On the contrary, it requires an enormous financial investment along with years of planning, hours of meetings, and months of training. No matter how much preparation goes into it, there are sure to be bumps along the way. It is a traumatic and stressful time for all involved, but the end result is well worth the effort. Still, there are lessons to be learned and wisdom to be gleaned, and this month we’d like to share a few that we found most important. We believe that many of these are useful lessons even to those who will never live through a go-live.
 

Safety always comes first

Patient safety is a term so often used that it has a tendency to be taken for granted. Health systems build processes and procedures to ensure safety – some even win awards and recognition for their efforts. But the best (and safest) health care institutions build patient safety into their cultures. More than just being taught to use checklists or buzzwords, the staff at these institutions are encouraged to put the welfare of patients first, making all other activities secondary to this pursuit. We had the opportunity to witness the benefits of such a culture during this go-live and were incredibly impressed with the results.

To be successful in an EHR transition of any magnitude, an organization needs to hold patient safety as a core value and provide its employees with the tools to execute on that value. This enables staff to prepare adequately and to identify risks and opportunities before the conversion takes place. Once go-live occurs, staff also must feel empowered to speak up when they identify problem areas that might jeopardize patients’ care. They also must be given a clear escalation path to ensure their voices can be heard. Most importantly, everyone must understand that the electronic health record itself is just one piece of a major operational change.

As workflows are modified to adapt to the new technology, unsafe processes should be called out and fixed quickly. While the EHR may offer the latest in decision support and system integration, no advancement in technology can make up for bad outcomes, nor justify processes that lead to patient harm.
 

Training is no substitute for good support

It takes a long time to train thousands of employees, especially when that training must occur during the era of social distancing in the midst of a pandemic. Still, even in the best of times, education should be married to hands-on experience in order to have a real impact. Unfortunately, this is extremely challenging.

Trainees forget much of what they’ve learned in the weeks or months between education and go-live, so they must be given immediately accessible support to bridge the gap. This is known as “at-the-elbow” (ATE) support, and as the name implies, it consists of individuals who are familiar with the new system and are always available to end users, answering their questions and helping them navigate. Since health care never sleeps, this support needs to be offered 24/7, and it should also be flexible and plentiful.

There are many areas that will require more support than anticipated to accommodate the number of clinical and other staff who will use the system, so support staff must be nimble and available for redeployment. In addition, ensuring high-quality support is essential. As many ATE experts are hired contractors, their knowledge base and communications skills can vary widely. Accountability is key, and end users should feel empowered to identify gaps in coverage and deficits in knowledge base in the ATE.

As employees become more familiar with the new system, the need for ATE will wane, but there will still be questions that arise for many weeks to months, and new EHR users will also be added all the time. A good after–go-live support system should remain available so clinical and clerical employees can get just-in-time assistance whenever they need it.
 

Users should be given clear expectations

Clinicians going through an EHR conversion may be frustrated to discover that the data transferred from their old system into the new one is not quite what they expected. While structured elements such as allergies and immunizations may transfer, unstructured patient histories may not come over at all.

There may be gaps in data, or the opposite may even be true: an overabundance of useless information may transfer over, leaving doctors with dozens of meaningless data points to sift through and eliminate to clean up the chart. This can be extremely time-consuming and discouraging and may jeopardize the success of the go-live.

Providers deserve clear expectations prior to conversion. They should be told what will and will not transfer and be informed that there will be extra work required for documentation at the outset. They may also want the option to preemptively reduce patient volumes to accommodate the additional effort involved in preparing charts. No matter what, this will be a heavy lift, and physicians should understand the implications long before go-live to prepare accordingly.
 

Old habits die hard

One of the most common complaints we’ve heard following EHR conversions is that “things just worked better in the old system.” We always respond with a question: “Were things better, or just different?” The truth may lie somewhere in the middle, but there is no question that muscle memory develops over many years, and change is difficult no matter how much better the new system is. Still, appropriate expectations, access to just-in-time support, and a continual focus on safety will ensure that the long-term benefits of a patient-centered and integrated electronic record will far outweigh the initial challenges of go-live.

Dr. Notte is a family physician and chief medical officer of Abington (Pa.) Hospital–Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health. They have no conflicts related to the content of this piece.

Recently, we had the opportunity to take part in a major EHR conversion project. During this “go-live,” 5 hospitals and approximately 300 ambulatory service and physician practice locations made the transition, consolidating over 100 disparate electronic systems and dozens of interfaces into one world-class medical record.

If you’ve ever been part of such an event, you know it is anything but simple. On the contrary, it requires an enormous financial investment along with years of planning, hours of meetings, and months of training. No matter how much preparation goes into it, there are sure to be bumps along the way. It is a traumatic and stressful time for all involved, but the end result is well worth the effort. Still, there are lessons to be learned and wisdom to be gleaned, and this month we’d like to share a few that we found most important. We believe that many of these are useful lessons even to those who will never live through a go-live.
 

Safety always comes first

Patient safety is a term so often used that it has a tendency to be taken for granted. Health systems build processes and procedures to ensure safety – some even win awards and recognition for their efforts. But the best (and safest) health care institutions build patient safety into their cultures. More than just being taught to use checklists or buzzwords, the staff at these institutions are encouraged to put the welfare of patients first, making all other activities secondary to this pursuit. We had the opportunity to witness the benefits of such a culture during this go-live and were incredibly impressed with the results.

To be successful in an EHR transition of any magnitude, an organization needs to hold patient safety as a core value and provide its employees with the tools to execute on that value. This enables staff to prepare adequately and to identify risks and opportunities before the conversion takes place. Once go-live occurs, staff also must feel empowered to speak up when they identify problem areas that might jeopardize patients’ care. They also must be given a clear escalation path to ensure their voices can be heard. Most importantly, everyone must understand that the electronic health record itself is just one piece of a major operational change.

As workflows are modified to adapt to the new technology, unsafe processes should be called out and fixed quickly. While the EHR may offer the latest in decision support and system integration, no advancement in technology can make up for bad outcomes, nor justify processes that lead to patient harm.
 

Training is no substitute for good support

It takes a long time to train thousands of employees, especially when that training must occur during the era of social distancing in the midst of a pandemic. Still, even in the best of times, education should be married to hands-on experience in order to have a real impact. Unfortunately, this is extremely challenging.

Trainees forget much of what they’ve learned in the weeks or months between education and go-live, so they must be given immediately accessible support to bridge the gap. This is known as “at-the-elbow” (ATE) support, and as the name implies, it consists of individuals who are familiar with the new system and are always available to end users, answering their questions and helping them navigate. Since health care never sleeps, this support needs to be offered 24/7, and it should also be flexible and plentiful.

There are many areas that will require more support than anticipated to accommodate the number of clinical and other staff who will use the system, so support staff must be nimble and available for redeployment. In addition, ensuring high-quality support is essential. As many ATE experts are hired contractors, their knowledge base and communications skills can vary widely. Accountability is key, and end users should feel empowered to identify gaps in coverage and deficits in knowledge base in the ATE.

As employees become more familiar with the new system, the need for ATE will wane, but there will still be questions that arise for many weeks to months, and new EHR users will also be added all the time. A good after–go-live support system should remain available so clinical and clerical employees can get just-in-time assistance whenever they need it.
 

Users should be given clear expectations

Clinicians going through an EHR conversion may be frustrated to discover that the data transferred from their old system into the new one is not quite what they expected. While structured elements such as allergies and immunizations may transfer, unstructured patient histories may not come over at all.

There may be gaps in data, or the opposite may even be true: an overabundance of useless information may transfer over, leaving doctors with dozens of meaningless data points to sift through and eliminate to clean up the chart. This can be extremely time-consuming and discouraging and may jeopardize the success of the go-live.

Providers deserve clear expectations prior to conversion. They should be told what will and will not transfer and be informed that there will be extra work required for documentation at the outset. They may also want the option to preemptively reduce patient volumes to accommodate the additional effort involved in preparing charts. No matter what, this will be a heavy lift, and physicians should understand the implications long before go-live to prepare accordingly.
 

Old habits die hard

One of the most common complaints we’ve heard following EHR conversions is that “things just worked better in the old system.” We always respond with a question: “Were things better, or just different?” The truth may lie somewhere in the middle, but there is no question that muscle memory develops over many years, and change is difficult no matter how much better the new system is. Still, appropriate expectations, access to just-in-time support, and a continual focus on safety will ensure that the long-term benefits of a patient-centered and integrated electronic record will far outweigh the initial challenges of go-live.

Dr. Notte is a family physician and chief medical officer of Abington (Pa.) Hospital–Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health. They have no conflicts related to the content of this piece.

One of the top research journals in the United States has placed its editor-in-chief on administrative leave pending the outcome of an investigation into a controversial podcast episode that critics labeled as racist.

The American Medical Association’s Joint Oversight Committee announced that Howard Bauchner, MD, is on leave beginning at the end of the day on March 25. Dr. Bauchner is the top editor at JAMA, the journal of the AMA.

“The decision to place the editor-in-chief on administrative leave neither implicates nor exonerates individuals and is standard operating procedure for such investigations,” the committee said in a statement.

More than 2,000 people signed a petition on Change.org calling for an investigation at JAMA over the February podcast episode, called “Structural Racism for Doctors: What Is It?”

Already, Edward H. Livingston, MD, the host of the podcast, has resigned as deputy editor of the journal.

During the podcast, Dr. Livingston, who is White, said, “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released in the week prior to his being on leave, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

This story will be updated.

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

One of the top research journals in the United States has placed its editor-in-chief on administrative leave pending the outcome of an investigation into a controversial podcast episode that critics labeled as racist.

The American Medical Association’s Joint Oversight Committee announced that Howard Bauchner, MD, is on leave beginning at the end of the day on March 25. Dr. Bauchner is the top editor at JAMA, the journal of the AMA.

“The decision to place the editor-in-chief on administrative leave neither implicates nor exonerates individuals and is standard operating procedure for such investigations,” the committee said in a statement.

More than 2,000 people signed a petition on Change.org calling for an investigation at JAMA over the February podcast episode, called “Structural Racism for Doctors: What Is It?”

Already, Edward H. Livingston, MD, the host of the podcast, has resigned as deputy editor of the journal.

During the podcast, Dr. Livingston, who is White, said, “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released in the week prior to his being on leave, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

This story will be updated.

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

One of the top research journals in the United States has placed its editor-in-chief on administrative leave pending the outcome of an investigation into a controversial podcast episode that critics labeled as racist.

The American Medical Association’s Joint Oversight Committee announced that Howard Bauchner, MD, is on leave beginning at the end of the day on March 25. Dr. Bauchner is the top editor at JAMA, the journal of the AMA.

“The decision to place the editor-in-chief on administrative leave neither implicates nor exonerates individuals and is standard operating procedure for such investigations,” the committee said in a statement.

More than 2,000 people signed a petition on Change.org calling for an investigation at JAMA over the February podcast episode, called “Structural Racism for Doctors: What Is It?”

Already, Edward H. Livingston, MD, the host of the podcast, has resigned as deputy editor of the journal.

During the podcast, Dr. Livingston, who is White, said, “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released in the week prior to his being on leave, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

This story will be updated.

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

Clinicians should be aware that the discordance between high-sensitivity cardiac troponin (hs-cTn) assays is significant enough that management recommendations may change, for example, for a patient assessed for suspected acute coronary syndrome (ACS) in one hospital and transferred to another that uses a different assay, according to a team of international researchers.

When hs-cTn concentrations were measured using the three Food and Drug Administration–approved assays, only 37.4% (384 of 1,027 samples) of blood samples were classified into the same analytical benchmark category.

“We didn’t expect such low concordance, to be honest, but I have to stress that this first assessment used just one-time blood testing and serial testing is what is more commonly recommended now,” said Júlia Karády, MD, from Massachusetts General Hospital and Harvard Medical School, both in Boston.

To see if concordance improved with serial testing, the researchers looked at the 242 patients for whom serial samples were available and saw concordance of management recommendations across assays rise to 74.8%.

“We tested the 0/2-hour algorithm and found that the overall agreement almost doubled, so I think that a very important message from our study is that serial testing improves the agreement between the assays in terms of clinical management and patient stratification,” said Dr. Karády.

Dr. Karády and colleagues published their findings in the Journal of the American College of Cardiology.

The researchers tested three assays referred to clinically as high-sensitivity assays: Elecsys 2010 platform (Roche Diagnostics); ARCHITECT i2000SR (Abbott Diagnostics); and hsVista (Siemens Diagnostics). All three have received FDA approval, starting with Elecsys in 2017.

The proportion of patients with similar management recommendations differed between the assays for both “rule-out” (87.2%, 73.1%, and 78.5% for Roche, Abbott, and Siemens, respectively) and “observe” (9.5%, 24%, and 17.8%; both P < .001). For the purposes of “rule-in,” no difference was noted (3.3%, 2.9%, and 3.7%).

“It’s important to note that this was a highly selected population of patients with an intermediate likelihood for ACS, not an all-comer population. This group comprises about 20% of the [emergency department] population and actually is the group we struggle with the most, which is hardest to diagnose because it excludes the very low– and very high–risk patients,” said Dr. Karády.

The patients included in this study all had suspected ACS and were enrolled in the ROMICAT-I and II trials.

Among 1,027 samples from 624 patients (mean age, 52.8 years; 39.4% women), samples were classified as below the limit of detection (LOD) in 56.3%, 10.4%, and 41.2% (P < .001) by Roche, Abbott, and Siemens, respectively.

The proportion of sample with a troponin measurement between LOD to the 99th percentile also differed significantly between the assays at 36.5%, 83.5%, and 52.6%, respectively (P < .001).

Only the proportion classified greater than 99th percentile did not differ (7.2%, 6.0%, and 6.2%; P = .114).

When the researchers looked at sex-specific difference, no differences were seen in rule-in numbers for men, but significant differences were seen for women.

“One possible explanation for this could be differences in the representation of men and women in the various reference populations used to develop the 99th percentile values for these assays,” suggested Dr. Karády.

They estimate around 30%-40% of U.S. centers are currently using high-sensitivity troponin assays and this number is “rapidly rising.”

The diagnostic algorithms developed for use with high-sensitivity assays, such as the 0/2-h algorithm, acknowledge differences in performance characteristics and recommend that assay-specific cut points be used for clinical decision-making rather than relying on generally applicable thresholds.

Joseph S. Alpert, MD, University of Arizona, Tucson, and coauthors of an accompanying editorial said the take-home message here is caveat emptor.

“First, ‘let the buyer (i.e., the clinician) beware’ when patients are transferred from one hospital to another, where different hs-cTn assays may be used,” they wrote. This is particularly true in women and in those with troponin levels in the “observe (gray zone)” clinical management recommendation.

Dr. Karády has received grant support from the Fulbright Visiting Researcher Grant and the Rosztoczy Foundation. One of the coauthors of the editorial comment consults or has consulted for most of the major diagnostic companies, including the manufacturers of the three assays tested in this study. Dr. Alpert disclosed no relevant financial relationships. 

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

Clinicians should be aware that the discordance between high-sensitivity cardiac troponin (hs-cTn) assays is significant enough that management recommendations may change, for example, for a patient assessed for suspected acute coronary syndrome (ACS) in one hospital and transferred to another that uses a different assay, according to a team of international researchers.

When hs-cTn concentrations were measured using the three Food and Drug Administration–approved assays, only 37.4% (384 of 1,027 samples) of blood samples were classified into the same analytical benchmark category.

“We didn’t expect such low concordance, to be honest, but I have to stress that this first assessment used just one-time blood testing and serial testing is what is more commonly recommended now,” said Júlia Karády, MD, from Massachusetts General Hospital and Harvard Medical School, both in Boston.

To see if concordance improved with serial testing, the researchers looked at the 242 patients for whom serial samples were available and saw concordance of management recommendations across assays rise to 74.8%.

“We tested the 0/2-hour algorithm and found that the overall agreement almost doubled, so I think that a very important message from our study is that serial testing improves the agreement between the assays in terms of clinical management and patient stratification,” said Dr. Karády.

Dr. Karády and colleagues published their findings in the Journal of the American College of Cardiology.

The researchers tested three assays referred to clinically as high-sensitivity assays: Elecsys 2010 platform (Roche Diagnostics); ARCHITECT i2000SR (Abbott Diagnostics); and hsVista (Siemens Diagnostics). All three have received FDA approval, starting with Elecsys in 2017.

The proportion of patients with similar management recommendations differed between the assays for both “rule-out” (87.2%, 73.1%, and 78.5% for Roche, Abbott, and Siemens, respectively) and “observe” (9.5%, 24%, and 17.8%; both P < .001). For the purposes of “rule-in,” no difference was noted (3.3%, 2.9%, and 3.7%).

“It’s important to note that this was a highly selected population of patients with an intermediate likelihood for ACS, not an all-comer population. This group comprises about 20% of the [emergency department] population and actually is the group we struggle with the most, which is hardest to diagnose because it excludes the very low– and very high–risk patients,” said Dr. Karády.

The patients included in this study all had suspected ACS and were enrolled in the ROMICAT-I and II trials.

Among 1,027 samples from 624 patients (mean age, 52.8 years; 39.4% women), samples were classified as below the limit of detection (LOD) in 56.3%, 10.4%, and 41.2% (P < .001) by Roche, Abbott, and Siemens, respectively.

The proportion of sample with a troponin measurement between LOD to the 99th percentile also differed significantly between the assays at 36.5%, 83.5%, and 52.6%, respectively (P < .001).

Only the proportion classified greater than 99th percentile did not differ (7.2%, 6.0%, and 6.2%; P = .114).

When the researchers looked at sex-specific difference, no differences were seen in rule-in numbers for men, but significant differences were seen for women.

“One possible explanation for this could be differences in the representation of men and women in the various reference populations used to develop the 99th percentile values for these assays,” suggested Dr. Karády.

They estimate around 30%-40% of U.S. centers are currently using high-sensitivity troponin assays and this number is “rapidly rising.”

The diagnostic algorithms developed for use with high-sensitivity assays, such as the 0/2-h algorithm, acknowledge differences in performance characteristics and recommend that assay-specific cut points be used for clinical decision-making rather than relying on generally applicable thresholds.

Joseph S. Alpert, MD, University of Arizona, Tucson, and coauthors of an accompanying editorial said the take-home message here is caveat emptor.

“First, ‘let the buyer (i.e., the clinician) beware’ when patients are transferred from one hospital to another, where different hs-cTn assays may be used,” they wrote. This is particularly true in women and in those with troponin levels in the “observe (gray zone)” clinical management recommendation.

Dr. Karády has received grant support from the Fulbright Visiting Researcher Grant and the Rosztoczy Foundation. One of the coauthors of the editorial comment consults or has consulted for most of the major diagnostic companies, including the manufacturers of the three assays tested in this study. Dr. Alpert disclosed no relevant financial relationships. 

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

Clinicians should be aware that the discordance between high-sensitivity cardiac troponin (hs-cTn) assays is significant enough that management recommendations may change, for example, for a patient assessed for suspected acute coronary syndrome (ACS) in one hospital and transferred to another that uses a different assay, according to a team of international researchers.

When hs-cTn concentrations were measured using the three Food and Drug Administration–approved assays, only 37.4% (384 of 1,027 samples) of blood samples were classified into the same analytical benchmark category.

“We didn’t expect such low concordance, to be honest, but I have to stress that this first assessment used just one-time blood testing and serial testing is what is more commonly recommended now,” said Júlia Karády, MD, from Massachusetts General Hospital and Harvard Medical School, both in Boston.

To see if concordance improved with serial testing, the researchers looked at the 242 patients for whom serial samples were available and saw concordance of management recommendations across assays rise to 74.8%.

“We tested the 0/2-hour algorithm and found that the overall agreement almost doubled, so I think that a very important message from our study is that serial testing improves the agreement between the assays in terms of clinical management and patient stratification,” said Dr. Karády.

Dr. Karády and colleagues published their findings in the Journal of the American College of Cardiology.

The researchers tested three assays referred to clinically as high-sensitivity assays: Elecsys 2010 platform (Roche Diagnostics); ARCHITECT i2000SR (Abbott Diagnostics); and hsVista (Siemens Diagnostics). All three have received FDA approval, starting with Elecsys in 2017.

The proportion of patients with similar management recommendations differed between the assays for both “rule-out” (87.2%, 73.1%, and 78.5% for Roche, Abbott, and Siemens, respectively) and “observe” (9.5%, 24%, and 17.8%; both P < .001). For the purposes of “rule-in,” no difference was noted (3.3%, 2.9%, and 3.7%).

“It’s important to note that this was a highly selected population of patients with an intermediate likelihood for ACS, not an all-comer population. This group comprises about 20% of the [emergency department] population and actually is the group we struggle with the most, which is hardest to diagnose because it excludes the very low– and very high–risk patients,” said Dr. Karády.

The patients included in this study all had suspected ACS and were enrolled in the ROMICAT-I and II trials.

Among 1,027 samples from 624 patients (mean age, 52.8 years; 39.4% women), samples were classified as below the limit of detection (LOD) in 56.3%, 10.4%, and 41.2% (P < .001) by Roche, Abbott, and Siemens, respectively.

The proportion of sample with a troponin measurement between LOD to the 99th percentile also differed significantly between the assays at 36.5%, 83.5%, and 52.6%, respectively (P < .001).

Only the proportion classified greater than 99th percentile did not differ (7.2%, 6.0%, and 6.2%; P = .114).

When the researchers looked at sex-specific difference, no differences were seen in rule-in numbers for men, but significant differences were seen for women.

“One possible explanation for this could be differences in the representation of men and women in the various reference populations used to develop the 99th percentile values for these assays,” suggested Dr. Karády.

They estimate around 30%-40% of U.S. centers are currently using high-sensitivity troponin assays and this number is “rapidly rising.”

The diagnostic algorithms developed for use with high-sensitivity assays, such as the 0/2-h algorithm, acknowledge differences in performance characteristics and recommend that assay-specific cut points be used for clinical decision-making rather than relying on generally applicable thresholds.

Joseph S. Alpert, MD, University of Arizona, Tucson, and coauthors of an accompanying editorial said the take-home message here is caveat emptor.

“First, ‘let the buyer (i.e., the clinician) beware’ when patients are transferred from one hospital to another, where different hs-cTn assays may be used,” they wrote. This is particularly true in women and in those with troponin levels in the “observe (gray zone)” clinical management recommendation.

Dr. Karády has received grant support from the Fulbright Visiting Researcher Grant and the Rosztoczy Foundation. One of the coauthors of the editorial comment consults or has consulted for most of the major diagnostic companies, including the manufacturers of the three assays tested in this study. Dr. Alpert disclosed no relevant financial relationships. 

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

The new SARS-CoV-2 variants are not just problems for humans. 

New research shows they can also infect animals, and for the first time, variants have been able to infect mice, a development that may complicate efforts to rein in the global spread of the virus.

In addition, two new studies have implications for pets. Veterinarians in Texas and the United Kingdom have documented infections of B.1.1.7 – the fast-spreading variant first found in the United Kingdom – in dogs and cats. The animals in the U.K. study also had heart damage, but it’s unclear if the damage was caused by the virus or was already there and was found as a result of their infections.

Animal studies of SARS-CoV-2 and its emerging variants are urgent, said Sarah Hamer, DVM, PhD, a veterinarian and epidemiologist at Texas A&M University, College Station. 

She’s part of a network of scientists who are swabbing the pets of people who are diagnosed with COVID-19 to find out how often the virus passes from people to animals.

The collaboration is part of the One Health initiative through the Centers for Disease Control and Prevention. One Health aims to tackle infectious diseases by recognizing that people can’t be fully protected from pathogens unless animals and the environment are also safeguarded. “Over 70% of emerging diseases of humans have their origins in animal populations,” Dr. Hamer said. “So if we are only focusing on studying disease as it emerges in humans and ignoring where those pathogens have been transmitted or circulating for years, then we might miss the ability to detect early emergence. We might miss the ability to control these diseases before they become problems for human health.”
 

Variants move to mice

In new work, researchers at the Institut Pasteur in Paris have shown that the B.1.351 and P.1 variants of concern, which were first identified in South Africa and Brazil, respectively, can infect mice, giving the virus a potential new host. Older versions of the virus couldn’t infect mice because they weren’t able bind to receptors on their cells. These two variants can.

On one hand, that’s a good thing, because it will help scientists more easily conduct experiments in mice. Before, if they wanted to do an experiment with SARS-CoV-2 in mice, they had to use a special strain of mouse that was bred to carry human ACE2 receptors on their lung cells. Now that mice can become naturally infected, any breed will do, making it less costly and time-consuming to study the virus in animals.

On the other hand, the idea that the virus could have more and different ways to spread isn’t good news.

“From the beginning of the epidemic and since human coronaviruses emerged from animals, it has been very important to establish in which species the virus can replicate, in particular the species that live close to humans,” said Xavier Montagutelli, DVM, PhD, head of the Mouse Genetics Laboratory at the Institut Pasteur. His study was published as a preprint ahead of peer review on BioRXIV.

Once a virus establishes itself within a population of animals, it will continue to spread and change and may eventually be passed back to humans. It’s the reason that birds and pigs are closely monitored for influenza viruses.

So far, with SARS-CoV-2, only one animal has been found to catch and spread the virus and pass it back to people – farmed mink. Researchers have also documented SARS-CoV-2 antibodies in escaped mink living near mink farms in Utah, suggesting the virus has the potential to be transmitted to wild populations.

And the move of the virus into mice suggests that SARS-CoV-2 could establish itself in a population of wild animals that live close to humans.

“At this point, we have no evidence that wild mice are infected, or can become infected from humans,” Dr. Montagutelli said. He added that his findings emphasize the need to regularly test animals for signs of the infection. He said these surveys will need to be updated as more variants emerge.

“So far, we’ve been lucky that our livestock species aren’t really susceptible to this,” said Scott Weese, DVM, a professor at Ontario Veterinary College at the University of Guelph, who studies emerging infectious diseases that pass between animals and people.

While the outbreaks on mink farms have been bad, imagine what would happen, Dr. Weese said, if the virus moved to pigs.

“If this infects a barn with a few thousand pigs – which is like the mink scenario – but we have a lot more pig farms than mink farms,” he said.

“With these variants, we have to reset,” he said. “We’ve figured all this about animals and how it spreads or how it doesn’t, but now we need to repeat all those studies to make sure it’s the same thing.”
 

Pets catch variants, too

Pets living with people who are infected with SARS-CoV-2 can catch it from their owners, and cats are particularly susceptible, Dr. Weese said. 

Contact tracing studies, which also tested animals for signs of the virus, have found that about half of cats living with infected people have signs of infection, while 20%-30% of dogs were sick.

“It’s quite common,” for pets to get COVID, Dr. Weese said.

Now, two new studies have shown that pets can also be infected by the newer B.1.1.7 variant.

The first study, from researchers at Texas A&M, documented the variant in a dog and a cat from Brazos County, Texas. Neither the older black Lab mix or the older domestic shorthair cat had symptoms of COVID-19. They were tested as part of a project funded by the CDC.

Dr. Weese said pets are at risk by people who are infected, but they don’t seem to play a big role in spreading the disease to humans. So if you have pets, there’s no reason to worry that they could bring the virus home to you. You’re more likely to be a risk to them.

The second study, from a specialty animal hospital in southeast England, documented infection by the B.1.1.7 virus variant in 11 dogs and cats. Most of the pets had unusual symptoms, including inflamed hearts and heart damage.

Dr. Weese called this study interesting and said its findings deserve more investigation, but pointed out that the study can’t determine whether the infection caused the heart damage, or whether it was already there.

“This is a human virus. There’s no doubt about it. It can affect other species, but it likes people a lot better,” he said. “If you think about the big picture and what is the potential role of animals, pets are pretty low risk.”
 

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

The new SARS-CoV-2 variants are not just problems for humans. 

New research shows they can also infect animals, and for the first time, variants have been able to infect mice, a development that may complicate efforts to rein in the global spread of the virus.

In addition, two new studies have implications for pets. Veterinarians in Texas and the United Kingdom have documented infections of B.1.1.7 – the fast-spreading variant first found in the United Kingdom – in dogs and cats. The animals in the U.K. study also had heart damage, but it’s unclear if the damage was caused by the virus or was already there and was found as a result of their infections.

Animal studies of SARS-CoV-2 and its emerging variants are urgent, said Sarah Hamer, DVM, PhD, a veterinarian and epidemiologist at Texas A&M University, College Station. 

She’s part of a network of scientists who are swabbing the pets of people who are diagnosed with COVID-19 to find out how often the virus passes from people to animals.

The collaboration is part of the One Health initiative through the Centers for Disease Control and Prevention. One Health aims to tackle infectious diseases by recognizing that people can’t be fully protected from pathogens unless animals and the environment are also safeguarded. “Over 70% of emerging diseases of humans have their origins in animal populations,” Dr. Hamer said. “So if we are only focusing on studying disease as it emerges in humans and ignoring where those pathogens have been transmitted or circulating for years, then we might miss the ability to detect early emergence. We might miss the ability to control these diseases before they become problems for human health.”
 

Variants move to mice

In new work, researchers at the Institut Pasteur in Paris have shown that the B.1.351 and P.1 variants of concern, which were first identified in South Africa and Brazil, respectively, can infect mice, giving the virus a potential new host. Older versions of the virus couldn’t infect mice because they weren’t able bind to receptors on their cells. These two variants can.

On one hand, that’s a good thing, because it will help scientists more easily conduct experiments in mice. Before, if they wanted to do an experiment with SARS-CoV-2 in mice, they had to use a special strain of mouse that was bred to carry human ACE2 receptors on their lung cells. Now that mice can become naturally infected, any breed will do, making it less costly and time-consuming to study the virus in animals.

On the other hand, the idea that the virus could have more and different ways to spread isn’t good news.

“From the beginning of the epidemic and since human coronaviruses emerged from animals, it has been very important to establish in which species the virus can replicate, in particular the species that live close to humans,” said Xavier Montagutelli, DVM, PhD, head of the Mouse Genetics Laboratory at the Institut Pasteur. His study was published as a preprint ahead of peer review on BioRXIV.

Once a virus establishes itself within a population of animals, it will continue to spread and change and may eventually be passed back to humans. It’s the reason that birds and pigs are closely monitored for influenza viruses.

So far, with SARS-CoV-2, only one animal has been found to catch and spread the virus and pass it back to people – farmed mink. Researchers have also documented SARS-CoV-2 antibodies in escaped mink living near mink farms in Utah, suggesting the virus has the potential to be transmitted to wild populations.

And the move of the virus into mice suggests that SARS-CoV-2 could establish itself in a population of wild animals that live close to humans.

“At this point, we have no evidence that wild mice are infected, or can become infected from humans,” Dr. Montagutelli said. He added that his findings emphasize the need to regularly test animals for signs of the infection. He said these surveys will need to be updated as more variants emerge.

“So far, we’ve been lucky that our livestock species aren’t really susceptible to this,” said Scott Weese, DVM, a professor at Ontario Veterinary College at the University of Guelph, who studies emerging infectious diseases that pass between animals and people.

While the outbreaks on mink farms have been bad, imagine what would happen, Dr. Weese said, if the virus moved to pigs.

“If this infects a barn with a few thousand pigs – which is like the mink scenario – but we have a lot more pig farms than mink farms,” he said.

“With these variants, we have to reset,” he said. “We’ve figured all this about animals and how it spreads or how it doesn’t, but now we need to repeat all those studies to make sure it’s the same thing.”
 

Pets catch variants, too

Pets living with people who are infected with SARS-CoV-2 can catch it from their owners, and cats are particularly susceptible, Dr. Weese said. 

Contact tracing studies, which also tested animals for signs of the virus, have found that about half of cats living with infected people have signs of infection, while 20%-30% of dogs were sick.

“It’s quite common,” for pets to get COVID, Dr. Weese said.

Now, two new studies have shown that pets can also be infected by the newer B.1.1.7 variant.

The first study, from researchers at Texas A&M, documented the variant in a dog and a cat from Brazos County, Texas. Neither the older black Lab mix or the older domestic shorthair cat had symptoms of COVID-19. They were tested as part of a project funded by the CDC.

Dr. Weese said pets are at risk by people who are infected, but they don’t seem to play a big role in spreading the disease to humans. So if you have pets, there’s no reason to worry that they could bring the virus home to you. You’re more likely to be a risk to them.

The second study, from a specialty animal hospital in southeast England, documented infection by the B.1.1.7 virus variant in 11 dogs and cats. Most of the pets had unusual symptoms, including inflamed hearts and heart damage.

Dr. Weese called this study interesting and said its findings deserve more investigation, but pointed out that the study can’t determine whether the infection caused the heart damage, or whether it was already there.

“This is a human virus. There’s no doubt about it. It can affect other species, but it likes people a lot better,” he said. “If you think about the big picture and what is the potential role of animals, pets are pretty low risk.”
 

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

The new SARS-CoV-2 variants are not just problems for humans. 

New research shows they can also infect animals, and for the first time, variants have been able to infect mice, a development that may complicate efforts to rein in the global spread of the virus.

In addition, two new studies have implications for pets. Veterinarians in Texas and the United Kingdom have documented infections of B.1.1.7 – the fast-spreading variant first found in the United Kingdom – in dogs and cats. The animals in the U.K. study also had heart damage, but it’s unclear if the damage was caused by the virus or was already there and was found as a result of their infections.

Animal studies of SARS-CoV-2 and its emerging variants are urgent, said Sarah Hamer, DVM, PhD, a veterinarian and epidemiologist at Texas A&M University, College Station. 

She’s part of a network of scientists who are swabbing the pets of people who are diagnosed with COVID-19 to find out how often the virus passes from people to animals.

The collaboration is part of the One Health initiative through the Centers for Disease Control and Prevention. One Health aims to tackle infectious diseases by recognizing that people can’t be fully protected from pathogens unless animals and the environment are also safeguarded. “Over 70% of emerging diseases of humans have their origins in animal populations,” Dr. Hamer said. “So if we are only focusing on studying disease as it emerges in humans and ignoring where those pathogens have been transmitted or circulating for years, then we might miss the ability to detect early emergence. We might miss the ability to control these diseases before they become problems for human health.”
 

Variants move to mice

In new work, researchers at the Institut Pasteur in Paris have shown that the B.1.351 and P.1 variants of concern, which were first identified in South Africa and Brazil, respectively, can infect mice, giving the virus a potential new host. Older versions of the virus couldn’t infect mice because they weren’t able bind to receptors on their cells. These two variants can.

On one hand, that’s a good thing, because it will help scientists more easily conduct experiments in mice. Before, if they wanted to do an experiment with SARS-CoV-2 in mice, they had to use a special strain of mouse that was bred to carry human ACE2 receptors on their lung cells. Now that mice can become naturally infected, any breed will do, making it less costly and time-consuming to study the virus in animals.

On the other hand, the idea that the virus could have more and different ways to spread isn’t good news.

“From the beginning of the epidemic and since human coronaviruses emerged from animals, it has been very important to establish in which species the virus can replicate, in particular the species that live close to humans,” said Xavier Montagutelli, DVM, PhD, head of the Mouse Genetics Laboratory at the Institut Pasteur. His study was published as a preprint ahead of peer review on BioRXIV.

Once a virus establishes itself within a population of animals, it will continue to spread and change and may eventually be passed back to humans. It’s the reason that birds and pigs are closely monitored for influenza viruses.

So far, with SARS-CoV-2, only one animal has been found to catch and spread the virus and pass it back to people – farmed mink. Researchers have also documented SARS-CoV-2 antibodies in escaped mink living near mink farms in Utah, suggesting the virus has the potential to be transmitted to wild populations.

And the move of the virus into mice suggests that SARS-CoV-2 could establish itself in a population of wild animals that live close to humans.

“At this point, we have no evidence that wild mice are infected, or can become infected from humans,” Dr. Montagutelli said. He added that his findings emphasize the need to regularly test animals for signs of the infection. He said these surveys will need to be updated as more variants emerge.

“So far, we’ve been lucky that our livestock species aren’t really susceptible to this,” said Scott Weese, DVM, a professor at Ontario Veterinary College at the University of Guelph, who studies emerging infectious diseases that pass between animals and people.

While the outbreaks on mink farms have been bad, imagine what would happen, Dr. Weese said, if the virus moved to pigs.

“If this infects a barn with a few thousand pigs – which is like the mink scenario – but we have a lot more pig farms than mink farms,” he said.

“With these variants, we have to reset,” he said. “We’ve figured all this about animals and how it spreads or how it doesn’t, but now we need to repeat all those studies to make sure it’s the same thing.”
 

Pets catch variants, too

Pets living with people who are infected with SARS-CoV-2 can catch it from their owners, and cats are particularly susceptible, Dr. Weese said. 

Contact tracing studies, which also tested animals for signs of the virus, have found that about half of cats living with infected people have signs of infection, while 20%-30% of dogs were sick.

“It’s quite common,” for pets to get COVID, Dr. Weese said.

Now, two new studies have shown that pets can also be infected by the newer B.1.1.7 variant.

The first study, from researchers at Texas A&M, documented the variant in a dog and a cat from Brazos County, Texas. Neither the older black Lab mix or the older domestic shorthair cat had symptoms of COVID-19. They were tested as part of a project funded by the CDC.

Dr. Weese said pets are at risk by people who are infected, but they don’t seem to play a big role in spreading the disease to humans. So if you have pets, there’s no reason to worry that they could bring the virus home to you. You’re more likely to be a risk to them.

The second study, from a specialty animal hospital in southeast England, documented infection by the B.1.1.7 virus variant in 11 dogs and cats. Most of the pets had unusual symptoms, including inflamed hearts and heart damage.

Dr. Weese called this study interesting and said its findings deserve more investigation, but pointed out that the study can’t determine whether the infection caused the heart damage, or whether it was already there.

“This is a human virus. There’s no doubt about it. It can affect other species, but it likes people a lot better,” he said. “If you think about the big picture and what is the potential role of animals, pets are pretty low risk.”
 

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

The increased risk of type 2 diabetes in women with polycystic ovary syndrome is well established, but a new analysis has shown that obesity is the major mediator and a target for preventing or reversing this comorbidity.

rumruay/Shutterstock

“Most women with PCOS are obese, complicating the effort to understand whether high rates of diabetes in this population are due to PCOS or excess weight, but our study now suggest that obesity isa targetable risk factor,” reported Panagiotis Anagnostis, MD, PhD, a reproductive endocrinologist at the Medical School of Aristotle University, Thessaloniki, Greece.

Obesity is also a known risk factor for type 2 diabetes (T2D), but there is reason to suspect that PCOS, which is associated with abnormal carbohydrate metabolism, has a direct impact on the risk of developing T2D, according to Dr. Anagnostis. It is also reasonable to expect “a synergistic deleterious effect” from PCOS and obesity on adverse changes in glucose metabolism that lead to T2D.

Even though rates of obesity among women with PCOS reach 80% in some studies, Dr. Anagnostis attempted to disentangle the relationship between obesity, PCOS, and risk of T2D using a large set of data drawn from a comprehensive search of published studies.

After screening with predefined criteria, 12 studies provided data on 224,284 women, of whom 45,361 had PCOS and 5,717 had T2D. Not least of the criteria for inclusion in this analysis, all studies stratified women as obese, defined as a body mass index (BMI) greater than 30 kg/m², or nonobese, he reported at the annual meeting of the Endocrine Society.



Diabetes risk tripled in PCOS

When compared without regard to BMI, the relative risk of having T2D among those with PCOS relative to those without this condition was more than three times greater (RR 3.13; P < .001). When women with PCOS were stratified for BMI, obesity was associated with a more than fourfold increased risk relative to controls without PCOS (RR, 4.06; P < .001).

In women who were nonobese, the risk of T2D was numerically higher for those with PCOS than those without (RR, 2.68), but it was only a trend with a large confidence interval (95% confidence interval, 0.97-7.49).

Among women with PCOS, those who were obese also had a more than fourfold and highly significant increased risk of T2D relative to those who were not obese (RR, 4.20; P < .001).

The message from these data is that obesity is a major and potentially modifiable risk factor for diabetes in women with PCOS, according to Dr. Anagnostis.

He said these data provide the basis for recommending weight loss specifically for managing this common PCOS comorbidity.

Almost the same relative risk of diabetes was derived from an analysis of a women’s health database published 2 years ago in Diabetes Care. In that study with 1,916 person-years of follow-up, the hazard ratio for T2D was also more than three times greater (HR, 3.23; P < .001) for those with PCOS relative to those without the syndrome.

However, normal BMI did not eliminate risk of developing diabetes in this study. Rather, the relative risk of T2D in women with PCOS was higher in those of normal weight, compared with those who were obese (HR, 4.68 vs. 2.36; P < .005). The investigators recommend screening all women with PCOS at least every 3 years with more frequent screening in those with risk factors.



PCOS complexity challenges simple conclusions

The complexity of disturbed metabolic pathways in patients with PCOS and obesity might explain some of the difficulty in unraveling the relationship between these two disease states and diabetes risk. In one recent review, it was suggested that obesity and PCOS share interrelated adverse effects on glucose metabolism. As a result, these associations are “more complex than a simple cause-and-effect process.” the authors of that article concluded.

Furthermore, in their examination of metabolic pathways, genetic susceptibility, and behavioral factors that might link PCOS, weight gain, and T2D, the authors did not ignore the psychological impact of PCOS in causing obesity and, as a byproduct, diabetes. These psychological factors might be relevant to treatment.

For example, depression and stress “might hamper ongoing attempts at lifestyle change and therefore effective weight loss” in at least some women, they cautioned.

However, in encouraging weight loss in overweight women with PCOS, the debate about cause of T2D might be moot in practical terms, according to Michael Dansinger, MD, founding director of the diabetes reversal program at Tufts Medical Center, Boston.

“Reducing excess body fat reduces the risk of type 2 diabetes,” Dr. Dansinger said in an interview. “Since women with obesity and PCOS are clearly at risk for future type 2 diabetes, that’s another reason to lose excess body fat through healthy eating and exercise.”

Dr. Anagnostis and Dr. Dansinger reported no relevant conflicts of interest.

The increased risk of type 2 diabetes in women with polycystic ovary syndrome is well established, but a new analysis has shown that obesity is the major mediator and a target for preventing or reversing this comorbidity.

rumruay/Shutterstock

“Most women with PCOS are obese, complicating the effort to understand whether high rates of diabetes in this population are due to PCOS or excess weight, but our study now suggest that obesity isa targetable risk factor,” reported Panagiotis Anagnostis, MD, PhD, a reproductive endocrinologist at the Medical School of Aristotle University, Thessaloniki, Greece.

Obesity is also a known risk factor for type 2 diabetes (T2D), but there is reason to suspect that PCOS, which is associated with abnormal carbohydrate metabolism, has a direct impact on the risk of developing T2D, according to Dr. Anagnostis. It is also reasonable to expect “a synergistic deleterious effect” from PCOS and obesity on adverse changes in glucose metabolism that lead to T2D.

Even though rates of obesity among women with PCOS reach 80% in some studies, Dr. Anagnostis attempted to disentangle the relationship between obesity, PCOS, and risk of T2D using a large set of data drawn from a comprehensive search of published studies.

After screening with predefined criteria, 12 studies provided data on 224,284 women, of whom 45,361 had PCOS and 5,717 had T2D. Not least of the criteria for inclusion in this analysis, all studies stratified women as obese, defined as a body mass index (BMI) greater than 30 kg/m², or nonobese, he reported at the annual meeting of the Endocrine Society.



Diabetes risk tripled in PCOS

When compared without regard to BMI, the relative risk of having T2D among those with PCOS relative to those without this condition was more than three times greater (RR 3.13; P < .001). When women with PCOS were stratified for BMI, obesity was associated with a more than fourfold increased risk relative to controls without PCOS (RR, 4.06; P < .001).

In women who were nonobese, the risk of T2D was numerically higher for those with PCOS than those without (RR, 2.68), but it was only a trend with a large confidence interval (95% confidence interval, 0.97-7.49).

Among women with PCOS, those who were obese also had a more than fourfold and highly significant increased risk of T2D relative to those who were not obese (RR, 4.20; P < .001).

The message from these data is that obesity is a major and potentially modifiable risk factor for diabetes in women with PCOS, according to Dr. Anagnostis.

He said these data provide the basis for recommending weight loss specifically for managing this common PCOS comorbidity.

Almost the same relative risk of diabetes was derived from an analysis of a women’s health database published 2 years ago in Diabetes Care. In that study with 1,916 person-years of follow-up, the hazard ratio for T2D was also more than three times greater (HR, 3.23; P < .001) for those with PCOS relative to those without the syndrome.

However, normal BMI did not eliminate risk of developing diabetes in this study. Rather, the relative risk of T2D in women with PCOS was higher in those of normal weight, compared with those who were obese (HR, 4.68 vs. 2.36; P < .005). The investigators recommend screening all women with PCOS at least every 3 years with more frequent screening in those with risk factors.



PCOS complexity challenges simple conclusions

The complexity of disturbed metabolic pathways in patients with PCOS and obesity might explain some of the difficulty in unraveling the relationship between these two disease states and diabetes risk. In one recent review, it was suggested that obesity and PCOS share interrelated adverse effects on glucose metabolism. As a result, these associations are “more complex than a simple cause-and-effect process.” the authors of that article concluded.

Furthermore, in their examination of metabolic pathways, genetic susceptibility, and behavioral factors that might link PCOS, weight gain, and T2D, the authors did not ignore the psychological impact of PCOS in causing obesity and, as a byproduct, diabetes. These psychological factors might be relevant to treatment.

For example, depression and stress “might hamper ongoing attempts at lifestyle change and therefore effective weight loss” in at least some women, they cautioned.

However, in encouraging weight loss in overweight women with PCOS, the debate about cause of T2D might be moot in practical terms, according to Michael Dansinger, MD, founding director of the diabetes reversal program at Tufts Medical Center, Boston.

“Reducing excess body fat reduces the risk of type 2 diabetes,” Dr. Dansinger said in an interview. “Since women with obesity and PCOS are clearly at risk for future type 2 diabetes, that’s another reason to lose excess body fat through healthy eating and exercise.”

Dr. Anagnostis and Dr. Dansinger reported no relevant conflicts of interest.

The increased risk of type 2 diabetes in women with polycystic ovary syndrome is well established, but a new analysis has shown that obesity is the major mediator and a target for preventing or reversing this comorbidity.

rumruay/Shutterstock

“Most women with PCOS are obese, complicating the effort to understand whether high rates of diabetes in this population are due to PCOS or excess weight, but our study now suggest that obesity isa targetable risk factor,” reported Panagiotis Anagnostis, MD, PhD, a reproductive endocrinologist at the Medical School of Aristotle University, Thessaloniki, Greece.

Obesity is also a known risk factor for type 2 diabetes (T2D), but there is reason to suspect that PCOS, which is associated with abnormal carbohydrate metabolism, has a direct impact on the risk of developing T2D, according to Dr. Anagnostis. It is also reasonable to expect “a synergistic deleterious effect” from PCOS and obesity on adverse changes in glucose metabolism that lead to T2D.

Even though rates of obesity among women with PCOS reach 80% in some studies, Dr. Anagnostis attempted to disentangle the relationship between obesity, PCOS, and risk of T2D using a large set of data drawn from a comprehensive search of published studies.

After screening with predefined criteria, 12 studies provided data on 224,284 women, of whom 45,361 had PCOS and 5,717 had T2D. Not least of the criteria for inclusion in this analysis, all studies stratified women as obese, defined as a body mass index (BMI) greater than 30 kg/m², or nonobese, he reported at the annual meeting of the Endocrine Society.



Diabetes risk tripled in PCOS

When compared without regard to BMI, the relative risk of having T2D among those with PCOS relative to those without this condition was more than three times greater (RR 3.13; P < .001). When women with PCOS were stratified for BMI, obesity was associated with a more than fourfold increased risk relative to controls without PCOS (RR, 4.06; P < .001).

In women who were nonobese, the risk of T2D was numerically higher for those with PCOS than those without (RR, 2.68), but it was only a trend with a large confidence interval (95% confidence interval, 0.97-7.49).

Among women with PCOS, those who were obese also had a more than fourfold and highly significant increased risk of T2D relative to those who were not obese (RR, 4.20; P < .001).

The message from these data is that obesity is a major and potentially modifiable risk factor for diabetes in women with PCOS, according to Dr. Anagnostis.

He said these data provide the basis for recommending weight loss specifically for managing this common PCOS comorbidity.

Almost the same relative risk of diabetes was derived from an analysis of a women’s health database published 2 years ago in Diabetes Care. In that study with 1,916 person-years of follow-up, the hazard ratio for T2D was also more than three times greater (HR, 3.23; P < .001) for those with PCOS relative to those without the syndrome.

However, normal BMI did not eliminate risk of developing diabetes in this study. Rather, the relative risk of T2D in women with PCOS was higher in those of normal weight, compared with those who were obese (HR, 4.68 vs. 2.36; P < .005). The investigators recommend screening all women with PCOS at least every 3 years with more frequent screening in those with risk factors.



PCOS complexity challenges simple conclusions

The complexity of disturbed metabolic pathways in patients with PCOS and obesity might explain some of the difficulty in unraveling the relationship between these two disease states and diabetes risk. In one recent review, it was suggested that obesity and PCOS share interrelated adverse effects on glucose metabolism. As a result, these associations are “more complex than a simple cause-and-effect process.” the authors of that article concluded.

Furthermore, in their examination of metabolic pathways, genetic susceptibility, and behavioral factors that might link PCOS, weight gain, and T2D, the authors did not ignore the psychological impact of PCOS in causing obesity and, as a byproduct, diabetes. These psychological factors might be relevant to treatment.

For example, depression and stress “might hamper ongoing attempts at lifestyle change and therefore effective weight loss” in at least some women, they cautioned.

However, in encouraging weight loss in overweight women with PCOS, the debate about cause of T2D might be moot in practical terms, according to Michael Dansinger, MD, founding director of the diabetes reversal program at Tufts Medical Center, Boston.

“Reducing excess body fat reduces the risk of type 2 diabetes,” Dr. Dansinger said in an interview. “Since women with obesity and PCOS are clearly at risk for future type 2 diabetes, that’s another reason to lose excess body fat through healthy eating and exercise.”

Dr. Anagnostis and Dr. Dansinger reported no relevant conflicts of interest.

More sleep at night, fewer or no sleep problems, and low levels of professional burnout were associated with a lower risk of developing COVID-19 among health care workers considered to be at high risk for exposure to patients with COVID-19, new evidence reveals.

PRImageFactory/iStock/Getty Images

For each additional hour of sleep at night, for example, risk for COVID-19 dropped by 12% in a study of 2844 frontline health care workers.

Furthermore, those who reported experiencing work-related burnout every day were 2.6 times more likely to report having COVID-19, to report having COVID-19 for a longer time, and to experience COVID-19 of more severity.

“This study underscores the importance of non–hygiene-related risk factors for COVID-19 and supports a holistic approach to health – including optimal sleep and job stress reduction to protect our health care workers from this and future pandemics,” senior author Sara B. Seidelmann, MD, said in an interview.

“Our findings add to the literature that sleep duration at night, sleep problems, and burnout may be risk factors for viral illnesses like COVID-19,” wrote Dr. Seidelmann and colleagues.

This is the first study to link COVID-19 risk to sleep habits – including number of hours of sleep at night, daytime napping hours, and severe sleep problems – among health care workers across multiple countries.

The study was published online March 22 in BMJ Nutrition, Prevention, and Health.

The researchers surveyed health care professionals in specialties considered to place personnel at high risk for exposure to SARS-CoV-2: critical care, emergency care, and internal medicine.

The association between sleep and burnout risk factors and COVID-19 did not vary significantly by specialty. “We didn’t detect any significant interactions between age, sex, specialty, or country,” said Dr. Seidelmann, assistant professor of clinical medicine at Columbia University College of Physicians and Surgeons, New York, and an internist at Stamford (Conn.) Hospital.

In addition to the 12% lower risk associated with each additional hour of sleep at night, each 1 additional hour of daytime napping was linked with a 6% increased risk for COVID-19 in an adjusted analysis (odds ratio [OR], 1.06; 95% confidence interval [CI], 1.01-1.12).

Daytime napping slightly increased risk for COVID-19 in five of the six countries included in the study: France, Germany, Italy, the United Kingdom, and the United States. In contrast, in Spain, napping had a nonsignificant protective effect.

The survey asked health care workers to recall nighttime sleep duration, sleep disorders, and burnout in the year prior to onset of the COVID-19 pandemic.
 

‘Significant, close contact’ with COVID-19?

Lead author Hyunju Kim, NP, Dr. Seidelmann, and colleagues conducted the population-based, case-control study from July 17 to Sept. 25, 2020. They identified health care workers from the SurveyHealthcareGlobus (SHG) network.

Of the respondents, 72% were men. The mean age of the participants was 48 years, and the study population was 77% White, 12% Asian, 6% mixed background, 2% Black, and 1% other. (The remainder preferred not to say).

The 568 health care workers considered to have COVID-19 were classified on the basis of self-reported symptoms. Control participants had no symptoms associated with COVID-19.

All 2,844 participants answered yes to a question about having “significant close contact” with COVID-19 patients in their workplace.

Compared to reporting no sleep problems, having three such problems – difficulty sleeping at night, poor sleep continuity, and frequent use of sleeping pills – was associated with 88% greater odds of COVID-19 (OR, 1.88; 95% CI, 1.17–3.01).

Having one sleep problem was not associated with COVID-19.
 

More burnout, greater risk

The health care workers reported the severity of any work-related burnout. “There was a significant dose-response relationship between frequency of burnout and COVID-19,” the researchers noted.

Those who reported having burnout rarely or weekly had a 1.3-1.4 greater chance of reporting COVID-19 compared to those who reported having no burnout, for example.

In addition, reporting a high level of burnout was linked to about three times the risk for having COVID-19 of longer duration and of greater severity.

What drives the association between sleep problems, burnout, and higher risk for COVID-19 and severe COVID-19 remains unknown.

“The mechanism underlying these associations isn’t clear, but suboptimal sleep, sleep disorders, and stress may result in immune system dysregulation, increased inflammation, and alterations in hormones such as cortisol and melatonin that may increase vulnerability to viral infections,” Dr. Seidelmann said.
 

Strengths and limitations

Using a large network of health care workers in the early phase of the pandemic is a strength of the study. How generalizable the findings are outside the SHG database of 1.5 million health care workers remains unknown.

Another limitation was reliance on self-reporting of COVID-19 patient exposure, outcomes, and covariates, which could have introduced bias.

“However,” the researchers noted, “health care workers are likely a reliable source of information.”
 

Insomnia a common challenge

A 2020 meta-analysis examined the effect of insomnia and psychological factors on COVID-19 risk among health care workers. Lead author Kavita Batra, PhD, of the University of Nevada, Las Vegas (UNLV), and colleagues found that the pooled prevalence of insomnia was almost 28%.

“The recent six-country study by Kim and colleagues also underscores this relationship between lack of sleep and having higher odds of COVID-19 infection,” Manoj Sharma, MBBS, PhD, professor of social and behavioral health in the UNLV department of environmental and occupational health, and one of the study authors, said in an interview.

More research is warranted to learn the direction of the association, he said. Does reduced sleep lower immunity and make a health care worker more susceptible to SARS-CoV-2 infection, or does the anxiety associated with COVID-19 contribute to insomnia?

“Practicing sleep hygiene is a must not only for health workers but also for everyone,” Dr. Sharma added. Recommendations include having fixed hours of going to bed, fixed hours of waking up, not overdoing naps, having at least 30 minutes of winding down before sleeping, having a dark bedroom devoid of all electronics and other disturbances, avoiding smoking, alcohol, and stimulants (such as caffeine) before sleeping, and practicing relaxation right before sleeping, he said.

“It is hard for some health care workers, especially those who work night shifts, but it must be a priority to follow as many sleep hygiene measures as possible,” Dr. Sharma said. “After all, if you do not take care of yourself how can you take care of others?”

Dr. Seidelmann, Dr. Batra, and Dr. Sharma have disclosed no relevant financial relationships.

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

More sleep at night, fewer or no sleep problems, and low levels of professional burnout were associated with a lower risk of developing COVID-19 among health care workers considered to be at high risk for exposure to patients with COVID-19, new evidence reveals.

PRImageFactory/iStock/Getty Images

For each additional hour of sleep at night, for example, risk for COVID-19 dropped by 12% in a study of 2844 frontline health care workers.

Furthermore, those who reported experiencing work-related burnout every day were 2.6 times more likely to report having COVID-19, to report having COVID-19 for a longer time, and to experience COVID-19 of more severity.

“This study underscores the importance of non–hygiene-related risk factors for COVID-19 and supports a holistic approach to health – including optimal sleep and job stress reduction to protect our health care workers from this and future pandemics,” senior author Sara B. Seidelmann, MD, said in an interview.

“Our findings add to the literature that sleep duration at night, sleep problems, and burnout may be risk factors for viral illnesses like COVID-19,” wrote Dr. Seidelmann and colleagues.

This is the first study to link COVID-19 risk to sleep habits – including number of hours of sleep at night, daytime napping hours, and severe sleep problems – among health care workers across multiple countries.

The study was published online March 22 in BMJ Nutrition, Prevention, and Health.

The researchers surveyed health care professionals in specialties considered to place personnel at high risk for exposure to SARS-CoV-2: critical care, emergency care, and internal medicine.

The association between sleep and burnout risk factors and COVID-19 did not vary significantly by specialty. “We didn’t detect any significant interactions between age, sex, specialty, or country,” said Dr. Seidelmann, assistant professor of clinical medicine at Columbia University College of Physicians and Surgeons, New York, and an internist at Stamford (Conn.) Hospital.

In addition to the 12% lower risk associated with each additional hour of sleep at night, each 1 additional hour of daytime napping was linked with a 6% increased risk for COVID-19 in an adjusted analysis (odds ratio [OR], 1.06; 95% confidence interval [CI], 1.01-1.12).

Daytime napping slightly increased risk for COVID-19 in five of the six countries included in the study: France, Germany, Italy, the United Kingdom, and the United States. In contrast, in Spain, napping had a nonsignificant protective effect.

The survey asked health care workers to recall nighttime sleep duration, sleep disorders, and burnout in the year prior to onset of the COVID-19 pandemic.
 

‘Significant, close contact’ with COVID-19?

Lead author Hyunju Kim, NP, Dr. Seidelmann, and colleagues conducted the population-based, case-control study from July 17 to Sept. 25, 2020. They identified health care workers from the SurveyHealthcareGlobus (SHG) network.

Of the respondents, 72% were men. The mean age of the participants was 48 years, and the study population was 77% White, 12% Asian, 6% mixed background, 2% Black, and 1% other. (The remainder preferred not to say).

The 568 health care workers considered to have COVID-19 were classified on the basis of self-reported symptoms. Control participants had no symptoms associated with COVID-19.

All 2,844 participants answered yes to a question about having “significant close contact” with COVID-19 patients in their workplace.

Compared to reporting no sleep problems, having three such problems – difficulty sleeping at night, poor sleep continuity, and frequent use of sleeping pills – was associated with 88% greater odds of COVID-19 (OR, 1.88; 95% CI, 1.17–3.01).

Having one sleep problem was not associated with COVID-19.
 

More burnout, greater risk

The health care workers reported the severity of any work-related burnout. “There was a significant dose-response relationship between frequency of burnout and COVID-19,” the researchers noted.

Those who reported having burnout rarely or weekly had a 1.3-1.4 greater chance of reporting COVID-19 compared to those who reported having no burnout, for example.

In addition, reporting a high level of burnout was linked to about three times the risk for having COVID-19 of longer duration and of greater severity.

What drives the association between sleep problems, burnout, and higher risk for COVID-19 and severe COVID-19 remains unknown.

“The mechanism underlying these associations isn’t clear, but suboptimal sleep, sleep disorders, and stress may result in immune system dysregulation, increased inflammation, and alterations in hormones such as cortisol and melatonin that may increase vulnerability to viral infections,” Dr. Seidelmann said.
 

Strengths and limitations

Using a large network of health care workers in the early phase of the pandemic is a strength of the study. How generalizable the findings are outside the SHG database of 1.5 million health care workers remains unknown.

Another limitation was reliance on self-reporting of COVID-19 patient exposure, outcomes, and covariates, which could have introduced bias.

“However,” the researchers noted, “health care workers are likely a reliable source of information.”
 

Insomnia a common challenge

A 2020 meta-analysis examined the effect of insomnia and psychological factors on COVID-19 risk among health care workers. Lead author Kavita Batra, PhD, of the University of Nevada, Las Vegas (UNLV), and colleagues found that the pooled prevalence of insomnia was almost 28%.

“The recent six-country study by Kim and colleagues also underscores this relationship between lack of sleep and having higher odds of COVID-19 infection,” Manoj Sharma, MBBS, PhD, professor of social and behavioral health in the UNLV department of environmental and occupational health, and one of the study authors, said in an interview.

More research is warranted to learn the direction of the association, he said. Does reduced sleep lower immunity and make a health care worker more susceptible to SARS-CoV-2 infection, or does the anxiety associated with COVID-19 contribute to insomnia?

“Practicing sleep hygiene is a must not only for health workers but also for everyone,” Dr. Sharma added. Recommendations include having fixed hours of going to bed, fixed hours of waking up, not overdoing naps, having at least 30 minutes of winding down before sleeping, having a dark bedroom devoid of all electronics and other disturbances, avoiding smoking, alcohol, and stimulants (such as caffeine) before sleeping, and practicing relaxation right before sleeping, he said.

“It is hard for some health care workers, especially those who work night shifts, but it must be a priority to follow as many sleep hygiene measures as possible,” Dr. Sharma said. “After all, if you do not take care of yourself how can you take care of others?”

Dr. Seidelmann, Dr. Batra, and Dr. Sharma have disclosed no relevant financial relationships.

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

More sleep at night, fewer or no sleep problems, and low levels of professional burnout were associated with a lower risk of developing COVID-19 among health care workers considered to be at high risk for exposure to patients with COVID-19, new evidence reveals.

PRImageFactory/iStock/Getty Images

For each additional hour of sleep at night, for example, risk for COVID-19 dropped by 12% in a study of 2844 frontline health care workers.

Furthermore, those who reported experiencing work-related burnout every day were 2.6 times more likely to report having COVID-19, to report having COVID-19 for a longer time, and to experience COVID-19 of more severity.

“This study underscores the importance of non–hygiene-related risk factors for COVID-19 and supports a holistic approach to health – including optimal sleep and job stress reduction to protect our health care workers from this and future pandemics,” senior author Sara B. Seidelmann, MD, said in an interview.

“Our findings add to the literature that sleep duration at night, sleep problems, and burnout may be risk factors for viral illnesses like COVID-19,” wrote Dr. Seidelmann and colleagues.

This is the first study to link COVID-19 risk to sleep habits – including number of hours of sleep at night, daytime napping hours, and severe sleep problems – among health care workers across multiple countries.

The study was published online March 22 in BMJ Nutrition, Prevention, and Health.

The researchers surveyed health care professionals in specialties considered to place personnel at high risk for exposure to SARS-CoV-2: critical care, emergency care, and internal medicine.

The association between sleep and burnout risk factors and COVID-19 did not vary significantly by specialty. “We didn’t detect any significant interactions between age, sex, specialty, or country,” said Dr. Seidelmann, assistant professor of clinical medicine at Columbia University College of Physicians and Surgeons, New York, and an internist at Stamford (Conn.) Hospital.

In addition to the 12% lower risk associated with each additional hour of sleep at night, each 1 additional hour of daytime napping was linked with a 6% increased risk for COVID-19 in an adjusted analysis (odds ratio [OR], 1.06; 95% confidence interval [CI], 1.01-1.12).

Daytime napping slightly increased risk for COVID-19 in five of the six countries included in the study: France, Germany, Italy, the United Kingdom, and the United States. In contrast, in Spain, napping had a nonsignificant protective effect.

The survey asked health care workers to recall nighttime sleep duration, sleep disorders, and burnout in the year prior to onset of the COVID-19 pandemic.
 

‘Significant, close contact’ with COVID-19?

Lead author Hyunju Kim, NP, Dr. Seidelmann, and colleagues conducted the population-based, case-control study from July 17 to Sept. 25, 2020. They identified health care workers from the SurveyHealthcareGlobus (SHG) network.

Of the respondents, 72% were men. The mean age of the participants was 48 years, and the study population was 77% White, 12% Asian, 6% mixed background, 2% Black, and 1% other. (The remainder preferred not to say).

The 568 health care workers considered to have COVID-19 were classified on the basis of self-reported symptoms. Control participants had no symptoms associated with COVID-19.

All 2,844 participants answered yes to a question about having “significant close contact” with COVID-19 patients in their workplace.

Compared to reporting no sleep problems, having three such problems – difficulty sleeping at night, poor sleep continuity, and frequent use of sleeping pills – was associated with 88% greater odds of COVID-19 (OR, 1.88; 95% CI, 1.17–3.01).

Having one sleep problem was not associated with COVID-19.
 

More burnout, greater risk

The health care workers reported the severity of any work-related burnout. “There was a significant dose-response relationship between frequency of burnout and COVID-19,” the researchers noted.

Those who reported having burnout rarely or weekly had a 1.3-1.4 greater chance of reporting COVID-19 compared to those who reported having no burnout, for example.

In addition, reporting a high level of burnout was linked to about three times the risk for having COVID-19 of longer duration and of greater severity.

What drives the association between sleep problems, burnout, and higher risk for COVID-19 and severe COVID-19 remains unknown.

“The mechanism underlying these associations isn’t clear, but suboptimal sleep, sleep disorders, and stress may result in immune system dysregulation, increased inflammation, and alterations in hormones such as cortisol and melatonin that may increase vulnerability to viral infections,” Dr. Seidelmann said.
 

Strengths and limitations

Using a large network of health care workers in the early phase of the pandemic is a strength of the study. How generalizable the findings are outside the SHG database of 1.5 million health care workers remains unknown.

Another limitation was reliance on self-reporting of COVID-19 patient exposure, outcomes, and covariates, which could have introduced bias.

“However,” the researchers noted, “health care workers are likely a reliable source of information.”
 

Insomnia a common challenge

A 2020 meta-analysis examined the effect of insomnia and psychological factors on COVID-19 risk among health care workers. Lead author Kavita Batra, PhD, of the University of Nevada, Las Vegas (UNLV), and colleagues found that the pooled prevalence of insomnia was almost 28%.

“The recent six-country study by Kim and colleagues also underscores this relationship between lack of sleep and having higher odds of COVID-19 infection,” Manoj Sharma, MBBS, PhD, professor of social and behavioral health in the UNLV department of environmental and occupational health, and one of the study authors, said in an interview.

More research is warranted to learn the direction of the association, he said. Does reduced sleep lower immunity and make a health care worker more susceptible to SARS-CoV-2 infection, or does the anxiety associated with COVID-19 contribute to insomnia?

“Practicing sleep hygiene is a must not only for health workers but also for everyone,” Dr. Sharma added. Recommendations include having fixed hours of going to bed, fixed hours of waking up, not overdoing naps, having at least 30 minutes of winding down before sleeping, having a dark bedroom devoid of all electronics and other disturbances, avoiding smoking, alcohol, and stimulants (such as caffeine) before sleeping, and practicing relaxation right before sleeping, he said.

“It is hard for some health care workers, especially those who work night shifts, but it must be a priority to follow as many sleep hygiene measures as possible,” Dr. Sharma said. “After all, if you do not take care of yourself how can you take care of others?”

Dr. Seidelmann, Dr. Batra, and Dr. Sharma have disclosed no relevant financial relationships.

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

A new study shows apolipoprotein B (apoB) and non-HDL cholesterol – but not LDL cholesterol – are associated with increased risk for all-cause mortality and myocardial infarction in patients taking statins.

Bruce Jancin/Frontline Medical News

Moreover, apoB was a more accurate marker of all-cause mortality risk than non-HDL or LDL cholesterol and was more accurate at identifying MI risk than LDL cholesterol.

“Any patient that comes to a doctor for evaluation, if statin treatment is sufficient, the doctor should look not only at LDL cholesterol but HDL cholesterol and apoB, if its available – that is the take-home message,” senior author Børge Grønne Nordestgaard, MD, DMSC, University of Copenhagen, said in an interview.

The findings are very relevant to clinical practice because international guidelines focus on LDL cholesterol and “many doctors are brainwashed that that is the only thing they should look at, just to keep LDL cholesterol down,” he said. “I’ve worked for years with triglyceride lipoproteins, what I call remnant cholesterol, and I think that the risk is very high also when you have high remnant cholesterol.”

Previous work has shown that apoB and non-HDL cholesterol better reflect atherosclerotic cardiovascular disease risk than LDL cholesterol. This is the first study, however, to show that elevated apoB and non-HDL cholesterol are associated with a higher risk for all-cause death in statin-treated patients with low LDL cholesterol, Dr. Nordestgaard noted.

The investigators compared outcomes among 13,015 statin-treated participants in the Copenhagen General Population Study using median baseline values of 92 mg/dL for apoB, 3.1 mmol/L (120 mg/dL) for non-HDL cholesterol, and 2.3 mmol/L (89 mg/dL) for LDL cholesterol. Over a median follow-up of 8 years, there were 2,499 deaths and 537 MIs.

As reported in the Journal of the American College of Cardiology, discordant apoB above the median with LDL cholesterol below was associated with a 21% increased risk for all-cause mortality (hazard ratio, 1.21; 95% confidence interval, 1.07-1.36) and 49% increased risk for MI (HR, 1.49; 95% CI, 1.15-1.92), compared with concordant apoB and LDL cholesterol below the medians.

Similar results were found for discordant non-HDL cholesterol above the median with low LDL cholesterol for all-cause mortality (HR, 1.18; 95% CI, 1.02-1.36) and MI (1.78; 95% CI, 1.35-2.34).

No such associations with mortality or MI were observed when LDL cholesterol was above the median and apoB or non-HDL below.

Additional analyses showed that high apoB with low non-HDL cholesterol was associated with a higher risk for all-cause mortality (HR, 1.21; 95% CI, 1.03-1.41), whereas high non-HDL cholesterol with low apoB was associated with a lower risk (HR, 0.75; 95% CI, 0.62-0.92).

Current guidelines define apoB greater than 130 mg/dL as a risk modifier in patients not using statins but, the authors wrote, “based on our results, the threshold for apoB as a risk modifier in statin-treated patients should be closer to 92 mg/dL than to 130 mg/dL.”

In an accompanying editorial, Neil J. Stone, MD, and Donald Lloyd-Jones, MD, both from Northwestern University, Chicago, said that American and European guidelines acknowledge the usefulness of apoB and non-HDL cholesterol in their risk algorithms and as possible targets to indicate efficacy, but don’t give a strong recommendation for apoB to assess residual risk.

“This paper suggests that, in the next iteration, we’ve got to give a stronger thought to measuring apoB for residual risk in those with secondary prevention,” Dr. Stone, vice chair of the 2018 American Heart Association/ACC cholesterol guidelines, said in an interview.

“The whole part of the guidelines was not to focus on any one number but to focus on the clinical risk as a whole,” he said. “You can enlarge your understanding of the patient by looking at their non-HDL, which you have anyway, and in certain circumstances, for example, people with metabolic syndrome, diabetes, obesity, or high triglycerides, those people might very well benefit from an apoB to further understand their risk. This paper simply highlights that and, therefore, was very valuable.”

Dr. Stone and Dr. Lloyd-Jones, however, pointed out that statin use was self-reported and information was lacking on adherence, dose intensity, and the amount of LDL cholesterol lowering from baseline. LDL cholesterol levels were also above current recommendations for optimizing risk reduction. “If statin dosing and LDL [cholesterol] were not optimized already, then there may have been ‘room’ for non-HDL [cholesterol] and apoB to add value in understanding residual risk,” they wrote.

The editorialists suggested that sequential use, rather than regular use, of apoB and non-HDL cholesterol may be best and that incorporating this information may be particularly beneficial for patients with metabolic disorders and elevated triglycerides after statin therapy.

“Maybe this paper is a wake-up call that there are other markers out there that can tell you that you still have higher risk and need to tighten up lifestyle and maybe be more adherent,” Dr. Stone said. “I think this is a wonderful chance to say that preventive cardiology isn’t just ‘set it and forget it’.”

C. Noel Bairey Merz, MD, who coauthored the 2018 cholesterol guidelines, agreed there’s “an overexuberant focus on LDL [cholesterol] for residual risk” and highlighted a recent systematic review of statins, ezetimibe, and PCSK9 cardiovascular outcomes trials that showed very little gain from aggressively driving down LDL below 100 mg/dL, unless the patient is at extremely high risk.

“If I, as a treating cardiologist who spends a lot of time on lipids, had a patient on a high-intensity statin and they didn’t drop [their LDL cholesterol] 50% and I already had them going to cardiac rehab and they were already losing weight, would I measure apoB? Yeah, I might, to motivate them to do more or to take Vascepa,” she said.

“This study is a useful addition to a relatively important problem, which is residual risk, and really supports personalized or precision medicine,” added Bairey Merz, MD, Cedars-Sinai Medical Center, Los Angeles. “But now we have to do the work and do an intervention trial in these people and see whether these markers make a difference.”

The study was supported by Herlev and Gentofte Hospital’s Research Fund and the department of clinical biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital. Dr. Nordestgaard has had consultancies or talks sponsored by AstraZeneca, Sanofi, Regeneron, Akcea, Amarin, Amgen, Esperion, Kowa, Novartis, Novo Nordisk, and Silence Therapeutics. All other authors, Dr. Stone, and Dr. Lloyd-Jones reported no conflicts. Dr. Merz reported no relevant disclosures.

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

A new study shows apolipoprotein B (apoB) and non-HDL cholesterol – but not LDL cholesterol – are associated with increased risk for all-cause mortality and myocardial infarction in patients taking statins.

Bruce Jancin/Frontline Medical News

Moreover, apoB was a more accurate marker of all-cause mortality risk than non-HDL or LDL cholesterol and was more accurate at identifying MI risk than LDL cholesterol.

“Any patient that comes to a doctor for evaluation, if statin treatment is sufficient, the doctor should look not only at LDL cholesterol but HDL cholesterol and apoB, if its available – that is the take-home message,” senior author Børge Grønne Nordestgaard, MD, DMSC, University of Copenhagen, said in an interview.

The findings are very relevant to clinical practice because international guidelines focus on LDL cholesterol and “many doctors are brainwashed that that is the only thing they should look at, just to keep LDL cholesterol down,” he said. “I’ve worked for years with triglyceride lipoproteins, what I call remnant cholesterol, and I think that the risk is very high also when you have high remnant cholesterol.”

Previous work has shown that apoB and non-HDL cholesterol better reflect atherosclerotic cardiovascular disease risk than LDL cholesterol. This is the first study, however, to show that elevated apoB and non-HDL cholesterol are associated with a higher risk for all-cause death in statin-treated patients with low LDL cholesterol, Dr. Nordestgaard noted.

The investigators compared outcomes among 13,015 statin-treated participants in the Copenhagen General Population Study using median baseline values of 92 mg/dL for apoB, 3.1 mmol/L (120 mg/dL) for non-HDL cholesterol, and 2.3 mmol/L (89 mg/dL) for LDL cholesterol. Over a median follow-up of 8 years, there were 2,499 deaths and 537 MIs.

As reported in the Journal of the American College of Cardiology, discordant apoB above the median with LDL cholesterol below was associated with a 21% increased risk for all-cause mortality (hazard ratio, 1.21; 95% confidence interval, 1.07-1.36) and 49% increased risk for MI (HR, 1.49; 95% CI, 1.15-1.92), compared with concordant apoB and LDL cholesterol below the medians.

Similar results were found for discordant non-HDL cholesterol above the median with low LDL cholesterol for all-cause mortality (HR, 1.18; 95% CI, 1.02-1.36) and MI (1.78; 95% CI, 1.35-2.34).

No such associations with mortality or MI were observed when LDL cholesterol was above the median and apoB or non-HDL below.

Additional analyses showed that high apoB with low non-HDL cholesterol was associated with a higher risk for all-cause mortality (HR, 1.21; 95% CI, 1.03-1.41), whereas high non-HDL cholesterol with low apoB was associated with a lower risk (HR, 0.75; 95% CI, 0.62-0.92).

Current guidelines define apoB greater than 130 mg/dL as a risk modifier in patients not using statins but, the authors wrote, “based on our results, the threshold for apoB as a risk modifier in statin-treated patients should be closer to 92 mg/dL than to 130 mg/dL.”

In an accompanying editorial, Neil J. Stone, MD, and Donald Lloyd-Jones, MD, both from Northwestern University, Chicago, said that American and European guidelines acknowledge the usefulness of apoB and non-HDL cholesterol in their risk algorithms and as possible targets to indicate efficacy, but don’t give a strong recommendation for apoB to assess residual risk.

“This paper suggests that, in the next iteration, we’ve got to give a stronger thought to measuring apoB for residual risk in those with secondary prevention,” Dr. Stone, vice chair of the 2018 American Heart Association/ACC cholesterol guidelines, said in an interview.

“The whole part of the guidelines was not to focus on any one number but to focus on the clinical risk as a whole,” he said. “You can enlarge your understanding of the patient by looking at their non-HDL, which you have anyway, and in certain circumstances, for example, people with metabolic syndrome, diabetes, obesity, or high triglycerides, those people might very well benefit from an apoB to further understand their risk. This paper simply highlights that and, therefore, was very valuable.”

Dr. Stone and Dr. Lloyd-Jones, however, pointed out that statin use was self-reported and information was lacking on adherence, dose intensity, and the amount of LDL cholesterol lowering from baseline. LDL cholesterol levels were also above current recommendations for optimizing risk reduction. “If statin dosing and LDL [cholesterol] were not optimized already, then there may have been ‘room’ for non-HDL [cholesterol] and apoB to add value in understanding residual risk,” they wrote.

The editorialists suggested that sequential use, rather than regular use, of apoB and non-HDL cholesterol may be best and that incorporating this information may be particularly beneficial for patients with metabolic disorders and elevated triglycerides after statin therapy.

“Maybe this paper is a wake-up call that there are other markers out there that can tell you that you still have higher risk and need to tighten up lifestyle and maybe be more adherent,” Dr. Stone said. “I think this is a wonderful chance to say that preventive cardiology isn’t just ‘set it and forget it’.”

C. Noel Bairey Merz, MD, who coauthored the 2018 cholesterol guidelines, agreed there’s “an overexuberant focus on LDL [cholesterol] for residual risk” and highlighted a recent systematic review of statins, ezetimibe, and PCSK9 cardiovascular outcomes trials that showed very little gain from aggressively driving down LDL below 100 mg/dL, unless the patient is at extremely high risk.

“If I, as a treating cardiologist who spends a lot of time on lipids, had a patient on a high-intensity statin and they didn’t drop [their LDL cholesterol] 50% and I already had them going to cardiac rehab and they were already losing weight, would I measure apoB? Yeah, I might, to motivate them to do more or to take Vascepa,” she said.

“This study is a useful addition to a relatively important problem, which is residual risk, and really supports personalized or precision medicine,” added Bairey Merz, MD, Cedars-Sinai Medical Center, Los Angeles. “But now we have to do the work and do an intervention trial in these people and see whether these markers make a difference.”

The study was supported by Herlev and Gentofte Hospital’s Research Fund and the department of clinical biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital. Dr. Nordestgaard has had consultancies or talks sponsored by AstraZeneca, Sanofi, Regeneron, Akcea, Amarin, Amgen, Esperion, Kowa, Novartis, Novo Nordisk, and Silence Therapeutics. All other authors, Dr. Stone, and Dr. Lloyd-Jones reported no conflicts. Dr. Merz reported no relevant disclosures.

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

A new study shows apolipoprotein B (apoB) and non-HDL cholesterol – but not LDL cholesterol – are associated with increased risk for all-cause mortality and myocardial infarction in patients taking statins.

Bruce Jancin/Frontline Medical News

Moreover, apoB was a more accurate marker of all-cause mortality risk than non-HDL or LDL cholesterol and was more accurate at identifying MI risk than LDL cholesterol.

“Any patient that comes to a doctor for evaluation, if statin treatment is sufficient, the doctor should look not only at LDL cholesterol but HDL cholesterol and apoB, if its available – that is the take-home message,” senior author Børge Grønne Nordestgaard, MD, DMSC, University of Copenhagen, said in an interview.

The findings are very relevant to clinical practice because international guidelines focus on LDL cholesterol and “many doctors are brainwashed that that is the only thing they should look at, just to keep LDL cholesterol down,” he said. “I’ve worked for years with triglyceride lipoproteins, what I call remnant cholesterol, and I think that the risk is very high also when you have high remnant cholesterol.”

Previous work has shown that apoB and non-HDL cholesterol better reflect atherosclerotic cardiovascular disease risk than LDL cholesterol. This is the first study, however, to show that elevated apoB and non-HDL cholesterol are associated with a higher risk for all-cause death in statin-treated patients with low LDL cholesterol, Dr. Nordestgaard noted.

The investigators compared outcomes among 13,015 statin-treated participants in the Copenhagen General Population Study using median baseline values of 92 mg/dL for apoB, 3.1 mmol/L (120 mg/dL) for non-HDL cholesterol, and 2.3 mmol/L (89 mg/dL) for LDL cholesterol. Over a median follow-up of 8 years, there were 2,499 deaths and 537 MIs.

As reported in the Journal of the American College of Cardiology, discordant apoB above the median with LDL cholesterol below was associated with a 21% increased risk for all-cause mortality (hazard ratio, 1.21; 95% confidence interval, 1.07-1.36) and 49% increased risk for MI (HR, 1.49; 95% CI, 1.15-1.92), compared with concordant apoB and LDL cholesterol below the medians.

Similar results were found for discordant non-HDL cholesterol above the median with low LDL cholesterol for all-cause mortality (HR, 1.18; 95% CI, 1.02-1.36) and MI (1.78; 95% CI, 1.35-2.34).

No such associations with mortality or MI were observed when LDL cholesterol was above the median and apoB or non-HDL below.

Additional analyses showed that high apoB with low non-HDL cholesterol was associated with a higher risk for all-cause mortality (HR, 1.21; 95% CI, 1.03-1.41), whereas high non-HDL cholesterol with low apoB was associated with a lower risk (HR, 0.75; 95% CI, 0.62-0.92).

Current guidelines define apoB greater than 130 mg/dL as a risk modifier in patients not using statins but, the authors wrote, “based on our results, the threshold for apoB as a risk modifier in statin-treated patients should be closer to 92 mg/dL than to 130 mg/dL.”

In an accompanying editorial, Neil J. Stone, MD, and Donald Lloyd-Jones, MD, both from Northwestern University, Chicago, said that American and European guidelines acknowledge the usefulness of apoB and non-HDL cholesterol in their risk algorithms and as possible targets to indicate efficacy, but don’t give a strong recommendation for apoB to assess residual risk.

“This paper suggests that, in the next iteration, we’ve got to give a stronger thought to measuring apoB for residual risk in those with secondary prevention,” Dr. Stone, vice chair of the 2018 American Heart Association/ACC cholesterol guidelines, said in an interview.

“The whole part of the guidelines was not to focus on any one number but to focus on the clinical risk as a whole,” he said. “You can enlarge your understanding of the patient by looking at their non-HDL, which you have anyway, and in certain circumstances, for example, people with metabolic syndrome, diabetes, obesity, or high triglycerides, those people might very well benefit from an apoB to further understand their risk. This paper simply highlights that and, therefore, was very valuable.”

Dr. Stone and Dr. Lloyd-Jones, however, pointed out that statin use was self-reported and information was lacking on adherence, dose intensity, and the amount of LDL cholesterol lowering from baseline. LDL cholesterol levels were also above current recommendations for optimizing risk reduction. “If statin dosing and LDL [cholesterol] were not optimized already, then there may have been ‘room’ for non-HDL [cholesterol] and apoB to add value in understanding residual risk,” they wrote.

The editorialists suggested that sequential use, rather than regular use, of apoB and non-HDL cholesterol may be best and that incorporating this information may be particularly beneficial for patients with metabolic disorders and elevated triglycerides after statin therapy.

“Maybe this paper is a wake-up call that there are other markers out there that can tell you that you still have higher risk and need to tighten up lifestyle and maybe be more adherent,” Dr. Stone said. “I think this is a wonderful chance to say that preventive cardiology isn’t just ‘set it and forget it’.”

C. Noel Bairey Merz, MD, who coauthored the 2018 cholesterol guidelines, agreed there’s “an overexuberant focus on LDL [cholesterol] for residual risk” and highlighted a recent systematic review of statins, ezetimibe, and PCSK9 cardiovascular outcomes trials that showed very little gain from aggressively driving down LDL below 100 mg/dL, unless the patient is at extremely high risk.

“If I, as a treating cardiologist who spends a lot of time on lipids, had a patient on a high-intensity statin and they didn’t drop [their LDL cholesterol] 50% and I already had them going to cardiac rehab and they were already losing weight, would I measure apoB? Yeah, I might, to motivate them to do more or to take Vascepa,” she said.

“This study is a useful addition to a relatively important problem, which is residual risk, and really supports personalized or precision medicine,” added Bairey Merz, MD, Cedars-Sinai Medical Center, Los Angeles. “But now we have to do the work and do an intervention trial in these people and see whether these markers make a difference.”

The study was supported by Herlev and Gentofte Hospital’s Research Fund and the department of clinical biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital. Dr. Nordestgaard has had consultancies or talks sponsored by AstraZeneca, Sanofi, Regeneron, Akcea, Amarin, Amgen, Esperion, Kowa, Novartis, Novo Nordisk, and Silence Therapeutics. All other authors, Dr. Stone, and Dr. Lloyd-Jones reported no conflicts. Dr. Merz reported no relevant disclosures.

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

High-intensity interval training (HIIT) was better than moderate-intensity continuous training (MICT) for improving several measures of cardiometabolic health in women with polycystic ovary syndrome (PCOS) in a prospective, randomized, single-center study with 27 women.

yacobchuk/Getty Images

After 12 weeks on a supervised exercise regimen, the women with PCOS who followed the HIIT program had significantly better improvements in aerobic capacity, insulin sensitivity, and level of sex hormone–binding globulin, Rhiannon K. Patten, MSc, said at the annual meeting of the Endocrine Society.

“HIIT can offer superior improvements in health outcomes, and should be considered as an effective tool to reduce cardiometabolic risk in women with PCOS,” concluded Ms. Patten, a researcher in the Institute for Health and Sport at Victoria University in Melbourne in her presentation (Abstract OR10-1).

“The changes we see [after 12 weeks on the HIIT regimen] seem to occur despite no change in body mass index, so rather than focus on weight loss we encourage participants to focus on the health improvements that seem to be greater with HIIT. We actively encourage the HIIT protocol right now,” she said.

Both regimens use a stationary cycle ergometer. In the HIIT protocol patients twice weekly pedal through 12 1-minute intervals at a heart rate of 90%-100% maximum, interspersed with 1 minute rest intervals. On a third day per week, patients pedal to a heart rate of 90%-95% maximum for 6-8 intervals maintained for 2 minutes and interspersed with rest intervals of 2 minutes. The MICT regimen used as a comparator has participants pedal to 60%-70% of their maximum heart rate continuously for 50 minutes 3 days weekly.



HIIT saves time

“These findings are relevant to clinical practice, because they demonstrate that HIIT is effective in women with PCOS. Reducing the time devoted to exercise to achieve fitness goals is attractive to patients. The reduced time to achieve training benefits with HIIT should improve patient compliance,” commented Andrea Dunaif, MD, professor and chief of the division of endocrinology, diabetes, and bone disease of the Mount Sinai Health System in New York, who was not involved with the study.

The overall weekly exercise time on the MICT regimen, 150 minutes, halves down to 75 minutes a week in the HIIT program. Guideline recommendations released in 2018 by the International PCOS Network recommended these as acceptable alternative exercise strategies. Ms. Patten and her associates sought to determine whether one strategy surpassed the other, the first time this has been examined in women with PCOS, she said.

They randomized 27 sedentary women 18-45 years old with a body mass index (BMI) above 25 kg/m² and diagnosed with PCOS by the Rotterdam criteria to a 12-week supervised exercise program on either the HIIT or MICT protocol. Their average BMI at entry was 36-37 kg/m². The study excluded women who smoked, were pregnant, had an illness or injury that would prevent exercise, or were on an oral contraceptive or insulin-sensitizing medication.

At the end of 12 weeks, neither group had a significant change in average weight or BMI, and waist circumference dropped by an average of just over 2 cm in both treatment groups. Lean mass increased by a mean 1 kg in the HIIT group, a significant change, compared with a nonsignificant 0.3 kg average increase in the MICT group.
 

Increased aerobic capacity ‘partially explains’ improved insulin sensitivity

Aerobic capacity, measured as peak oxygen consumption (VO₂peak), increased by an average 5.7 mL/kg per min among the HIIT patients, significantly more than the mean 3.2 mL/kg per min increase among those in the MICT program.

The insulin sensitivity index rose by a significant, relative 35% among the HIIT patients, but barely budged in the MICT group. Fasting glucose fell significantly and the glucose infusion rate increased significantly among the women who performed HIIT, but again showed little change among those doing MICT.

Analysis showed a significant link between the increase in VO₂peak and the increase in insulin sensitivity among the women engaged in HIIT, Ms. Patten reported. The improvement in the insulin sensitivity index was “partially explained” by the increase in VO₂peak, she said.

Assessment of hormone levels showed a significant increase in sex hormone–binding globulin in the HIIT patients while those in the MICT group showed a small decline in this level. The free androgen index fell by a relative 39% on average in the HIIT group, a significant drop, but decreased by a much smaller and not significant amount among the women who did MICT. The women who performed HIIT also showed a significant drop in their free testosterone level, a change not seen with MICT.

Women who performed the HIIT protocol also had a significant improvement in their menstrual cyclicity, and significant improvements in depression, stress, and anxiety, Ms Patten reported. She next plans to do longer follow-up on study participants, out to 6 and 12 months after the end of the exercise protocol.

“Overall, the findings suggest that HIIT is superior to MICT for improving fitness and insulin sensitivity in the short term. Results from a number of studies in individuals without PCOS suggest that HIIT is superior to MICT for improving fitness short term,” commented Dr. Dunaif. “This study makes an important contribution by directly investigating the impact of training intensity in women with PCOS. Larger studies will be needed before the superiority of HIIT is established for women with PCOS, and study durations of at least several months will be needed to assess the impact on reproductive outcomes such as ovulation,” she said in an interview. She also called for assessing the effects of HIIT in more diverse populations of women with PCOS.

Ms. Patten had no disclosures. Dr. Dunaif has been a consultant to Equator Therapeutics, Fractyl Laboratories, and Globe Life Sciences.

[email protected]
 

High-intensity interval training (HIIT) was better than moderate-intensity continuous training (MICT) for improving several measures of cardiometabolic health in women with polycystic ovary syndrome (PCOS) in a prospective, randomized, single-center study with 27 women.

yacobchuk/Getty Images

After 12 weeks on a supervised exercise regimen, the women with PCOS who followed the HIIT program had significantly better improvements in aerobic capacity, insulin sensitivity, and level of sex hormone–binding globulin, Rhiannon K. Patten, MSc, said at the annual meeting of the Endocrine Society.

“HIIT can offer superior improvements in health outcomes, and should be considered as an effective tool to reduce cardiometabolic risk in women with PCOS,” concluded Ms. Patten, a researcher in the Institute for Health and Sport at Victoria University in Melbourne in her presentation (Abstract OR10-1).

“The changes we see [after 12 weeks on the HIIT regimen] seem to occur despite no change in body mass index, so rather than focus on weight loss we encourage participants to focus on the health improvements that seem to be greater with HIIT. We actively encourage the HIIT protocol right now,” she said.

Both regimens use a stationary cycle ergometer. In the HIIT protocol patients twice weekly pedal through 12 1-minute intervals at a heart rate of 90%-100% maximum, interspersed with 1 minute rest intervals. On a third day per week, patients pedal to a heart rate of 90%-95% maximum for 6-8 intervals maintained for 2 minutes and interspersed with rest intervals of 2 minutes. The MICT regimen used as a comparator has participants pedal to 60%-70% of their maximum heart rate continuously for 50 minutes 3 days weekly.



HIIT saves time

“These findings are relevant to clinical practice, because they demonstrate that HIIT is effective in women with PCOS. Reducing the time devoted to exercise to achieve fitness goals is attractive to patients. The reduced time to achieve training benefits with HIIT should improve patient compliance,” commented Andrea Dunaif, MD, professor and chief of the division of endocrinology, diabetes, and bone disease of the Mount Sinai Health System in New York, who was not involved with the study.

The overall weekly exercise time on the MICT regimen, 150 minutes, halves down to 75 minutes a week in the HIIT program. Guideline recommendations released in 2018 by the International PCOS Network recommended these as acceptable alternative exercise strategies. Ms. Patten and her associates sought to determine whether one strategy surpassed the other, the first time this has been examined in women with PCOS, she said.

They randomized 27 sedentary women 18-45 years old with a body mass index (BMI) above 25 kg/m² and diagnosed with PCOS by the Rotterdam criteria to a 12-week supervised exercise program on either the HIIT or MICT protocol. Their average BMI at entry was 36-37 kg/m². The study excluded women who smoked, were pregnant, had an illness or injury that would prevent exercise, or were on an oral contraceptive or insulin-sensitizing medication.

At the end of 12 weeks, neither group had a significant change in average weight or BMI, and waist circumference dropped by an average of just over 2 cm in both treatment groups. Lean mass increased by a mean 1 kg in the HIIT group, a significant change, compared with a nonsignificant 0.3 kg average increase in the MICT group.
 

Increased aerobic capacity ‘partially explains’ improved insulin sensitivity

Aerobic capacity, measured as peak oxygen consumption (VO₂peak), increased by an average 5.7 mL/kg per min among the HIIT patients, significantly more than the mean 3.2 mL/kg per min increase among those in the MICT program.

The insulin sensitivity index rose by a significant, relative 35% among the HIIT patients, but barely budged in the MICT group. Fasting glucose fell significantly and the glucose infusion rate increased significantly among the women who performed HIIT, but again showed little change among those doing MICT.

Analysis showed a significant link between the increase in VO₂peak and the increase in insulin sensitivity among the women engaged in HIIT, Ms. Patten reported. The improvement in the insulin sensitivity index was “partially explained” by the increase in VO₂peak, she said.

Assessment of hormone levels showed a significant increase in sex hormone–binding globulin in the HIIT patients while those in the MICT group showed a small decline in this level. The free androgen index fell by a relative 39% on average in the HIIT group, a significant drop, but decreased by a much smaller and not significant amount among the women who did MICT. The women who performed HIIT also showed a significant drop in their free testosterone level, a change not seen with MICT.

Women who performed the HIIT protocol also had a significant improvement in their menstrual cyclicity, and significant improvements in depression, stress, and anxiety, Ms Patten reported. She next plans to do longer follow-up on study participants, out to 6 and 12 months after the end of the exercise protocol.

“Overall, the findings suggest that HIIT is superior to MICT for improving fitness and insulin sensitivity in the short term. Results from a number of studies in individuals without PCOS suggest that HIIT is superior to MICT for improving fitness short term,” commented Dr. Dunaif. “This study makes an important contribution by directly investigating the impact of training intensity in women with PCOS. Larger studies will be needed before the superiority of HIIT is established for women with PCOS, and study durations of at least several months will be needed to assess the impact on reproductive outcomes such as ovulation,” she said in an interview. She also called for assessing the effects of HIIT in more diverse populations of women with PCOS.

Ms. Patten had no disclosures. Dr. Dunaif has been a consultant to Equator Therapeutics, Fractyl Laboratories, and Globe Life Sciences.

[email protected]
 

High-intensity interval training (HIIT) was better than moderate-intensity continuous training (MICT) for improving several measures of cardiometabolic health in women with polycystic ovary syndrome (PCOS) in a prospective, randomized, single-center study with 27 women.

yacobchuk/Getty Images

After 12 weeks on a supervised exercise regimen, the women with PCOS who followed the HIIT program had significantly better improvements in aerobic capacity, insulin sensitivity, and level of sex hormone–binding globulin, Rhiannon K. Patten, MSc, said at the annual meeting of the Endocrine Society.

“HIIT can offer superior improvements in health outcomes, and should be considered as an effective tool to reduce cardiometabolic risk in women with PCOS,” concluded Ms. Patten, a researcher in the Institute for Health and Sport at Victoria University in Melbourne in her presentation (Abstract OR10-1).

“The changes we see [after 12 weeks on the HIIT regimen] seem to occur despite no change in body mass index, so rather than focus on weight loss we encourage participants to focus on the health improvements that seem to be greater with HIIT. We actively encourage the HIIT protocol right now,” she said.

Both regimens use a stationary cycle ergometer. In the HIIT protocol patients twice weekly pedal through 12 1-minute intervals at a heart rate of 90%-100% maximum, interspersed with 1 minute rest intervals. On a third day per week, patients pedal to a heart rate of 90%-95% maximum for 6-8 intervals maintained for 2 minutes and interspersed with rest intervals of 2 minutes. The MICT regimen used as a comparator has participants pedal to 60%-70% of their maximum heart rate continuously for 50 minutes 3 days weekly.



HIIT saves time

“These findings are relevant to clinical practice, because they demonstrate that HIIT is effective in women with PCOS. Reducing the time devoted to exercise to achieve fitness goals is attractive to patients. The reduced time to achieve training benefits with HIIT should improve patient compliance,” commented Andrea Dunaif, MD, professor and chief of the division of endocrinology, diabetes, and bone disease of the Mount Sinai Health System in New York, who was not involved with the study.

The overall weekly exercise time on the MICT regimen, 150 minutes, halves down to 75 minutes a week in the HIIT program. Guideline recommendations released in 2018 by the International PCOS Network recommended these as acceptable alternative exercise strategies. Ms. Patten and her associates sought to determine whether one strategy surpassed the other, the first time this has been examined in women with PCOS, she said.

They randomized 27 sedentary women 18-45 years old with a body mass index (BMI) above 25 kg/m² and diagnosed with PCOS by the Rotterdam criteria to a 12-week supervised exercise program on either the HIIT or MICT protocol. Their average BMI at entry was 36-37 kg/m². The study excluded women who smoked, were pregnant, had an illness or injury that would prevent exercise, or were on an oral contraceptive or insulin-sensitizing medication.

At the end of 12 weeks, neither group had a significant change in average weight or BMI, and waist circumference dropped by an average of just over 2 cm in both treatment groups. Lean mass increased by a mean 1 kg in the HIIT group, a significant change, compared with a nonsignificant 0.3 kg average increase in the MICT group.
 

Increased aerobic capacity ‘partially explains’ improved insulin sensitivity

Aerobic capacity, measured as peak oxygen consumption (VO₂peak), increased by an average 5.7 mL/kg per min among the HIIT patients, significantly more than the mean 3.2 mL/kg per min increase among those in the MICT program.

The insulin sensitivity index rose by a significant, relative 35% among the HIIT patients, but barely budged in the MICT group. Fasting glucose fell significantly and the glucose infusion rate increased significantly among the women who performed HIIT, but again showed little change among those doing MICT.

Analysis showed a significant link between the increase in VO₂peak and the increase in insulin sensitivity among the women engaged in HIIT, Ms. Patten reported. The improvement in the insulin sensitivity index was “partially explained” by the increase in VO₂peak, she said.

Assessment of hormone levels showed a significant increase in sex hormone–binding globulin in the HIIT patients while those in the MICT group showed a small decline in this level. The free androgen index fell by a relative 39% on average in the HIIT group, a significant drop, but decreased by a much smaller and not significant amount among the women who did MICT. The women who performed HIIT also showed a significant drop in their free testosterone level, a change not seen with MICT.

Women who performed the HIIT protocol also had a significant improvement in their menstrual cyclicity, and significant improvements in depression, stress, and anxiety, Ms Patten reported. She next plans to do longer follow-up on study participants, out to 6 and 12 months after the end of the exercise protocol.

“Overall, the findings suggest that HIIT is superior to MICT for improving fitness and insulin sensitivity in the short term. Results from a number of studies in individuals without PCOS suggest that HIIT is superior to MICT for improving fitness short term,” commented Dr. Dunaif. “This study makes an important contribution by directly investigating the impact of training intensity in women with PCOS. Larger studies will be needed before the superiority of HIIT is established for women with PCOS, and study durations of at least several months will be needed to assess the impact on reproductive outcomes such as ovulation,” she said in an interview. She also called for assessing the effects of HIIT in more diverse populations of women with PCOS.

Ms. Patten had no disclosures. Dr. Dunaif has been a consultant to Equator Therapeutics, Fractyl Laboratories, and Globe Life Sciences.

[email protected]