MDedge Endocrinology

You can observe a lot by watching. – Yogi Berra

He was a fit man in his 40s. Thick legs. Maybe he was a long-distance walker? The bones of his right arm were more developed than his left – a right-handed thrower. His lower left fibula was fractured from a severely rolled ankle. He carried a walking stick that was glossy in the middle from where he gripped it with his left hand, dragging his bad left foot along. Dental cavities tell the story of his diet: honey, carobs, dates. Carbon 14 dating confirms that he lived during the Chalcolithic period, approximately 6,000 years ago. He was likely a shepherd in the Judean Desert.

Isn’t it amazing how much we can know about another human even across such an enormous chasm of time? If you’d asked me when I was 11 what I wanted to be, I’d have said archaeologist. How cool to study artifacts and recreate stories from eons ago! I sometimes still get to be that kid in my office. Noticing people, their scars, their flaws, knowing there is a story behind each one.

A 64-year-old woman with a 4-cm red, brown shiny plaque on her right calf. She burned it on her boyfriend’s Harley Davidson nearly 40 years ago. She wonders where he is now.

A 58-year-old man with a 3-inch scar on his right wrist. He fell off his 6-year-old’s skimboard. ORIF.

A 40-year-old woman with bilateral mastectomy scars.

A 66-year-old with a lichenified nodule on his left forearm. When I shaved it off, a quarter inch spicule of glass came out. It was from a car accident in his first car, a Chevy Impala. He saved the piece of glass as a souvenir.

A fit 50-year-old with extensive scars on his feet and ankles. “Yeah, I went ‘whistling-in’ on a training jump,” he said. He was a retired Navy Seal and raconteur with quite a tale about the day his parachute malfunctioned. Some well placed live oak trees is why he’s around for his skin screening.

A classic, rope-like open-heart scar on the chest of a thin, young, healthy, flaxen-haired woman. Dissected aorta.

A 30-something woman dressed in a pants suit with razor-thin parallel scars on her volar forearms and proximal thighs. She asks if any laser could remove them.

A rotund, hard-living, bearded man with chest and upper-arm tattoos of flames and nudie girls now mixed with the striking face of an old woman and three little kids: His mom and grandkids. He shows me where the fourth grandkid will go and gives me a bear hug to thank me for the care when he leaves.

Attending to these details shifts us from autopilot to present. It keeps us involved, holding our attention even if it’s the 20th skin screening or diabetic foot exam of the day. And what a gift to share in the intimate details of another’s life.

Like examining the minute details of an ancient bone, dig for the history with curiosity, pity, humility. The perfect moment for asking might be when you stand with your #15 blade ready to introduce a new scar and become part of this human’s story forever.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

You can observe a lot by watching. – Yogi Berra

He was a fit man in his 40s. Thick legs. Maybe he was a long-distance walker? The bones of his right arm were more developed than his left – a right-handed thrower. His lower left fibula was fractured from a severely rolled ankle. He carried a walking stick that was glossy in the middle from where he gripped it with his left hand, dragging his bad left foot along. Dental cavities tell the story of his diet: honey, carobs, dates. Carbon 14 dating confirms that he lived during the Chalcolithic period, approximately 6,000 years ago. He was likely a shepherd in the Judean Desert.

Isn’t it amazing how much we can know about another human even across such an enormous chasm of time? If you’d asked me when I was 11 what I wanted to be, I’d have said archaeologist. How cool to study artifacts and recreate stories from eons ago! I sometimes still get to be that kid in my office. Noticing people, their scars, their flaws, knowing there is a story behind each one.

A 64-year-old woman with a 4-cm red, brown shiny plaque on her right calf. She burned it on her boyfriend’s Harley Davidson nearly 40 years ago. She wonders where he is now.

A 58-year-old man with a 3-inch scar on his right wrist. He fell off his 6-year-old’s skimboard. ORIF.

A 40-year-old woman with bilateral mastectomy scars.

A 66-year-old with a lichenified nodule on his left forearm. When I shaved it off, a quarter inch spicule of glass came out. It was from a car accident in his first car, a Chevy Impala. He saved the piece of glass as a souvenir.

A fit 50-year-old with extensive scars on his feet and ankles. “Yeah, I went ‘whistling-in’ on a training jump,” he said. He was a retired Navy Seal and raconteur with quite a tale about the day his parachute malfunctioned. Some well placed live oak trees is why he’s around for his skin screening.

A classic, rope-like open-heart scar on the chest of a thin, young, healthy, flaxen-haired woman. Dissected aorta.

A 30-something woman dressed in a pants suit with razor-thin parallel scars on her volar forearms and proximal thighs. She asks if any laser could remove them.

A rotund, hard-living, bearded man with chest and upper-arm tattoos of flames and nudie girls now mixed with the striking face of an old woman and three little kids: His mom and grandkids. He shows me where the fourth grandkid will go and gives me a bear hug to thank me for the care when he leaves.

Attending to these details shifts us from autopilot to present. It keeps us involved, holding our attention even if it’s the 20th skin screening or diabetic foot exam of the day. And what a gift to share in the intimate details of another’s life.

Like examining the minute details of an ancient bone, dig for the history with curiosity, pity, humility. The perfect moment for asking might be when you stand with your #15 blade ready to introduce a new scar and become part of this human’s story forever.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

You can observe a lot by watching. – Yogi Berra

He was a fit man in his 40s. Thick legs. Maybe he was a long-distance walker? The bones of his right arm were more developed than his left – a right-handed thrower. His lower left fibula was fractured from a severely rolled ankle. He carried a walking stick that was glossy in the middle from where he gripped it with his left hand, dragging his bad left foot along. Dental cavities tell the story of his diet: honey, carobs, dates. Carbon 14 dating confirms that he lived during the Chalcolithic period, approximately 6,000 years ago. He was likely a shepherd in the Judean Desert.

Isn’t it amazing how much we can know about another human even across such an enormous chasm of time? If you’d asked me when I was 11 what I wanted to be, I’d have said archaeologist. How cool to study artifacts and recreate stories from eons ago! I sometimes still get to be that kid in my office. Noticing people, their scars, their flaws, knowing there is a story behind each one.

A 64-year-old woman with a 4-cm red, brown shiny plaque on her right calf. She burned it on her boyfriend’s Harley Davidson nearly 40 years ago. She wonders where he is now.

A 58-year-old man with a 3-inch scar on his right wrist. He fell off his 6-year-old’s skimboard. ORIF.

A 40-year-old woman with bilateral mastectomy scars.

A 66-year-old with a lichenified nodule on his left forearm. When I shaved it off, a quarter inch spicule of glass came out. It was from a car accident in his first car, a Chevy Impala. He saved the piece of glass as a souvenir.

A fit 50-year-old with extensive scars on his feet and ankles. “Yeah, I went ‘whistling-in’ on a training jump,” he said. He was a retired Navy Seal and raconteur with quite a tale about the day his parachute malfunctioned. Some well placed live oak trees is why he’s around for his skin screening.

A classic, rope-like open-heart scar on the chest of a thin, young, healthy, flaxen-haired woman. Dissected aorta.

A 30-something woman dressed in a pants suit with razor-thin parallel scars on her volar forearms and proximal thighs. She asks if any laser could remove them.

A rotund, hard-living, bearded man with chest and upper-arm tattoos of flames and nudie girls now mixed with the striking face of an old woman and three little kids: His mom and grandkids. He shows me where the fourth grandkid will go and gives me a bear hug to thank me for the care when he leaves.

Attending to these details shifts us from autopilot to present. It keeps us involved, holding our attention even if it’s the 20th skin screening or diabetic foot exam of the day. And what a gift to share in the intimate details of another’s life.

Like examining the minute details of an ancient bone, dig for the history with curiosity, pity, humility. The perfect moment for asking might be when you stand with your #15 blade ready to introduce a new scar and become part of this human’s story forever.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

The PREDICT score does not seem to be particularly accurate when it comes to estimating overall survival (OS) in patients with HER2-positive early breast cancer who are treated with modern chemotherapy and anti-HER2 targeted therapies. This is the conclusion of an international study published in the journal npj Breast Cancer. The work was supervised by Matteo Lambertini, MD, PhD, an oncologist at the IRCCS San Martino Polyclinic Hospital in Genoa, Italy.

As the authors explain, “PREDICT is a publicly available online tool that helps to predict the individual prognosis of patients with early breast cancer and to show the impact of adjuvant treatments administered after breast cancer surgery.” The tool uses traditional clinical-pathological factors. The authors also point out that the original version of this tool was validated in several datasets of patients with breast cancer. In 2011, it was updated to include HER2 status.

The investigators noted that, although the use of PREDICT is recommended to aid decision-making in the adjuvant setting, its prognostic role in patients with HER2-positive early breast cancer who are treated with modern chemotherapy and anti-HER2 therapies – even trastuzumab-based ones – remains unclear.

Therefore, they decided to analyze PREDICT’s prognostic performance using data extracted from the ALTTO trial, the largest adjuvant study ever conducted in the field of HER2-positive early breast cancer. That trial “represented a unique opportunity to investigate the reliability and prognostic performance of PREDICT in women with HER2-positive disease,” according to the investigators. They went on to specify that ALTTO evaluated adjuvant lapatinib plus trastuzumab vs. trastuzumab alone in 8,381 patients – 2,794 of whom were included in their own analysis.

What the analysis found was that, overall, PREDICT underestimated 5-year OS by 6.7%. The observed 5-year OS was 94.7%, and the predicted 5-year OS was 88.0%.

“The underestimation was consistent across all subgroups, including those according to the type of anti-HER2 therapy. The highest absolute differences were observed for patients with hormone receptor–negative disease, nodal involvement, and large tumor size (13.0%, 15.8%, and 15.3%, respectively),” they wrote. Furthermore, they reported that “the suboptimal performance of this prognostic tool was observed irrespective of type of anti-HER2 treatment, type of chemotherapy regimen, age of the patients at the time of diagnosis, central hormone receptor status, pathological nodal status, and pathological tumor size.”

To potentially explain the reasons for the underestimation of patients’ OS, the authors questioned whether the population used to validate PREDICT accurately mirrored the real-world population of patients with HER2-positive disease treated in the modern era with effective chemotherapy and anti-HER2 targeted therapies. “Moreover, the current standard of care for early breast cancer is even superior to the treatment received by many patients in the ALTTO study. … As such, the discordance between OS estimated by PREDICT and the current real-world OS is expected to be even higher. Therefore,” the researchers concluded, “our results suggest that the current version of PREDICT should be used with caution for prognostication in HER2-positive early breast cancer patients treated in the modern era with effective chemotherapy and anti-HER2 targeted therapies.”

A version of this article first appeared on Medscape.com. This article was translated from Univadis Italy.

The PREDICT score does not seem to be particularly accurate when it comes to estimating overall survival (OS) in patients with HER2-positive early breast cancer who are treated with modern chemotherapy and anti-HER2 targeted therapies. This is the conclusion of an international study published in the journal npj Breast Cancer. The work was supervised by Matteo Lambertini, MD, PhD, an oncologist at the IRCCS San Martino Polyclinic Hospital in Genoa, Italy.

As the authors explain, “PREDICT is a publicly available online tool that helps to predict the individual prognosis of patients with early breast cancer and to show the impact of adjuvant treatments administered after breast cancer surgery.” The tool uses traditional clinical-pathological factors. The authors also point out that the original version of this tool was validated in several datasets of patients with breast cancer. In 2011, it was updated to include HER2 status.

The investigators noted that, although the use of PREDICT is recommended to aid decision-making in the adjuvant setting, its prognostic role in patients with HER2-positive early breast cancer who are treated with modern chemotherapy and anti-HER2 therapies – even trastuzumab-based ones – remains unclear.

Therefore, they decided to analyze PREDICT’s prognostic performance using data extracted from the ALTTO trial, the largest adjuvant study ever conducted in the field of HER2-positive early breast cancer. That trial “represented a unique opportunity to investigate the reliability and prognostic performance of PREDICT in women with HER2-positive disease,” according to the investigators. They went on to specify that ALTTO evaluated adjuvant lapatinib plus trastuzumab vs. trastuzumab alone in 8,381 patients – 2,794 of whom were included in their own analysis.

What the analysis found was that, overall, PREDICT underestimated 5-year OS by 6.7%. The observed 5-year OS was 94.7%, and the predicted 5-year OS was 88.0%.

“The underestimation was consistent across all subgroups, including those according to the type of anti-HER2 therapy. The highest absolute differences were observed for patients with hormone receptor–negative disease, nodal involvement, and large tumor size (13.0%, 15.8%, and 15.3%, respectively),” they wrote. Furthermore, they reported that “the suboptimal performance of this prognostic tool was observed irrespective of type of anti-HER2 treatment, type of chemotherapy regimen, age of the patients at the time of diagnosis, central hormone receptor status, pathological nodal status, and pathological tumor size.”

To potentially explain the reasons for the underestimation of patients’ OS, the authors questioned whether the population used to validate PREDICT accurately mirrored the real-world population of patients with HER2-positive disease treated in the modern era with effective chemotherapy and anti-HER2 targeted therapies. “Moreover, the current standard of care for early breast cancer is even superior to the treatment received by many patients in the ALTTO study. … As such, the discordance between OS estimated by PREDICT and the current real-world OS is expected to be even higher. Therefore,” the researchers concluded, “our results suggest that the current version of PREDICT should be used with caution for prognostication in HER2-positive early breast cancer patients treated in the modern era with effective chemotherapy and anti-HER2 targeted therapies.”

A version of this article first appeared on Medscape.com. This article was translated from Univadis Italy.

The PREDICT score does not seem to be particularly accurate when it comes to estimating overall survival (OS) in patients with HER2-positive early breast cancer who are treated with modern chemotherapy and anti-HER2 targeted therapies. This is the conclusion of an international study published in the journal npj Breast Cancer. The work was supervised by Matteo Lambertini, MD, PhD, an oncologist at the IRCCS San Martino Polyclinic Hospital in Genoa, Italy.

As the authors explain, “PREDICT is a publicly available online tool that helps to predict the individual prognosis of patients with early breast cancer and to show the impact of adjuvant treatments administered after breast cancer surgery.” The tool uses traditional clinical-pathological factors. The authors also point out that the original version of this tool was validated in several datasets of patients with breast cancer. In 2011, it was updated to include HER2 status.

The investigators noted that, although the use of PREDICT is recommended to aid decision-making in the adjuvant setting, its prognostic role in patients with HER2-positive early breast cancer who are treated with modern chemotherapy and anti-HER2 therapies – even trastuzumab-based ones – remains unclear.

Therefore, they decided to analyze PREDICT’s prognostic performance using data extracted from the ALTTO trial, the largest adjuvant study ever conducted in the field of HER2-positive early breast cancer. That trial “represented a unique opportunity to investigate the reliability and prognostic performance of PREDICT in women with HER2-positive disease,” according to the investigators. They went on to specify that ALTTO evaluated adjuvant lapatinib plus trastuzumab vs. trastuzumab alone in 8,381 patients – 2,794 of whom were included in their own analysis.

What the analysis found was that, overall, PREDICT underestimated 5-year OS by 6.7%. The observed 5-year OS was 94.7%, and the predicted 5-year OS was 88.0%.

“The underestimation was consistent across all subgroups, including those according to the type of anti-HER2 therapy. The highest absolute differences were observed for patients with hormone receptor–negative disease, nodal involvement, and large tumor size (13.0%, 15.8%, and 15.3%, respectively),” they wrote. Furthermore, they reported that “the suboptimal performance of this prognostic tool was observed irrespective of type of anti-HER2 treatment, type of chemotherapy regimen, age of the patients at the time of diagnosis, central hormone receptor status, pathological nodal status, and pathological tumor size.”

To potentially explain the reasons for the underestimation of patients’ OS, the authors questioned whether the population used to validate PREDICT accurately mirrored the real-world population of patients with HER2-positive disease treated in the modern era with effective chemotherapy and anti-HER2 targeted therapies. “Moreover, the current standard of care for early breast cancer is even superior to the treatment received by many patients in the ALTTO study. … As such, the discordance between OS estimated by PREDICT and the current real-world OS is expected to be even higher. Therefore,” the researchers concluded, “our results suggest that the current version of PREDICT should be used with caution for prognostication in HER2-positive early breast cancer patients treated in the modern era with effective chemotherapy and anti-HER2 targeted therapies.”

A version of this article first appeared on Medscape.com. This article was translated from Univadis Italy.

The relationship between body mass index (BMI) and all-cause mortality in patients with atrial fibrillation (AFib) is U-shaped, with the risk highest in those who are underweight or severely obese and lowest in patients defined simply as obese, a registry analysis suggests. It also showed a similar relationship between BMI and risk for new or worsening heart failure (HF).

Mortality bottomed out at a BMI of about 30-35 kg/m², which suggests that mild obesity was protective, compared even with “normal-weight” or “overweight” BMI. Still, mortality went up sharply from there with rising BMI.

But higher BMI, a surrogate for obesity, apparently didn’t worsen outcomes by itself. The risk for death from any cause at higher obesity levels was found to depend a lot on related risk factors and comorbidities when the analysis controlled for conditions such as diabetes and hypertension.

The findings suggest an inverse relationship between BMI and all-cause mortality in AFib only for patients with BMI less than about 30. They therefore argue against any “obesity paradox” in AFib that posits consistently better survival with increasing levels of obesity, say researchers, based on their analysis of patients with new-onset AFib in the GARFIELD-AF registry.

“It’s common practice now for clinicians to discuss weight within a clinic setting when they’re talking to their AFib patients,” observed Christian Fielder Camm, BM, BCh, University of Oxford (England), and Royal Berkshire NHS Foundation Trust, Reading, England. So studies suggesting an inverse association between BMI and AFib-related risk can be a concern.

Such studies “seem to suggest that once you’ve got AFib, maintaining a high or very high BMI may in some way be protective – which is contrary to what would seem to make sense and certainly contrary to what our results have shown,” Dr. Camm told this news organization.

“I think that having further evidence now to suggest, actually, that greater BMI is associated with a greater risk of all-cause mortality and heart failure helps reframe that discussion at the physician-patient interaction level more clearly, and ensures that we’re able to talk to our patients appropriately about risks associated with BMI and atrial fibrillation,” said Dr. Camm, who is lead author on the analysis published in Open Heart.

“Obesity is a cause of most cardiovascular diseases, but [these] data would support that being overweight or having mild obesity does not increase the risk,” observed Carl J. Lavie, MD, of the John Ochsner Heart and Vascular Institute, New Orleans, La., and the Ochsner Clinical School at the University of Queensland, Brisbane, Australia.

“At a BMI of 40, it’s very important for them to lose weight for their long-term prognosis,” Dr. Lavie noted, but “at a BMI of 30, the important thing would be to prevent further weight gain. And if they could keep their BMI of 30, they should have a good prognosis. Their prognosis would be particularly good if they didn’t gain weight and put themselves in a more extreme obesity class that is associated with worse risk.”

The current analysis, Dr. Lavie said, “is way better than the AFFIRM study,” which yielded an obesity-paradox report on its patients with AFib about a dozen years ago. “It’s got more data, more numbers, more statistical power,” and breaks BMI into more categories.

That previous analysis based on the influential AFFIRM randomized trial separated its 4,060 patients with AFib into normal (BMI, 18.5-25), overweight (BMI, 25-30), and obese (BMI, > 30) categories, per the convention at the time. It concluded that “obese patients with atrial fibrillation appear to have better long-term outcomes than nonobese patients.”
 

Bleeding risk on oral anticoagulants

Also noteworthy in the current analysis, variation in BMI didn’t seem to affect mortality or risk for major bleeding or nonhemorrhagic stroke according to choice of oral anticoagulant – whether a new oral anticoagulant (NOAC) or a vitamin K antagonist (VKA).

“We saw that even in the obese and extremely obese group, all-cause mortality was lower in the group taking NOACs, compared with taking warfarin,” Dr. Camm observed, “which goes against the idea that we would need any kind of dose adjustments for increased BMI.”

Indeed, the report notes, use of NOACs, compared with VKA, was associated with a 23% drop in risk for death among patients who were either normal weight or overweight and also in those who were obese or extremely obese.

Those findings “are basically saying that the NOACs look better than warfarin regardless of weight,” agreed Dr. Lavie. “The problem is that the study is not very powered.”

Whereas the benefits of NOACs, compared to VKA, seem similar for patients with a BMI of 30 or 34, compared with a BMI of 23, for example, “none of the studies has many people with 50 BMI.” Many clinicians “feel uncomfortable giving the same dose of NOAC to somebody who has a 60 BMI,” he said. At least with warfarin, “you can check the INR [international normalized ratio].”

The current analysis included 40,482 patients with recently diagnosed AFib and at least one other stroke risk factor from among the registry’s more than 50,000 patients from 35 countries, enrolled from 2010 to 2016. They were followed for 2 years.

The 703 patients with BMI under 18.5 at AFib diagnosis were classified per World Health Organization definitions as underweight; the 13,095 with BMI 18.5-25 as normal weight; the 15,043 with BMI 25-30 as overweight; the 7,560 with BMI 30-35 as obese; and the 4,081 with BMI above 35 as extremely obese. Their ages averaged 71 years, and 55.6% were men.
 

BMI effects on different outcomes

Relationships between BMI and all-cause mortality and between BMI and new or worsening HF emerged as U-shaped, the risk climbing with both increasing and decreasing BMI. The nadir BMI for risk was about 30 in the case of mortality and about 25 for new or worsening HF.

The all-cause mortality risk rose by 32% for every 5 BMI points lower than a BMI of 30, and by 16% for every 5 BMI points higher than 30, in a partially adjusted analysis. The risk for new or worsening HF rose significantly with increasing but not decreasing BMI, and the reverse was observed for the endpoint of major bleeding.

The effect of BMI on all-cause mortality was “substantially attenuated” when the analysis was further adjusted with “likely mediators of any association between BMI and outcomes,” including hypertension, diabetes, HF, cerebrovascular events, and history of bleeding, Dr. Camm said.

That blunted BMI-mortality relationship, he said, “suggests that a lot of the effect is mediated through relatively traditional risk factors like hypertension and diabetes.”

The 2010 AFFIRM analysis by BMI, Dr. Lavie noted, “didn’t even look at the underweight; they actually threw them out.” Yet, such patients with AFib, who tend to be extremely frail or have chronic diseases or conditions other than the arrhythmia, are common. A take-home of the current study is that “the underweight with atrial fibrillation have a really bad prognosis.”

That message isn’t heard as much, he observed, “but is as important as saying that BMI 30 has the best prognosis. The worst prognosis is with the underweight or the really extreme obese.”

Dr. Camm discloses research funding from the British Heart Foundation. Disclosures for the other authors are in the report. Dr. Lavie has previously disclosed serving as a speaker and consultant for PAI Health and DSM Nutritional Products and is the author of “The Obesity Paradox: When Thinner Means Sicker and Heavier Means Healthier” (Avery, 2014).

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

The relationship between body mass index (BMI) and all-cause mortality in patients with atrial fibrillation (AFib) is U-shaped, with the risk highest in those who are underweight or severely obese and lowest in patients defined simply as obese, a registry analysis suggests. It also showed a similar relationship between BMI and risk for new or worsening heart failure (HF).

Mortality bottomed out at a BMI of about 30-35 kg/m², which suggests that mild obesity was protective, compared even with “normal-weight” or “overweight” BMI. Still, mortality went up sharply from there with rising BMI.

But higher BMI, a surrogate for obesity, apparently didn’t worsen outcomes by itself. The risk for death from any cause at higher obesity levels was found to depend a lot on related risk factors and comorbidities when the analysis controlled for conditions such as diabetes and hypertension.

The findings suggest an inverse relationship between BMI and all-cause mortality in AFib only for patients with BMI less than about 30. They therefore argue against any “obesity paradox” in AFib that posits consistently better survival with increasing levels of obesity, say researchers, based on their analysis of patients with new-onset AFib in the GARFIELD-AF registry.

“It’s common practice now for clinicians to discuss weight within a clinic setting when they’re talking to their AFib patients,” observed Christian Fielder Camm, BM, BCh, University of Oxford (England), and Royal Berkshire NHS Foundation Trust, Reading, England. So studies suggesting an inverse association between BMI and AFib-related risk can be a concern.

Such studies “seem to suggest that once you’ve got AFib, maintaining a high or very high BMI may in some way be protective – which is contrary to what would seem to make sense and certainly contrary to what our results have shown,” Dr. Camm told this news organization.

“I think that having further evidence now to suggest, actually, that greater BMI is associated with a greater risk of all-cause mortality and heart failure helps reframe that discussion at the physician-patient interaction level more clearly, and ensures that we’re able to talk to our patients appropriately about risks associated with BMI and atrial fibrillation,” said Dr. Camm, who is lead author on the analysis published in Open Heart.

“Obesity is a cause of most cardiovascular diseases, but [these] data would support that being overweight or having mild obesity does not increase the risk,” observed Carl J. Lavie, MD, of the John Ochsner Heart and Vascular Institute, New Orleans, La., and the Ochsner Clinical School at the University of Queensland, Brisbane, Australia.

“At a BMI of 40, it’s very important for them to lose weight for their long-term prognosis,” Dr. Lavie noted, but “at a BMI of 30, the important thing would be to prevent further weight gain. And if they could keep their BMI of 30, they should have a good prognosis. Their prognosis would be particularly good if they didn’t gain weight and put themselves in a more extreme obesity class that is associated with worse risk.”

The current analysis, Dr. Lavie said, “is way better than the AFFIRM study,” which yielded an obesity-paradox report on its patients with AFib about a dozen years ago. “It’s got more data, more numbers, more statistical power,” and breaks BMI into more categories.

That previous analysis based on the influential AFFIRM randomized trial separated its 4,060 patients with AFib into normal (BMI, 18.5-25), overweight (BMI, 25-30), and obese (BMI, > 30) categories, per the convention at the time. It concluded that “obese patients with atrial fibrillation appear to have better long-term outcomes than nonobese patients.”
 

Bleeding risk on oral anticoagulants

Also noteworthy in the current analysis, variation in BMI didn’t seem to affect mortality or risk for major bleeding or nonhemorrhagic stroke according to choice of oral anticoagulant – whether a new oral anticoagulant (NOAC) or a vitamin K antagonist (VKA).

“We saw that even in the obese and extremely obese group, all-cause mortality was lower in the group taking NOACs, compared with taking warfarin,” Dr. Camm observed, “which goes against the idea that we would need any kind of dose adjustments for increased BMI.”

Indeed, the report notes, use of NOACs, compared with VKA, was associated with a 23% drop in risk for death among patients who were either normal weight or overweight and also in those who were obese or extremely obese.

Those findings “are basically saying that the NOACs look better than warfarin regardless of weight,” agreed Dr. Lavie. “The problem is that the study is not very powered.”

Whereas the benefits of NOACs, compared to VKA, seem similar for patients with a BMI of 30 or 34, compared with a BMI of 23, for example, “none of the studies has many people with 50 BMI.” Many clinicians “feel uncomfortable giving the same dose of NOAC to somebody who has a 60 BMI,” he said. At least with warfarin, “you can check the INR [international normalized ratio].”

The current analysis included 40,482 patients with recently diagnosed AFib and at least one other stroke risk factor from among the registry’s more than 50,000 patients from 35 countries, enrolled from 2010 to 2016. They were followed for 2 years.

The 703 patients with BMI under 18.5 at AFib diagnosis were classified per World Health Organization definitions as underweight; the 13,095 with BMI 18.5-25 as normal weight; the 15,043 with BMI 25-30 as overweight; the 7,560 with BMI 30-35 as obese; and the 4,081 with BMI above 35 as extremely obese. Their ages averaged 71 years, and 55.6% were men.
 

BMI effects on different outcomes

Relationships between BMI and all-cause mortality and between BMI and new or worsening HF emerged as U-shaped, the risk climbing with both increasing and decreasing BMI. The nadir BMI for risk was about 30 in the case of mortality and about 25 for new or worsening HF.

The all-cause mortality risk rose by 32% for every 5 BMI points lower than a BMI of 30, and by 16% for every 5 BMI points higher than 30, in a partially adjusted analysis. The risk for new or worsening HF rose significantly with increasing but not decreasing BMI, and the reverse was observed for the endpoint of major bleeding.

The effect of BMI on all-cause mortality was “substantially attenuated” when the analysis was further adjusted with “likely mediators of any association between BMI and outcomes,” including hypertension, diabetes, HF, cerebrovascular events, and history of bleeding, Dr. Camm said.

That blunted BMI-mortality relationship, he said, “suggests that a lot of the effect is mediated through relatively traditional risk factors like hypertension and diabetes.”

The 2010 AFFIRM analysis by BMI, Dr. Lavie noted, “didn’t even look at the underweight; they actually threw them out.” Yet, such patients with AFib, who tend to be extremely frail or have chronic diseases or conditions other than the arrhythmia, are common. A take-home of the current study is that “the underweight with atrial fibrillation have a really bad prognosis.”

That message isn’t heard as much, he observed, “but is as important as saying that BMI 30 has the best prognosis. The worst prognosis is with the underweight or the really extreme obese.”

Dr. Camm discloses research funding from the British Heart Foundation. Disclosures for the other authors are in the report. Dr. Lavie has previously disclosed serving as a speaker and consultant for PAI Health and DSM Nutritional Products and is the author of “The Obesity Paradox: When Thinner Means Sicker and Heavier Means Healthier” (Avery, 2014).

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

The relationship between body mass index (BMI) and all-cause mortality in patients with atrial fibrillation (AFib) is U-shaped, with the risk highest in those who are underweight or severely obese and lowest in patients defined simply as obese, a registry analysis suggests. It also showed a similar relationship between BMI and risk for new or worsening heart failure (HF).

Mortality bottomed out at a BMI of about 30-35 kg/m², which suggests that mild obesity was protective, compared even with “normal-weight” or “overweight” BMI. Still, mortality went up sharply from there with rising BMI.

But higher BMI, a surrogate for obesity, apparently didn’t worsen outcomes by itself. The risk for death from any cause at higher obesity levels was found to depend a lot on related risk factors and comorbidities when the analysis controlled for conditions such as diabetes and hypertension.

The findings suggest an inverse relationship between BMI and all-cause mortality in AFib only for patients with BMI less than about 30. They therefore argue against any “obesity paradox” in AFib that posits consistently better survival with increasing levels of obesity, say researchers, based on their analysis of patients with new-onset AFib in the GARFIELD-AF registry.

“It’s common practice now for clinicians to discuss weight within a clinic setting when they’re talking to their AFib patients,” observed Christian Fielder Camm, BM, BCh, University of Oxford (England), and Royal Berkshire NHS Foundation Trust, Reading, England. So studies suggesting an inverse association between BMI and AFib-related risk can be a concern.

Such studies “seem to suggest that once you’ve got AFib, maintaining a high or very high BMI may in some way be protective – which is contrary to what would seem to make sense and certainly contrary to what our results have shown,” Dr. Camm told this news organization.

“I think that having further evidence now to suggest, actually, that greater BMI is associated with a greater risk of all-cause mortality and heart failure helps reframe that discussion at the physician-patient interaction level more clearly, and ensures that we’re able to talk to our patients appropriately about risks associated with BMI and atrial fibrillation,” said Dr. Camm, who is lead author on the analysis published in Open Heart.

“Obesity is a cause of most cardiovascular diseases, but [these] data would support that being overweight or having mild obesity does not increase the risk,” observed Carl J. Lavie, MD, of the John Ochsner Heart and Vascular Institute, New Orleans, La., and the Ochsner Clinical School at the University of Queensland, Brisbane, Australia.

“At a BMI of 40, it’s very important for them to lose weight for their long-term prognosis,” Dr. Lavie noted, but “at a BMI of 30, the important thing would be to prevent further weight gain. And if they could keep their BMI of 30, they should have a good prognosis. Their prognosis would be particularly good if they didn’t gain weight and put themselves in a more extreme obesity class that is associated with worse risk.”

The current analysis, Dr. Lavie said, “is way better than the AFFIRM study,” which yielded an obesity-paradox report on its patients with AFib about a dozen years ago. “It’s got more data, more numbers, more statistical power,” and breaks BMI into more categories.

That previous analysis based on the influential AFFIRM randomized trial separated its 4,060 patients with AFib into normal (BMI, 18.5-25), overweight (BMI, 25-30), and obese (BMI, > 30) categories, per the convention at the time. It concluded that “obese patients with atrial fibrillation appear to have better long-term outcomes than nonobese patients.”
 

Bleeding risk on oral anticoagulants

Also noteworthy in the current analysis, variation in BMI didn’t seem to affect mortality or risk for major bleeding or nonhemorrhagic stroke according to choice of oral anticoagulant – whether a new oral anticoagulant (NOAC) or a vitamin K antagonist (VKA).

“We saw that even in the obese and extremely obese group, all-cause mortality was lower in the group taking NOACs, compared with taking warfarin,” Dr. Camm observed, “which goes against the idea that we would need any kind of dose adjustments for increased BMI.”

Indeed, the report notes, use of NOACs, compared with VKA, was associated with a 23% drop in risk for death among patients who were either normal weight or overweight and also in those who were obese or extremely obese.

Those findings “are basically saying that the NOACs look better than warfarin regardless of weight,” agreed Dr. Lavie. “The problem is that the study is not very powered.”

Whereas the benefits of NOACs, compared to VKA, seem similar for patients with a BMI of 30 or 34, compared with a BMI of 23, for example, “none of the studies has many people with 50 BMI.” Many clinicians “feel uncomfortable giving the same dose of NOAC to somebody who has a 60 BMI,” he said. At least with warfarin, “you can check the INR [international normalized ratio].”

The current analysis included 40,482 patients with recently diagnosed AFib and at least one other stroke risk factor from among the registry’s more than 50,000 patients from 35 countries, enrolled from 2010 to 2016. They were followed for 2 years.

The 703 patients with BMI under 18.5 at AFib diagnosis were classified per World Health Organization definitions as underweight; the 13,095 with BMI 18.5-25 as normal weight; the 15,043 with BMI 25-30 as overweight; the 7,560 with BMI 30-35 as obese; and the 4,081 with BMI above 35 as extremely obese. Their ages averaged 71 years, and 55.6% were men.
 

BMI effects on different outcomes

Relationships between BMI and all-cause mortality and between BMI and new or worsening HF emerged as U-shaped, the risk climbing with both increasing and decreasing BMI. The nadir BMI for risk was about 30 in the case of mortality and about 25 for new or worsening HF.

The all-cause mortality risk rose by 32% for every 5 BMI points lower than a BMI of 30, and by 16% for every 5 BMI points higher than 30, in a partially adjusted analysis. The risk for new or worsening HF rose significantly with increasing but not decreasing BMI, and the reverse was observed for the endpoint of major bleeding.

The effect of BMI on all-cause mortality was “substantially attenuated” when the analysis was further adjusted with “likely mediators of any association between BMI and outcomes,” including hypertension, diabetes, HF, cerebrovascular events, and history of bleeding, Dr. Camm said.

That blunted BMI-mortality relationship, he said, “suggests that a lot of the effect is mediated through relatively traditional risk factors like hypertension and diabetes.”

The 2010 AFFIRM analysis by BMI, Dr. Lavie noted, “didn’t even look at the underweight; they actually threw them out.” Yet, such patients with AFib, who tend to be extremely frail or have chronic diseases or conditions other than the arrhythmia, are common. A take-home of the current study is that “the underweight with atrial fibrillation have a really bad prognosis.”

That message isn’t heard as much, he observed, “but is as important as saying that BMI 30 has the best prognosis. The worst prognosis is with the underweight or the really extreme obese.”

Dr. Camm discloses research funding from the British Heart Foundation. Disclosures for the other authors are in the report. Dr. Lavie has previously disclosed serving as a speaker and consultant for PAI Health and DSM Nutritional Products and is the author of “The Obesity Paradox: When Thinner Means Sicker and Heavier Means Healthier” (Avery, 2014).

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

People who maintain a vegan diet show significant deficits in bone microarchitecture, compared with omnivores; however, resistance training not only appears to improve those deficits but may have a stronger effect in vegans, suggesting an important strategy in maintaining bone health with a vegan diet.

“We expected better bone structure in both vegans and omnivores who reported resistance training,” first author Robert Wakolbinger-Habel, MD, PhD, of St. Vincent Hospital Vienna and the Medical University of Vienna, said in an interview.

Thinkstock.com

“However, we expected [there would still be] differences in structure between vegans and omnivores [who practiced resistance training], as previous literature reported higher fracture rates in vegans,” he said. “Still, the positive message is that ‘pumping iron’ could counterbalance these differences between vegans and omnivores.”

The research was published online in The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
 

Exercise significantly impacts bone health in vegans

The potential effects of the plant-based vegan diet on bone health have been reported in studies linking the diet to an increased risk of fractures and lower bone mineral density (BMD), with common theories including lower bone- and muscle-building protein in vegan diets.

However, most previous studies have not considered other key factors, such as the effects of exercise, the authors noted.

“While previous studies on bone health in vegans only took BMD, biochemical and nutritional parameters into account, they did not consider the significant effects of physical activity,” they wrote.

“By ignoring these effects, important factors influencing bone health are neglected.”

For the study, 88 participants were enrolled in Vienna, with vegan participants recruited with the help of the Austrian Vegan Society.

Importantly, the study documented participants’ bone microarchitecture, a key measure of bone strength that has also not been previously investigated in vegans, using high-resolution peripheral quantitative CT.

Inclusion criteria included maintaining an omnivore diet of meat and plant-based foods or a vegan diet for at least 5 years, not being underweight or obese (body mass index [BMI], 18.5-30 kg/m²), being age 30-50 years, and being premenopausal.

Of the participants, 43 were vegan and 45 were omnivores, with generally equal ratios of men and women.

Vegan bone deficits disappear with strength training

Overall, compared with omnivores, the vegan group showed significant deficits in 7 of 14 measures of BMI-adjusted trabecular and cortical structure (all P < .05).

Among participants who reported no resistance training, vegans still showed significant decreases in bone microarchitecture, compared with omnivores, including radius trabecular BMD, radius trabecular bone volume fraction, and other tibial and cortical bone microarchitecture measures.

However, among those who did report progressive resistant training (20 vegans and 25 omnivores), defined as using machines, free weights, or bodyweight resistance exercises at least once a week, those differences disappeared and there were no significant differences in BMI-adjusted bone microarchitecture between vegans and omnivores after the 5 years.

Of note, no significant differences in bone microarchitecture were observed between those who performed exclusively aerobic activities and those who reported no sports activities in the vegan or omnivore group.

Based on the findings, “other types of exercise such as aerobics, cycling, etc, would not be sufficient for a similar positive effect on bone [as resistance training],” Dr. Wakolbinger-Habel said.

Although the findings suggest that resistance training seemed to allow vegans to “catch up” with omnivores in terms of bone microarchitecture, Dr. Wakolbinger-Habel cautioned that a study limitation is the relatively low number of participants.

“The absolute numbers suggest that in vegans the differences, and the relative effect, respectively of resistance training might be larger,” he said. “However, the number of participants in the subgroups is small and it is still an observational study, so we need to be careful in drawing causal conclusions.”

Serum bone markers were within normal ranges across all subgroups. And although there were some correlations between nutrient intake and bone microarchitecture among vegans who did and did not practice resistance training, no conclusions could be drawn from that data, the authors noted.

“Based on our data, the structural [differences between vegans and omnivores] cannot solely be explained by deficits in certain nutrients according to lifestyle,” the authors concluded.
 

Mechanisms

The mechanisms by which progressive resistance training could result in the benefits include that mechanical loads trigger stimulation of key pathways involved in bone formation, or mechanotransduction, the authors explained.

The unique effects have been observed in other studies, including one study showing that, among young adult runners, the addition of resistance training once a week was associated with significantly greater BMD.

“Veganism is a global trend with strongly increasing numbers of people worldwide adhering to a purely plant-based diet,” first author Christian Muschitz, MD, also of St. Vincent Hospital Vienna and the Medical University of Vienna, said in a press statement.

“Our study showed resistance training offsets diminished bone structure in vegan people when compared to omnivores,” he said.

Dr. Wakolbinger-Habel recommended that, based on the findings, “exercise, including resistance training, should be strongly advocated [for vegans], I would say, at least two times per week.”

The authors reported no relevant financial relationships.

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

People who maintain a vegan diet show significant deficits in bone microarchitecture, compared with omnivores; however, resistance training not only appears to improve those deficits but may have a stronger effect in vegans, suggesting an important strategy in maintaining bone health with a vegan diet.

“We expected better bone structure in both vegans and omnivores who reported resistance training,” first author Robert Wakolbinger-Habel, MD, PhD, of St. Vincent Hospital Vienna and the Medical University of Vienna, said in an interview.

Thinkstock.com

“However, we expected [there would still be] differences in structure between vegans and omnivores [who practiced resistance training], as previous literature reported higher fracture rates in vegans,” he said. “Still, the positive message is that ‘pumping iron’ could counterbalance these differences between vegans and omnivores.”

The research was published online in The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
 

Exercise significantly impacts bone health in vegans

The potential effects of the plant-based vegan diet on bone health have been reported in studies linking the diet to an increased risk of fractures and lower bone mineral density (BMD), with common theories including lower bone- and muscle-building protein in vegan diets.

However, most previous studies have not considered other key factors, such as the effects of exercise, the authors noted.

“While previous studies on bone health in vegans only took BMD, biochemical and nutritional parameters into account, they did not consider the significant effects of physical activity,” they wrote.

“By ignoring these effects, important factors influencing bone health are neglected.”

For the study, 88 participants were enrolled in Vienna, with vegan participants recruited with the help of the Austrian Vegan Society.

Importantly, the study documented participants’ bone microarchitecture, a key measure of bone strength that has also not been previously investigated in vegans, using high-resolution peripheral quantitative CT.

Inclusion criteria included maintaining an omnivore diet of meat and plant-based foods or a vegan diet for at least 5 years, not being underweight or obese (body mass index [BMI], 18.5-30 kg/m²), being age 30-50 years, and being premenopausal.

Of the participants, 43 were vegan and 45 were omnivores, with generally equal ratios of men and women.

Vegan bone deficits disappear with strength training

Overall, compared with omnivores, the vegan group showed significant deficits in 7 of 14 measures of BMI-adjusted trabecular and cortical structure (all P < .05).

Among participants who reported no resistance training, vegans still showed significant decreases in bone microarchitecture, compared with omnivores, including radius trabecular BMD, radius trabecular bone volume fraction, and other tibial and cortical bone microarchitecture measures.

However, among those who did report progressive resistant training (20 vegans and 25 omnivores), defined as using machines, free weights, or bodyweight resistance exercises at least once a week, those differences disappeared and there were no significant differences in BMI-adjusted bone microarchitecture between vegans and omnivores after the 5 years.

Of note, no significant differences in bone microarchitecture were observed between those who performed exclusively aerobic activities and those who reported no sports activities in the vegan or omnivore group.

Based on the findings, “other types of exercise such as aerobics, cycling, etc, would not be sufficient for a similar positive effect on bone [as resistance training],” Dr. Wakolbinger-Habel said.

Although the findings suggest that resistance training seemed to allow vegans to “catch up” with omnivores in terms of bone microarchitecture, Dr. Wakolbinger-Habel cautioned that a study limitation is the relatively low number of participants.

“The absolute numbers suggest that in vegans the differences, and the relative effect, respectively of resistance training might be larger,” he said. “However, the number of participants in the subgroups is small and it is still an observational study, so we need to be careful in drawing causal conclusions.”

Serum bone markers were within normal ranges across all subgroups. And although there were some correlations between nutrient intake and bone microarchitecture among vegans who did and did not practice resistance training, no conclusions could be drawn from that data, the authors noted.

“Based on our data, the structural [differences between vegans and omnivores] cannot solely be explained by deficits in certain nutrients according to lifestyle,” the authors concluded.
 

Mechanisms

The mechanisms by which progressive resistance training could result in the benefits include that mechanical loads trigger stimulation of key pathways involved in bone formation, or mechanotransduction, the authors explained.

The unique effects have been observed in other studies, including one study showing that, among young adult runners, the addition of resistance training once a week was associated with significantly greater BMD.

“Veganism is a global trend with strongly increasing numbers of people worldwide adhering to a purely plant-based diet,” first author Christian Muschitz, MD, also of St. Vincent Hospital Vienna and the Medical University of Vienna, said in a press statement.

“Our study showed resistance training offsets diminished bone structure in vegan people when compared to omnivores,” he said.

Dr. Wakolbinger-Habel recommended that, based on the findings, “exercise, including resistance training, should be strongly advocated [for vegans], I would say, at least two times per week.”

The authors reported no relevant financial relationships.

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

People who maintain a vegan diet show significant deficits in bone microarchitecture, compared with omnivores; however, resistance training not only appears to improve those deficits but may have a stronger effect in vegans, suggesting an important strategy in maintaining bone health with a vegan diet.

“We expected better bone structure in both vegans and omnivores who reported resistance training,” first author Robert Wakolbinger-Habel, MD, PhD, of St. Vincent Hospital Vienna and the Medical University of Vienna, said in an interview.

Thinkstock.com

“However, we expected [there would still be] differences in structure between vegans and omnivores [who practiced resistance training], as previous literature reported higher fracture rates in vegans,” he said. “Still, the positive message is that ‘pumping iron’ could counterbalance these differences between vegans and omnivores.”

The research was published online in The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
 

Exercise significantly impacts bone health in vegans

The potential effects of the plant-based vegan diet on bone health have been reported in studies linking the diet to an increased risk of fractures and lower bone mineral density (BMD), with common theories including lower bone- and muscle-building protein in vegan diets.

However, most previous studies have not considered other key factors, such as the effects of exercise, the authors noted.

“While previous studies on bone health in vegans only took BMD, biochemical and nutritional parameters into account, they did not consider the significant effects of physical activity,” they wrote.

“By ignoring these effects, important factors influencing bone health are neglected.”

For the study, 88 participants were enrolled in Vienna, with vegan participants recruited with the help of the Austrian Vegan Society.

Importantly, the study documented participants’ bone microarchitecture, a key measure of bone strength that has also not been previously investigated in vegans, using high-resolution peripheral quantitative CT.

Inclusion criteria included maintaining an omnivore diet of meat and plant-based foods or a vegan diet for at least 5 years, not being underweight or obese (body mass index [BMI], 18.5-30 kg/m²), being age 30-50 years, and being premenopausal.

Of the participants, 43 were vegan and 45 were omnivores, with generally equal ratios of men and women.

Vegan bone deficits disappear with strength training

Overall, compared with omnivores, the vegan group showed significant deficits in 7 of 14 measures of BMI-adjusted trabecular and cortical structure (all P < .05).

Among participants who reported no resistance training, vegans still showed significant decreases in bone microarchitecture, compared with omnivores, including radius trabecular BMD, radius trabecular bone volume fraction, and other tibial and cortical bone microarchitecture measures.

However, among those who did report progressive resistant training (20 vegans and 25 omnivores), defined as using machines, free weights, or bodyweight resistance exercises at least once a week, those differences disappeared and there were no significant differences in BMI-adjusted bone microarchitecture between vegans and omnivores after the 5 years.

Of note, no significant differences in bone microarchitecture were observed between those who performed exclusively aerobic activities and those who reported no sports activities in the vegan or omnivore group.

Based on the findings, “other types of exercise such as aerobics, cycling, etc, would not be sufficient for a similar positive effect on bone [as resistance training],” Dr. Wakolbinger-Habel said.

Although the findings suggest that resistance training seemed to allow vegans to “catch up” with omnivores in terms of bone microarchitecture, Dr. Wakolbinger-Habel cautioned that a study limitation is the relatively low number of participants.

“The absolute numbers suggest that in vegans the differences, and the relative effect, respectively of resistance training might be larger,” he said. “However, the number of participants in the subgroups is small and it is still an observational study, so we need to be careful in drawing causal conclusions.”

Serum bone markers were within normal ranges across all subgroups. And although there were some correlations between nutrient intake and bone microarchitecture among vegans who did and did not practice resistance training, no conclusions could be drawn from that data, the authors noted.

“Based on our data, the structural [differences between vegans and omnivores] cannot solely be explained by deficits in certain nutrients according to lifestyle,” the authors concluded.
 

Mechanisms

The mechanisms by which progressive resistance training could result in the benefits include that mechanical loads trigger stimulation of key pathways involved in bone formation, or mechanotransduction, the authors explained.

The unique effects have been observed in other studies, including one study showing that, among young adult runners, the addition of resistance training once a week was associated with significantly greater BMD.

“Veganism is a global trend with strongly increasing numbers of people worldwide adhering to a purely plant-based diet,” first author Christian Muschitz, MD, also of St. Vincent Hospital Vienna and the Medical University of Vienna, said in a press statement.

“Our study showed resistance training offsets diminished bone structure in vegan people when compared to omnivores,” he said.

Dr. Wakolbinger-Habel recommended that, based on the findings, “exercise, including resistance training, should be strongly advocated [for vegans], I would say, at least two times per week.”

The authors reported no relevant financial relationships.

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

One day in 2020, Ronda S. Farah, MD, was spending some downtime from her dermatology practice scrolling through social media. When she opened TikTok, she came across something that piqued her interest: A popular content creator was promoting the supplement biotin as a way to grow hair. Dr. Farah was immediately alarmed, because not only was the evidence that biotin increases hair growth shoddy, but the FDA had also warned that biotin supplements may interfere with lab tests for troponin.

Dr. Farah was moved to action and made a brief TikTok stating that use of biotin does not result in hair growth for most patients, which quickly shot up to over half a million views. She was flooded with messages from influencers and people desperate for an answer to their hair growth questions.

From that point on, Dr. Farah was immersed in the world of hairfluencers, the social media personalities who promote hair care trends, which formed the basis of a review, published in the Journal of Cosmetic Dermatology that she conducted with her colleagues at the University of Minnesota, Minneapolis. .

They reviewed five treatments that represent some of the most frequently discussed hair-growth trends on social media: rosemary, onion juice, rice water, castor oil, and aloe vera. For each, they evaluated recommendations on how the treatments were applied, possible harmful effects to the user, claims that weren’t totally based on scientific evidence, and the theoretical mechanism of action. “Overall,” they concluded, “there is little to no literature supporting these social media trends for hair growth.”

Of the five, rosemary, applied to the scalp or hair, has perhaps the most significant research behind it, according to Dr. Farah and coauthors. Methods of applying rosemary described on social media included use of prepackaged oil, boiling fresh rosemary leaves, adding leaves to oils and spraying it on or massaging it on the scalp, applying it in the hair, or using it as a rinse. Dr. Farah noted that the literature supporting the use of rosemary for hair growth does not represent the most robust science; the studies had small sample sizes and used nonstandardized methods of measuring hair growth.

“It didn’t really meet rigorous, strong study methods that a board-certified dermatologist with their expertise would consider a really solid study,” she said.

For the remaining methods, there was little research to support their use for hair growth. A few, the authors pointed out, can cause scalp burns (aloe vera), damage to hair follicles (rice water), contact dermatitis (aloe vera, onion juice), and, in the case of castor oil, hair felting..

Dr. Farah thinks social media can be a great tool to reach patients, but that people should be wary of what kind of information they’re consuming “and need to be aware of who their hairfluencer is,” she said. And, as she and her coauthors wrote: “We call on dermatologists, as hair and scalp disease experts, to serve as authorities on ‘hairfluencer’ trends and appropriately counsel patients.”

The study was independently supported. Dr. Farah reports no relevant financial relationships.

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

One day in 2020, Ronda S. Farah, MD, was spending some downtime from her dermatology practice scrolling through social media. When she opened TikTok, she came across something that piqued her interest: A popular content creator was promoting the supplement biotin as a way to grow hair. Dr. Farah was immediately alarmed, because not only was the evidence that biotin increases hair growth shoddy, but the FDA had also warned that biotin supplements may interfere with lab tests for troponin.

Dr. Farah was moved to action and made a brief TikTok stating that use of biotin does not result in hair growth for most patients, which quickly shot up to over half a million views. She was flooded with messages from influencers and people desperate for an answer to their hair growth questions.

From that point on, Dr. Farah was immersed in the world of hairfluencers, the social media personalities who promote hair care trends, which formed the basis of a review, published in the Journal of Cosmetic Dermatology that she conducted with her colleagues at the University of Minnesota, Minneapolis. .

They reviewed five treatments that represent some of the most frequently discussed hair-growth trends on social media: rosemary, onion juice, rice water, castor oil, and aloe vera. For each, they evaluated recommendations on how the treatments were applied, possible harmful effects to the user, claims that weren’t totally based on scientific evidence, and the theoretical mechanism of action. “Overall,” they concluded, “there is little to no literature supporting these social media trends for hair growth.”

Of the five, rosemary, applied to the scalp or hair, has perhaps the most significant research behind it, according to Dr. Farah and coauthors. Methods of applying rosemary described on social media included use of prepackaged oil, boiling fresh rosemary leaves, adding leaves to oils and spraying it on or massaging it on the scalp, applying it in the hair, or using it as a rinse. Dr. Farah noted that the literature supporting the use of rosemary for hair growth does not represent the most robust science; the studies had small sample sizes and used nonstandardized methods of measuring hair growth.

“It didn’t really meet rigorous, strong study methods that a board-certified dermatologist with their expertise would consider a really solid study,” she said.

For the remaining methods, there was little research to support their use for hair growth. A few, the authors pointed out, can cause scalp burns (aloe vera), damage to hair follicles (rice water), contact dermatitis (aloe vera, onion juice), and, in the case of castor oil, hair felting..

Dr. Farah thinks social media can be a great tool to reach patients, but that people should be wary of what kind of information they’re consuming “and need to be aware of who their hairfluencer is,” she said. And, as she and her coauthors wrote: “We call on dermatologists, as hair and scalp disease experts, to serve as authorities on ‘hairfluencer’ trends and appropriately counsel patients.”

The study was independently supported. Dr. Farah reports no relevant financial relationships.

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

One day in 2020, Ronda S. Farah, MD, was spending some downtime from her dermatology practice scrolling through social media. When she opened TikTok, she came across something that piqued her interest: A popular content creator was promoting the supplement biotin as a way to grow hair. Dr. Farah was immediately alarmed, because not only was the evidence that biotin increases hair growth shoddy, but the FDA had also warned that biotin supplements may interfere with lab tests for troponin.

Dr. Farah was moved to action and made a brief TikTok stating that use of biotin does not result in hair growth for most patients, which quickly shot up to over half a million views. She was flooded with messages from influencers and people desperate for an answer to their hair growth questions.

From that point on, Dr. Farah was immersed in the world of hairfluencers, the social media personalities who promote hair care trends, which formed the basis of a review, published in the Journal of Cosmetic Dermatology that she conducted with her colleagues at the University of Minnesota, Minneapolis. .

They reviewed five treatments that represent some of the most frequently discussed hair-growth trends on social media: rosemary, onion juice, rice water, castor oil, and aloe vera. For each, they evaluated recommendations on how the treatments were applied, possible harmful effects to the user, claims that weren’t totally based on scientific evidence, and the theoretical mechanism of action. “Overall,” they concluded, “there is little to no literature supporting these social media trends for hair growth.”

Of the five, rosemary, applied to the scalp or hair, has perhaps the most significant research behind it, according to Dr. Farah and coauthors. Methods of applying rosemary described on social media included use of prepackaged oil, boiling fresh rosemary leaves, adding leaves to oils and spraying it on or massaging it on the scalp, applying it in the hair, or using it as a rinse. Dr. Farah noted that the literature supporting the use of rosemary for hair growth does not represent the most robust science; the studies had small sample sizes and used nonstandardized methods of measuring hair growth.

“It didn’t really meet rigorous, strong study methods that a board-certified dermatologist with their expertise would consider a really solid study,” she said.

For the remaining methods, there was little research to support their use for hair growth. A few, the authors pointed out, can cause scalp burns (aloe vera), damage to hair follicles (rice water), contact dermatitis (aloe vera, onion juice), and, in the case of castor oil, hair felting..

Dr. Farah thinks social media can be a great tool to reach patients, but that people should be wary of what kind of information they’re consuming “and need to be aware of who their hairfluencer is,” she said. And, as she and her coauthors wrote: “We call on dermatologists, as hair and scalp disease experts, to serve as authorities on ‘hairfluencer’ trends and appropriately counsel patients.”

The study was independently supported. Dr. Farah reports no relevant financial relationships.

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

Of all the headaches inherent in a private medical practice, few are more frustrating than patients who make appointments and then fail to keep them.

No-shows are a problem for all physicians, but especially for dermatologists. In one study, the no-show rate in dermatology offices averaged 10% – almost double the average for all medical offices.

The problem has become so pervasive that many physicians are now charging a fee for missed appointments. I have never been a fan of such fees for a variety of reasons, starting with the anger and bad will that they engender; but also, in my experience, they seldom accomplish their intended goal of changing the behavior.

That’s because fees imply some sort of conscious decision made by a patient to miss an appointment, but studies show that this is rarely the case. Some patients cite transportation issues or childcare obligations. One Canadian study found that nearly a quarter of patients who missed an appointment felt too sick to keep it. Another reason is lack of insurance coverage. Studies have shown that the no-show rate is far higher when the patient is paying out-of-pocket for the visit.

Patients who don’t show up for appointments tend to be younger and poorer, and live farther away from the office than those who attend consistently. Some patients may be unaware that they need to cancel, while others report that they don’t feel obliged to keep appointments because they feel disrespected by the system. One person posted on a medical forum, “Everyone’s time is valuable. When the doctor makes me wait, there are consequences too. Why are there two standards in the situation?”

The most common reason for missed appointments, however, according to multiple studies, is that patients simply forget that they have one. One reason for that is a lag between appointment and visit. Many dermatologists are booked well in advance; by the time the appointment arrives, some patients’ complaints will have resolved spontaneously, while other patients will have found another office willing to see them sooner.

Another big reason is the absence of a strong physician-patient relationship. Perhaps the patient sees a different doctor or physician assistant at each visit and doesn’t feel a particular bond with any of them. Some patients may perceive a lack of concern on the part of the physician. And others may suffer from poor communication; for example, patients frequently become frustrated that a chronic condition has not resolved, when it has not been clearly explained to them that such problems cannot be expected to resolve rapidly or completely.

Whatever the reasons, no-shows are an economic and medicolegal liability. It is worth the considerable effort it often takes to minimize them.

Research suggests that no-show rates can be reduced by providing more same-day or next-day appointments. One large-scale analysis of national data found that same-day appointments accounted for just 2% of no-shows, while appointments booked 15 days or more in advance accounted for nearly a third of them. Canadian studies have likewise found the risk of no-shows increases the further in advance clinics book patients.

Deal with simple forgetfulness by calling your patients the day before to remind them of their appointments. Reasonably priced phone software is available from a variety of vendors to automate this process. Or hire a teenager to do it after school each day.

Whenever possible, use cellphone numbers for reminder calls. Patients often aren’t home during the day, and many don’t listen to their messages when they come in. And patients who have moved will often have a new home phone number, but their cellphone number will be the same.

Decrease the wait for new appointments. Keep some slots open each week for new patients, who will often “shop around” for a faster appointment while they’re waiting for an appointment they already have elsewhere.

But above all, seek to maximize the strength of your physician-patient relationships. Try not to shuttle patients between different physicians or PAs, and make it clear that you are genuinely concerned about their health. Impress upon them the crucial role they play in their own care, which includes keeping all their appointments.

In our office, significant no-shows (for example, a patient with a melanoma who misses a follow-up visit) receive a phone call and a certified letter, and their records go into a special file for close follow-up by the nursing staff.

If you choose to go the missed-appointment-fee route, be sure to post notices in your office and on your website clearly delineating your policy. Emphasize that it is not a service fee, and cannot be billed to insurance.

All missed appointments should be documented in the patient’s record; it’s important clinical and medicolegal information. And habitual no-shows should be dismissed from your practice. You cannot afford them.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Of all the headaches inherent in a private medical practice, few are more frustrating than patients who make appointments and then fail to keep them.

No-shows are a problem for all physicians, but especially for dermatologists. In one study, the no-show rate in dermatology offices averaged 10% – almost double the average for all medical offices.

The problem has become so pervasive that many physicians are now charging a fee for missed appointments. I have never been a fan of such fees for a variety of reasons, starting with the anger and bad will that they engender; but also, in my experience, they seldom accomplish their intended goal of changing the behavior.

That’s because fees imply some sort of conscious decision made by a patient to miss an appointment, but studies show that this is rarely the case. Some patients cite transportation issues or childcare obligations. One Canadian study found that nearly a quarter of patients who missed an appointment felt too sick to keep it. Another reason is lack of insurance coverage. Studies have shown that the no-show rate is far higher when the patient is paying out-of-pocket for the visit.

Patients who don’t show up for appointments tend to be younger and poorer, and live farther away from the office than those who attend consistently. Some patients may be unaware that they need to cancel, while others report that they don’t feel obliged to keep appointments because they feel disrespected by the system. One person posted on a medical forum, “Everyone’s time is valuable. When the doctor makes me wait, there are consequences too. Why are there two standards in the situation?”

The most common reason for missed appointments, however, according to multiple studies, is that patients simply forget that they have one. One reason for that is a lag between appointment and visit. Many dermatologists are booked well in advance; by the time the appointment arrives, some patients’ complaints will have resolved spontaneously, while other patients will have found another office willing to see them sooner.

Another big reason is the absence of a strong physician-patient relationship. Perhaps the patient sees a different doctor or physician assistant at each visit and doesn’t feel a particular bond with any of them. Some patients may perceive a lack of concern on the part of the physician. And others may suffer from poor communication; for example, patients frequently become frustrated that a chronic condition has not resolved, when it has not been clearly explained to them that such problems cannot be expected to resolve rapidly or completely.

Whatever the reasons, no-shows are an economic and medicolegal liability. It is worth the considerable effort it often takes to minimize them.

Research suggests that no-show rates can be reduced by providing more same-day or next-day appointments. One large-scale analysis of national data found that same-day appointments accounted for just 2% of no-shows, while appointments booked 15 days or more in advance accounted for nearly a third of them. Canadian studies have likewise found the risk of no-shows increases the further in advance clinics book patients.

Deal with simple forgetfulness by calling your patients the day before to remind them of their appointments. Reasonably priced phone software is available from a variety of vendors to automate this process. Or hire a teenager to do it after school each day.

Whenever possible, use cellphone numbers for reminder calls. Patients often aren’t home during the day, and many don’t listen to their messages when they come in. And patients who have moved will often have a new home phone number, but their cellphone number will be the same.

Decrease the wait for new appointments. Keep some slots open each week for new patients, who will often “shop around” for a faster appointment while they’re waiting for an appointment they already have elsewhere.

But above all, seek to maximize the strength of your physician-patient relationships. Try not to shuttle patients between different physicians or PAs, and make it clear that you are genuinely concerned about their health. Impress upon them the crucial role they play in their own care, which includes keeping all their appointments.

In our office, significant no-shows (for example, a patient with a melanoma who misses a follow-up visit) receive a phone call and a certified letter, and their records go into a special file for close follow-up by the nursing staff.

If you choose to go the missed-appointment-fee route, be sure to post notices in your office and on your website clearly delineating your policy. Emphasize that it is not a service fee, and cannot be billed to insurance.

All missed appointments should be documented in the patient’s record; it’s important clinical and medicolegal information. And habitual no-shows should be dismissed from your practice. You cannot afford them.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Of all the headaches inherent in a private medical practice, few are more frustrating than patients who make appointments and then fail to keep them.

No-shows are a problem for all physicians, but especially for dermatologists. In one study, the no-show rate in dermatology offices averaged 10% – almost double the average for all medical offices.

The problem has become so pervasive that many physicians are now charging a fee for missed appointments. I have never been a fan of such fees for a variety of reasons, starting with the anger and bad will that they engender; but also, in my experience, they seldom accomplish their intended goal of changing the behavior.

That’s because fees imply some sort of conscious decision made by a patient to miss an appointment, but studies show that this is rarely the case. Some patients cite transportation issues or childcare obligations. One Canadian study found that nearly a quarter of patients who missed an appointment felt too sick to keep it. Another reason is lack of insurance coverage. Studies have shown that the no-show rate is far higher when the patient is paying out-of-pocket for the visit.

Patients who don’t show up for appointments tend to be younger and poorer, and live farther away from the office than those who attend consistently. Some patients may be unaware that they need to cancel, while others report that they don’t feel obliged to keep appointments because they feel disrespected by the system. One person posted on a medical forum, “Everyone’s time is valuable. When the doctor makes me wait, there are consequences too. Why are there two standards in the situation?”

The most common reason for missed appointments, however, according to multiple studies, is that patients simply forget that they have one. One reason for that is a lag between appointment and visit. Many dermatologists are booked well in advance; by the time the appointment arrives, some patients’ complaints will have resolved spontaneously, while other patients will have found another office willing to see them sooner.

Another big reason is the absence of a strong physician-patient relationship. Perhaps the patient sees a different doctor or physician assistant at each visit and doesn’t feel a particular bond with any of them. Some patients may perceive a lack of concern on the part of the physician. And others may suffer from poor communication; for example, patients frequently become frustrated that a chronic condition has not resolved, when it has not been clearly explained to them that such problems cannot be expected to resolve rapidly or completely.

Whatever the reasons, no-shows are an economic and medicolegal liability. It is worth the considerable effort it often takes to minimize them.

Research suggests that no-show rates can be reduced by providing more same-day or next-day appointments. One large-scale analysis of national data found that same-day appointments accounted for just 2% of no-shows, while appointments booked 15 days or more in advance accounted for nearly a third of them. Canadian studies have likewise found the risk of no-shows increases the further in advance clinics book patients.

Deal with simple forgetfulness by calling your patients the day before to remind them of their appointments. Reasonably priced phone software is available from a variety of vendors to automate this process. Or hire a teenager to do it after school each day.

Whenever possible, use cellphone numbers for reminder calls. Patients often aren’t home during the day, and many don’t listen to their messages when they come in. And patients who have moved will often have a new home phone number, but their cellphone number will be the same.

Decrease the wait for new appointments. Keep some slots open each week for new patients, who will often “shop around” for a faster appointment while they’re waiting for an appointment they already have elsewhere.

But above all, seek to maximize the strength of your physician-patient relationships. Try not to shuttle patients between different physicians or PAs, and make it clear that you are genuinely concerned about their health. Impress upon them the crucial role they play in their own care, which includes keeping all their appointments.

In our office, significant no-shows (for example, a patient with a melanoma who misses a follow-up visit) receive a phone call and a certified letter, and their records go into a special file for close follow-up by the nursing staff.

If you choose to go the missed-appointment-fee route, be sure to post notices in your office and on your website clearly delineating your policy. Emphasize that it is not a service fee, and cannot be billed to insurance.

All missed appointments should be documented in the patient’s record; it’s important clinical and medicolegal information. And habitual no-shows should be dismissed from your practice. You cannot afford them.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

You may have noticed that collecting patient payments has been tough this year. Owing to the pandemic, job loss, and the possible loss of health insurance, patients have had more difficulty managing copays, coinsurance, and deductibles, not to mention other out-of-pocket health care charges.

“Many of our patients have lost their jobs or have had their hours cut back, and as a result, they are struggling to make ends meet,” said Ahmad Chaudhry, MD, a cardiothoracic surgeon in Lexington, Ky. “However, we cannot continue to provide care if our patients do not pay their bills.”

This news organization asked physicians what they do when their patients don’t pay. About 43% said that they continue to treat them and develop a payment plan; 13% send their bill to collections; 12% continue their care and write off their balance, and 25% choose other actions. Only 8% of physicians drop patients if they don’t pay.

Because you need to pay your own bills, what can you do about nonpaying patients?
 

Start with price transparency

In the past, patients never knew what their lab work or a chest EKG would cost because it wasn’t listed anywhere, and it was usually more than expected. Because of new legislation concerning health care price transparency, hospitals, health plans, and insurers must pony up with the actual fees, making them transparent to patients. Physician practices should follow suit and keep prices transparent too. Patients are more likely to pay their bills when prepared for the expense.

Patients with insurance often don’t know what they’ll be paying for their visit or their tests because they don’t know how much insurance will cover and what will be left for them to pay. Also, they may not know if they’ve met their deductible yet so they’re unsure whether insurance will even kick in. And patients without insurance still need to know what their costs will be upfront.

According to 10 insights from the Primary Care Consumer Choice Survey, 74% of health care consumers were willing to pay a $50 out-of-pocket charge to know the cost of their primary care visit.
 

Provide payment plans

Many patients have always needed payment plans. It’s one thing to post a sign at check-in telling patients that all monies are due at the time of service, but it’s another reality for a patient who can’t fork over the $250 charge they just unexpectedly spent in your office.

Discover Financial Services recently ran a survey, with results presented in the press release Americans are Delaying Non-Emergency Medical Care in Higher Numbers than Last Year, and found that many Americans with medical debt are delaying nonemergency medical care. For example, they put off seeing a specialist (52%), seeing a doctor for sickness (41%), and undergoing treatment plans recommended by their doctor (31%). 

Turning an account over to collections should be a last resort. In addition, agencies typically charge 30%-40% of the total collected off the top.

Though collecting that amount is better than nothing, using a collection agency may have unexpected consequences. For instance, you’re trusting the agency you hire to collect to represent you and act on your practice’s behalf. If they’re rude or their tactics are harsh in the eyes of the patient or their relatives, it’s your reputation that is on the line.

Rather than use a collection agency, you could collect the payments yourself. When a patient fails to pay within about 3 months, begin mailing statements from the office, followed by firm but generous phone calls trying to collect. Industry estimates put the average cost of sending an invoice, including staff labor, printing, and postage, at about $35 per mailer. Some practices combat the added costs by offering a 20% prompt-pay discount. Offering payment plans is another option that helps garner eventual payment. Plus, practices should direct patients to third-party lenders such as CareCredit for larger bills.

On occasion, some small practices may allow a swap, such as allowing a patient to provide a service such as plumbing, electrical, or painting in exchange for working off the bill. Though it’s not ideal when it comes to finances, you may find it can work in a pinch for a cash-strapped patient. Make sure to keep records of what bills the patient’s work goes toward.

It often helps to incentivize your billing staff to follow up regularly, with various suggestions and tactics, to get patients to pay their bills. The incentive amount you offer will probably be less than if you had to use a collection agency.
 

Have a payment policy

Because your practice’s primary job is caring for patients’ physical and emotional needs, payment collection without coming off as insensitive can be tricky. “We understand these are difficult times for everyone, and we are doing our best to work with our patients,” said Dr. Chaudhry. Having a written payment policy can help build the bridge. A policy lets patients know what they can expect and can help prevent surprises over what occurs in the event of nonpayment. Your written policy should include:

• When payment is due.
• How the practice handles copays and deductibles.
• What forms of payment are accepted.
• Your policy regarding nonpayment.

Why patients don’t pay

A 2021 Healthcare Consumer Experience Study from Cedar found that medical bills are a source of anxiety and frustration for most patients, affecting their financial experience. More than half of the respondents said that paying a medical bill is stressful. Complicating matters, many health care practices rely on outdated payment systems, which may not provide patients with a clear view of what they owe and how to pay it.

The study found that 53% of respondents find understanding their plan’s coverage and benefits stressful, and 37% of patients won’t pay their bill if they can’t understand it.

People may think the patient is trying to get out of paying, which, of course, is sometimes true, but most of the time they want to pay, concluded the study. Most patients need a better explanation, communication, and accurate accounting of their out-of-pocket costs.
 

What can doctors do?

If you’re a physician who regularly sees patients who have problems paying their bills, you can take a few steps to minimize the financial impact on your practice:

• Bill the patient’s insurance directly to ensure you receive at least partial payment.
• Keep adequate records of services in case you need to pursue legal action.
• “Be understanding and flexible when it comes to payment arrangements, as this can often be the difference between getting paid and not getting paid at all,” said Dr. Chaudhry.

Distance yourself

When discussing payment policies, physicians should try to distance themselves from the actual collection process as much as possible. Well-meaning physicians often tell patients things like they can “figure something out “ financially or “work them in” during a scheduling conflict, but that often undermines the authority and credibility of the practice’s office staff. Plus, it teaches patients they can get their way if they work on the doctor’s soft spot – something you don’t want to encourage.

By following some of these measures, you can help ensure that your practice continues to thrive despite the challenges posed by nonpaying patients.

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

You may have noticed that collecting patient payments has been tough this year. Owing to the pandemic, job loss, and the possible loss of health insurance, patients have had more difficulty managing copays, coinsurance, and deductibles, not to mention other out-of-pocket health care charges.

“Many of our patients have lost their jobs or have had their hours cut back, and as a result, they are struggling to make ends meet,” said Ahmad Chaudhry, MD, a cardiothoracic surgeon in Lexington, Ky. “However, we cannot continue to provide care if our patients do not pay their bills.”

This news organization asked physicians what they do when their patients don’t pay. About 43% said that they continue to treat them and develop a payment plan; 13% send their bill to collections; 12% continue their care and write off their balance, and 25% choose other actions. Only 8% of physicians drop patients if they don’t pay.

Because you need to pay your own bills, what can you do about nonpaying patients?
 

Start with price transparency

In the past, patients never knew what their lab work or a chest EKG would cost because it wasn’t listed anywhere, and it was usually more than expected. Because of new legislation concerning health care price transparency, hospitals, health plans, and insurers must pony up with the actual fees, making them transparent to patients. Physician practices should follow suit and keep prices transparent too. Patients are more likely to pay their bills when prepared for the expense.

Patients with insurance often don’t know what they’ll be paying for their visit or their tests because they don’t know how much insurance will cover and what will be left for them to pay. Also, they may not know if they’ve met their deductible yet so they’re unsure whether insurance will even kick in. And patients without insurance still need to know what their costs will be upfront.

According to 10 insights from the Primary Care Consumer Choice Survey, 74% of health care consumers were willing to pay a $50 out-of-pocket charge to know the cost of their primary care visit.
 

Provide payment plans

Many patients have always needed payment plans. It’s one thing to post a sign at check-in telling patients that all monies are due at the time of service, but it’s another reality for a patient who can’t fork over the $250 charge they just unexpectedly spent in your office.

Discover Financial Services recently ran a survey, with results presented in the press release Americans are Delaying Non-Emergency Medical Care in Higher Numbers than Last Year, and found that many Americans with medical debt are delaying nonemergency medical care. For example, they put off seeing a specialist (52%), seeing a doctor for sickness (41%), and undergoing treatment plans recommended by their doctor (31%). 

Turning an account over to collections should be a last resort. In addition, agencies typically charge 30%-40% of the total collected off the top.

Though collecting that amount is better than nothing, using a collection agency may have unexpected consequences. For instance, you’re trusting the agency you hire to collect to represent you and act on your practice’s behalf. If they’re rude or their tactics are harsh in the eyes of the patient or their relatives, it’s your reputation that is on the line.

Rather than use a collection agency, you could collect the payments yourself. When a patient fails to pay within about 3 months, begin mailing statements from the office, followed by firm but generous phone calls trying to collect. Industry estimates put the average cost of sending an invoice, including staff labor, printing, and postage, at about $35 per mailer. Some practices combat the added costs by offering a 20% prompt-pay discount. Offering payment plans is another option that helps garner eventual payment. Plus, practices should direct patients to third-party lenders such as CareCredit for larger bills.

On occasion, some small practices may allow a swap, such as allowing a patient to provide a service such as plumbing, electrical, or painting in exchange for working off the bill. Though it’s not ideal when it comes to finances, you may find it can work in a pinch for a cash-strapped patient. Make sure to keep records of what bills the patient’s work goes toward.

It often helps to incentivize your billing staff to follow up regularly, with various suggestions and tactics, to get patients to pay their bills. The incentive amount you offer will probably be less than if you had to use a collection agency.
 

Have a payment policy

Because your practice’s primary job is caring for patients’ physical and emotional needs, payment collection without coming off as insensitive can be tricky. “We understand these are difficult times for everyone, and we are doing our best to work with our patients,” said Dr. Chaudhry. Having a written payment policy can help build the bridge. A policy lets patients know what they can expect and can help prevent surprises over what occurs in the event of nonpayment. Your written policy should include:

• When payment is due.
• How the practice handles copays and deductibles.
• What forms of payment are accepted.
• Your policy regarding nonpayment.

Why patients don’t pay

A 2021 Healthcare Consumer Experience Study from Cedar found that medical bills are a source of anxiety and frustration for most patients, affecting their financial experience. More than half of the respondents said that paying a medical bill is stressful. Complicating matters, many health care practices rely on outdated payment systems, which may not provide patients with a clear view of what they owe and how to pay it.

The study found that 53% of respondents find understanding their plan’s coverage and benefits stressful, and 37% of patients won’t pay their bill if they can’t understand it.

People may think the patient is trying to get out of paying, which, of course, is sometimes true, but most of the time they want to pay, concluded the study. Most patients need a better explanation, communication, and accurate accounting of their out-of-pocket costs.
 

What can doctors do?

If you’re a physician who regularly sees patients who have problems paying their bills, you can take a few steps to minimize the financial impact on your practice:

• Bill the patient’s insurance directly to ensure you receive at least partial payment.
• Keep adequate records of services in case you need to pursue legal action.
• “Be understanding and flexible when it comes to payment arrangements, as this can often be the difference between getting paid and not getting paid at all,” said Dr. Chaudhry.

Distance yourself

When discussing payment policies, physicians should try to distance themselves from the actual collection process as much as possible. Well-meaning physicians often tell patients things like they can “figure something out “ financially or “work them in” during a scheduling conflict, but that often undermines the authority and credibility of the practice’s office staff. Plus, it teaches patients they can get their way if they work on the doctor’s soft spot – something you don’t want to encourage.

By following some of these measures, you can help ensure that your practice continues to thrive despite the challenges posed by nonpaying patients.

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

You may have noticed that collecting patient payments has been tough this year. Owing to the pandemic, job loss, and the possible loss of health insurance, patients have had more difficulty managing copays, coinsurance, and deductibles, not to mention other out-of-pocket health care charges.

“Many of our patients have lost their jobs or have had their hours cut back, and as a result, they are struggling to make ends meet,” said Ahmad Chaudhry, MD, a cardiothoracic surgeon in Lexington, Ky. “However, we cannot continue to provide care if our patients do not pay their bills.”

This news organization asked physicians what they do when their patients don’t pay. About 43% said that they continue to treat them and develop a payment plan; 13% send their bill to collections; 12% continue their care and write off their balance, and 25% choose other actions. Only 8% of physicians drop patients if they don’t pay.

Because you need to pay your own bills, what can you do about nonpaying patients?
 

Start with price transparency

In the past, patients never knew what their lab work or a chest EKG would cost because it wasn’t listed anywhere, and it was usually more than expected. Because of new legislation concerning health care price transparency, hospitals, health plans, and insurers must pony up with the actual fees, making them transparent to patients. Physician practices should follow suit and keep prices transparent too. Patients are more likely to pay their bills when prepared for the expense.

Patients with insurance often don’t know what they’ll be paying for their visit or their tests because they don’t know how much insurance will cover and what will be left for them to pay. Also, they may not know if they’ve met their deductible yet so they’re unsure whether insurance will even kick in. And patients without insurance still need to know what their costs will be upfront.

According to 10 insights from the Primary Care Consumer Choice Survey, 74% of health care consumers were willing to pay a $50 out-of-pocket charge to know the cost of their primary care visit.
 

Provide payment plans

Many patients have always needed payment plans. It’s one thing to post a sign at check-in telling patients that all monies are due at the time of service, but it’s another reality for a patient who can’t fork over the $250 charge they just unexpectedly spent in your office.

Discover Financial Services recently ran a survey, with results presented in the press release Americans are Delaying Non-Emergency Medical Care in Higher Numbers than Last Year, and found that many Americans with medical debt are delaying nonemergency medical care. For example, they put off seeing a specialist (52%), seeing a doctor for sickness (41%), and undergoing treatment plans recommended by their doctor (31%). 

Turning an account over to collections should be a last resort. In addition, agencies typically charge 30%-40% of the total collected off the top.

Though collecting that amount is better than nothing, using a collection agency may have unexpected consequences. For instance, you’re trusting the agency you hire to collect to represent you and act on your practice’s behalf. If they’re rude or their tactics are harsh in the eyes of the patient or their relatives, it’s your reputation that is on the line.

Rather than use a collection agency, you could collect the payments yourself. When a patient fails to pay within about 3 months, begin mailing statements from the office, followed by firm but generous phone calls trying to collect. Industry estimates put the average cost of sending an invoice, including staff labor, printing, and postage, at about $35 per mailer. Some practices combat the added costs by offering a 20% prompt-pay discount. Offering payment plans is another option that helps garner eventual payment. Plus, practices should direct patients to third-party lenders such as CareCredit for larger bills.

On occasion, some small practices may allow a swap, such as allowing a patient to provide a service such as plumbing, electrical, or painting in exchange for working off the bill. Though it’s not ideal when it comes to finances, you may find it can work in a pinch for a cash-strapped patient. Make sure to keep records of what bills the patient’s work goes toward.

It often helps to incentivize your billing staff to follow up regularly, with various suggestions and tactics, to get patients to pay their bills. The incentive amount you offer will probably be less than if you had to use a collection agency.
 

Have a payment policy

Because your practice’s primary job is caring for patients’ physical and emotional needs, payment collection without coming off as insensitive can be tricky. “We understand these are difficult times for everyone, and we are doing our best to work with our patients,” said Dr. Chaudhry. Having a written payment policy can help build the bridge. A policy lets patients know what they can expect and can help prevent surprises over what occurs in the event of nonpayment. Your written policy should include:

• When payment is due.
• How the practice handles copays and deductibles.
• What forms of payment are accepted.
• Your policy regarding nonpayment.

Why patients don’t pay

A 2021 Healthcare Consumer Experience Study from Cedar found that medical bills are a source of anxiety and frustration for most patients, affecting their financial experience. More than half of the respondents said that paying a medical bill is stressful. Complicating matters, many health care practices rely on outdated payment systems, which may not provide patients with a clear view of what they owe and how to pay it.

The study found that 53% of respondents find understanding their plan’s coverage and benefits stressful, and 37% of patients won’t pay their bill if they can’t understand it.

People may think the patient is trying to get out of paying, which, of course, is sometimes true, but most of the time they want to pay, concluded the study. Most patients need a better explanation, communication, and accurate accounting of their out-of-pocket costs.
 

What can doctors do?

If you’re a physician who regularly sees patients who have problems paying their bills, you can take a few steps to minimize the financial impact on your practice:

• Bill the patient’s insurance directly to ensure you receive at least partial payment.
• Keep adequate records of services in case you need to pursue legal action.
• “Be understanding and flexible when it comes to payment arrangements, as this can often be the difference between getting paid and not getting paid at all,” said Dr. Chaudhry.

Distance yourself

When discussing payment policies, physicians should try to distance themselves from the actual collection process as much as possible. Well-meaning physicians often tell patients things like they can “figure something out “ financially or “work them in” during a scheduling conflict, but that often undermines the authority and credibility of the practice’s office staff. Plus, it teaches patients they can get their way if they work on the doctor’s soft spot – something you don’t want to encourage.

By following some of these measures, you can help ensure that your practice continues to thrive despite the challenges posed by nonpaying patients.

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

Using ultrasound (US) to evaluate sarcopenic obesity in patients with cirrhosis may offer accuracy on par with computed tomography (CT), according to investigators.

US-based assessment presents a more affordable point-of-care strategy that limits radiation exposure, which enables sequential monitoring, reported lead author Sukhpal Dhariwal, MBBS, MD, of the Postgraduate Institute of Medical Education and Research, Chandigarh, India.

“Preliminary data in patients with liver disease ... suggest that US muscle assessment–derived indices, especially thigh muscle thickness, identify sarcopenia CT-skeletal muscle index (SMI) and also predict hospitalization and mortality,” the investigators wrote in Journal of Clinical Gastroenterology. “However, the applicability of US-based techniques to measure muscle mass in the high-risk group of patients with cirrhosis and sarcopenic obesity has not been evaluated.”

To address this knowledge gap, the investigators performed both US- and CT-based muscle assessments in 52 patients with obesity and evidence of cirrhosis; 40 patients were male and the mean age was 50.9 years. In all, 20 (38.5%) were diagnosed with sarcopenia based on CT-determined SMI scores of less than 39 cm²/m² for women and 50 cm²/m² for men.

US showed that it was similarly capable of categorizing patients. The modality significantly differentiated individuals with or without sarcopenia based on high area under the curve values in four muscle indices: quadriceps muscle thickness (0.98), quadriceps muscle feather index (0.95), forearm muscle thickness (0.85), and forearm feather index (0.80).

Direct comparison of US-based assessment against CT-based SMI revealed positive correlations, with significant r values ranging from 0.40 to 0.58. These correlations were stronger in a male-only subgroup analysis, in which r values ranged from 0.52 to 0.70. R values were not calculated in the female subgroup because of the small sample size (n = 12).

The investigators adjusted indices for height, which may pose bias for overestimating muscle mass. Another limitation is the small sample size.

“US-based assessment of sarcopenia has excellent diagnostic accuracy and correlates highly with cross-sectional imaging-based SMI in cirrhosis patients with sarcopenic obesity,” the investigators concluded. “US may serve as an easy-to-use, point-of-care tool for assessing sarcopenia in sarcopenic obesity with the advantage of repeated sequential assessment.”

According to Jamile Wakim-Fleming, MD, of the Cleveland Clinic, “US-based muscle mass assessment seems to be reliable, reproducible, and simple to perform and should be encouraged along with nutrition assessments in all patients with cirrhosis and obesity.”

In a written comment, Dr. Wakim-Fleming noted the importance of timely monitoring and intervention in this patient population.

“Considering the morbidity and the poor outcomes associated with sarcopenic obesity and its frequency in cirrhosis, it is important to make early diagnosis and institute a management plan to improve muscle mass and function,” she said.

The study was supported the Patient-Centered Outcomes Research Institute, the American Medical Association, and the American Heart Association. The investigators disclosed additional relationships with Pfizer, Bristol Myers Squibb, and Novartis. Dr. Wakim-Fleming reported no relevant conflicts of interest.

Using ultrasound (US) to evaluate sarcopenic obesity in patients with cirrhosis may offer accuracy on par with computed tomography (CT), according to investigators.

US-based assessment presents a more affordable point-of-care strategy that limits radiation exposure, which enables sequential monitoring, reported lead author Sukhpal Dhariwal, MBBS, MD, of the Postgraduate Institute of Medical Education and Research, Chandigarh, India.

“Preliminary data in patients with liver disease ... suggest that US muscle assessment–derived indices, especially thigh muscle thickness, identify sarcopenia CT-skeletal muscle index (SMI) and also predict hospitalization and mortality,” the investigators wrote in Journal of Clinical Gastroenterology. “However, the applicability of US-based techniques to measure muscle mass in the high-risk group of patients with cirrhosis and sarcopenic obesity has not been evaluated.”

To address this knowledge gap, the investigators performed both US- and CT-based muscle assessments in 52 patients with obesity and evidence of cirrhosis; 40 patients were male and the mean age was 50.9 years. In all, 20 (38.5%) were diagnosed with sarcopenia based on CT-determined SMI scores of less than 39 cm²/m² for women and 50 cm²/m² for men.

US showed that it was similarly capable of categorizing patients. The modality significantly differentiated individuals with or without sarcopenia based on high area under the curve values in four muscle indices: quadriceps muscle thickness (0.98), quadriceps muscle feather index (0.95), forearm muscle thickness (0.85), and forearm feather index (0.80).

Direct comparison of US-based assessment against CT-based SMI revealed positive correlations, with significant r values ranging from 0.40 to 0.58. These correlations were stronger in a male-only subgroup analysis, in which r values ranged from 0.52 to 0.70. R values were not calculated in the female subgroup because of the small sample size (n = 12).

The investigators adjusted indices for height, which may pose bias for overestimating muscle mass. Another limitation is the small sample size.

“US-based assessment of sarcopenia has excellent diagnostic accuracy and correlates highly with cross-sectional imaging-based SMI in cirrhosis patients with sarcopenic obesity,” the investigators concluded. “US may serve as an easy-to-use, point-of-care tool for assessing sarcopenia in sarcopenic obesity with the advantage of repeated sequential assessment.”

According to Jamile Wakim-Fleming, MD, of the Cleveland Clinic, “US-based muscle mass assessment seems to be reliable, reproducible, and simple to perform and should be encouraged along with nutrition assessments in all patients with cirrhosis and obesity.”

In a written comment, Dr. Wakim-Fleming noted the importance of timely monitoring and intervention in this patient population.

“Considering the morbidity and the poor outcomes associated with sarcopenic obesity and its frequency in cirrhosis, it is important to make early diagnosis and institute a management plan to improve muscle mass and function,” she said.

The study was supported the Patient-Centered Outcomes Research Institute, the American Medical Association, and the American Heart Association. The investigators disclosed additional relationships with Pfizer, Bristol Myers Squibb, and Novartis. Dr. Wakim-Fleming reported no relevant conflicts of interest.

Using ultrasound (US) to evaluate sarcopenic obesity in patients with cirrhosis may offer accuracy on par with computed tomography (CT), according to investigators.

US-based assessment presents a more affordable point-of-care strategy that limits radiation exposure, which enables sequential monitoring, reported lead author Sukhpal Dhariwal, MBBS, MD, of the Postgraduate Institute of Medical Education and Research, Chandigarh, India.

“Preliminary data in patients with liver disease ... suggest that US muscle assessment–derived indices, especially thigh muscle thickness, identify sarcopenia CT-skeletal muscle index (SMI) and also predict hospitalization and mortality,” the investigators wrote in Journal of Clinical Gastroenterology. “However, the applicability of US-based techniques to measure muscle mass in the high-risk group of patients with cirrhosis and sarcopenic obesity has not been evaluated.”

To address this knowledge gap, the investigators performed both US- and CT-based muscle assessments in 52 patients with obesity and evidence of cirrhosis; 40 patients were male and the mean age was 50.9 years. In all, 20 (38.5%) were diagnosed with sarcopenia based on CT-determined SMI scores of less than 39 cm²/m² for women and 50 cm²/m² for men.

US showed that it was similarly capable of categorizing patients. The modality significantly differentiated individuals with or without sarcopenia based on high area under the curve values in four muscle indices: quadriceps muscle thickness (0.98), quadriceps muscle feather index (0.95), forearm muscle thickness (0.85), and forearm feather index (0.80).

Direct comparison of US-based assessment against CT-based SMI revealed positive correlations, with significant r values ranging from 0.40 to 0.58. These correlations were stronger in a male-only subgroup analysis, in which r values ranged from 0.52 to 0.70. R values were not calculated in the female subgroup because of the small sample size (n = 12).

The investigators adjusted indices for height, which may pose bias for overestimating muscle mass. Another limitation is the small sample size.

“US-based assessment of sarcopenia has excellent diagnostic accuracy and correlates highly with cross-sectional imaging-based SMI in cirrhosis patients with sarcopenic obesity,” the investigators concluded. “US may serve as an easy-to-use, point-of-care tool for assessing sarcopenia in sarcopenic obesity with the advantage of repeated sequential assessment.”

According to Jamile Wakim-Fleming, MD, of the Cleveland Clinic, “US-based muscle mass assessment seems to be reliable, reproducible, and simple to perform and should be encouraged along with nutrition assessments in all patients with cirrhosis and obesity.”

In a written comment, Dr. Wakim-Fleming noted the importance of timely monitoring and intervention in this patient population.

“Considering the morbidity and the poor outcomes associated with sarcopenic obesity and its frequency in cirrhosis, it is important to make early diagnosis and institute a management plan to improve muscle mass and function,” she said.

The study was supported the Patient-Centered Outcomes Research Institute, the American Medical Association, and the American Heart Association. The investigators disclosed additional relationships with Pfizer, Bristol Myers Squibb, and Novartis. Dr. Wakim-Fleming reported no relevant conflicts of interest.

Sleep behaviors, both individually and combined, are associated with an increased risk of developing metabolic dysfunction–associated fatty liver disease (MAFLD), according to a Chinese analysis that suggests the effect may be independent of obesity.

Yan Liu, PhD, from the School of Public Health at Sun Yat-sen University in Guangzhou, China, and colleagues studied data on over 5,000 individuals who self-reported sleep behaviors and underwent liver ultrasound.

Late bedtimes, snoring, and prolonged daytime napping were significantly associated with MAFLD, increasing the risk by 37%, 59%, and 17%, respectively, whereas people with both poor nighttime sleep and prolonged daytime napping had the “highest risk for developing fatty liver disease,” said Dr. Liu in a press release.

In contrast, having any of six healthy sleep behaviors decreased the risk by 16% each, and even a “moderate improvement in sleep quality was related to a 29% reduction in the risk for fatty liver disease,” he added.

The research, published online in the Journal of Clinical Endocrinology & Metabolism, also indicated that obesity accounted for only one fifth of the effect of sleep quality on MAFLD risk.

Rise in unhealthy lifestyles leads to increase in MALFD

The authors write that MAFLD is the “leading chronic liver disease worldwide,” affecting around a quarter of the adult population, and may lead to end-stage liver diseases and extrahepatic complications, thus “posing a major health and economic burden.”

Moreover, the disease prevalence is “soaring at an unanticipated rate,” increasing from 18% to 29% in China over the past decade, because of a “rapid rise in unhealthy lifestyles,” the authors note.

Sleep disturbance is increasingly prevalent, “and an emerging contributor to multiple metabolic disorders,” with insomnia and habitual snoring, for example, positively correlated with hypertension, impaired glucose metabolism, and dyslipidemia, report the authors.

However, whether sleep quality, which includes “several metabolic-related sleep behaviors,” constitutes an independent risk for MAFLD “over and above” the effect of obesity remains unclear.

To investigate further, the researchers examined data from the baseline survey of the community-based, prospective South China Cohort study, which was conducted in four regions of Southern China and involved 5,430 individuals aged 30-79 years.

Between March 2018 and October 2019, the participants self-reported sleep behaviors on the Pittsburgh Sleep Quality Index questionnaire and underwent ultrasound examination of the liver.

MAFLD was diagnosed in those with hepatic steatosis and one of the following:

• Overweight/obesity, defined by this study as a body mass index greater than or equal to 23 kg/m².
• Presence of diabetes.
• Evidence of metabolic dysregulation.

After excluding patients with insufficient data, and those with a history of liver cirrhosis, hepatectomy, or liver cancer, among others, the team included 5,011 individuals with an average age of 64 years and a mean body mass index of 24.31 kg/m². Forty percent were male.

Obesity was present in 13% of participants, whereas 15% had diabetes, 58% hypertension, and 35% metabolic syndrome.

MAFLD was diagnosed in 28% of the study population. They were older, more likely to be female with a higher education, and had a higher prevalence of preexisting metabolic disorders and worse metabolic profiles, than those without the disease.

Turning to the associations between sleep and the risk of MAFLD, the researchers say that “in contrast to previous reports, neither shorter nor longer sleep duration was found to be associated with the risk for MAFLD.”

However, after adjusting for demographics, lifestyles, medication, and preexisting metabolic comorbidities including hypertension, diabetes, and obesity, they found that the risk of MAFLD was significantly associated with late bedtime (defined as after 10 p.m.), at an odds ratio of 1.37 (P < .05).

MAFLD was also linked to snoring, at an odds ratio of 1.59, and to daytime napping for longer than 30 minutes, at an odds ratio of 1.17 (P < .05 for both).

When the team compared low-risk and high-risk sleep factors, they found that participants who had an early bedtime, slept 7-8 hours per night, never or rarely had insomnia or snoring, had infrequent daytime sleepiness, and daytime napping of half-hour or less had an odds ratio for MAFLD vs. other participants of 0.64 (P < .05).

Combining those factors into a healthy sleep score, the team found that each additional increase of healthy sleep score was associated with a fully adjusted odds ratio for MAFLD of 0.84 (P < .05).

In contrast, individuals with poor nocturnal sleep patterns and prolonged daytime napping had a higher risk for developing MAFLD, compared with those with a healthy nocturnal sleep pattern and daytime napping of half-hour or less, at an odds ratio of 2.38 (P < .05).

Further analysis indicated that individuals with a sedentary lifestyle and central obesity had a higher risk of MAFLD, but that the presence of obesity accounted for only 20.8% of the total effect of sleep quality on the risk of MAFLD.

“Taken together, our results suggests that obesity only partially mediates the effect of overall sleep quality on MAFLD,” the authors write.

“Given that large proportions of subjects suffering from poor sleep quality are underdiagnosed and undertreated, our study calls for more research into this field and strategies to improve sleep quality,” Dr. Liu said.

The study was supported by the “National Key R&D Program” of China, the Fundamental Research Funds for the Central Universities (Sun Yat-sen University), Natural Science Foundation of Guangdong Province, the Key Project of Medicine Discipline of Guangzhou, and Basic Research Project of Key Laboratory of Guangzhou.

The authors report no relevant financial relationships.

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

Sleep behaviors, both individually and combined, are associated with an increased risk of developing metabolic dysfunction–associated fatty liver disease (MAFLD), according to a Chinese analysis that suggests the effect may be independent of obesity.

Yan Liu, PhD, from the School of Public Health at Sun Yat-sen University in Guangzhou, China, and colleagues studied data on over 5,000 individuals who self-reported sleep behaviors and underwent liver ultrasound.

Late bedtimes, snoring, and prolonged daytime napping were significantly associated with MAFLD, increasing the risk by 37%, 59%, and 17%, respectively, whereas people with both poor nighttime sleep and prolonged daytime napping had the “highest risk for developing fatty liver disease,” said Dr. Liu in a press release.

In contrast, having any of six healthy sleep behaviors decreased the risk by 16% each, and even a “moderate improvement in sleep quality was related to a 29% reduction in the risk for fatty liver disease,” he added.

The research, published online in the Journal of Clinical Endocrinology & Metabolism, also indicated that obesity accounted for only one fifth of the effect of sleep quality on MAFLD risk.

Rise in unhealthy lifestyles leads to increase in MALFD

The authors write that MAFLD is the “leading chronic liver disease worldwide,” affecting around a quarter of the adult population, and may lead to end-stage liver diseases and extrahepatic complications, thus “posing a major health and economic burden.”

Moreover, the disease prevalence is “soaring at an unanticipated rate,” increasing from 18% to 29% in China over the past decade, because of a “rapid rise in unhealthy lifestyles,” the authors note.

Sleep disturbance is increasingly prevalent, “and an emerging contributor to multiple metabolic disorders,” with insomnia and habitual snoring, for example, positively correlated with hypertension, impaired glucose metabolism, and dyslipidemia, report the authors.

However, whether sleep quality, which includes “several metabolic-related sleep behaviors,” constitutes an independent risk for MAFLD “over and above” the effect of obesity remains unclear.

To investigate further, the researchers examined data from the baseline survey of the community-based, prospective South China Cohort study, which was conducted in four regions of Southern China and involved 5,430 individuals aged 30-79 years.

Between March 2018 and October 2019, the participants self-reported sleep behaviors on the Pittsburgh Sleep Quality Index questionnaire and underwent ultrasound examination of the liver.

MAFLD was diagnosed in those with hepatic steatosis and one of the following:

• Overweight/obesity, defined by this study as a body mass index greater than or equal to 23 kg/m².
• Presence of diabetes.
• Evidence of metabolic dysregulation.

After excluding patients with insufficient data, and those with a history of liver cirrhosis, hepatectomy, or liver cancer, among others, the team included 5,011 individuals with an average age of 64 years and a mean body mass index of 24.31 kg/m². Forty percent were male.

Obesity was present in 13% of participants, whereas 15% had diabetes, 58% hypertension, and 35% metabolic syndrome.

MAFLD was diagnosed in 28% of the study population. They were older, more likely to be female with a higher education, and had a higher prevalence of preexisting metabolic disorders and worse metabolic profiles, than those without the disease.

Turning to the associations between sleep and the risk of MAFLD, the researchers say that “in contrast to previous reports, neither shorter nor longer sleep duration was found to be associated with the risk for MAFLD.”

However, after adjusting for demographics, lifestyles, medication, and preexisting metabolic comorbidities including hypertension, diabetes, and obesity, they found that the risk of MAFLD was significantly associated with late bedtime (defined as after 10 p.m.), at an odds ratio of 1.37 (P < .05).

MAFLD was also linked to snoring, at an odds ratio of 1.59, and to daytime napping for longer than 30 minutes, at an odds ratio of 1.17 (P < .05 for both).

When the team compared low-risk and high-risk sleep factors, they found that participants who had an early bedtime, slept 7-8 hours per night, never or rarely had insomnia or snoring, had infrequent daytime sleepiness, and daytime napping of half-hour or less had an odds ratio for MAFLD vs. other participants of 0.64 (P < .05).

Combining those factors into a healthy sleep score, the team found that each additional increase of healthy sleep score was associated with a fully adjusted odds ratio for MAFLD of 0.84 (P < .05).

In contrast, individuals with poor nocturnal sleep patterns and prolonged daytime napping had a higher risk for developing MAFLD, compared with those with a healthy nocturnal sleep pattern and daytime napping of half-hour or less, at an odds ratio of 2.38 (P < .05).

Further analysis indicated that individuals with a sedentary lifestyle and central obesity had a higher risk of MAFLD, but that the presence of obesity accounted for only 20.8% of the total effect of sleep quality on the risk of MAFLD.

“Taken together, our results suggests that obesity only partially mediates the effect of overall sleep quality on MAFLD,” the authors write.

“Given that large proportions of subjects suffering from poor sleep quality are underdiagnosed and undertreated, our study calls for more research into this field and strategies to improve sleep quality,” Dr. Liu said.

The study was supported by the “National Key R&D Program” of China, the Fundamental Research Funds for the Central Universities (Sun Yat-sen University), Natural Science Foundation of Guangdong Province, the Key Project of Medicine Discipline of Guangzhou, and Basic Research Project of Key Laboratory of Guangzhou.

The authors report no relevant financial relationships.

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

Sleep behaviors, both individually and combined, are associated with an increased risk of developing metabolic dysfunction–associated fatty liver disease (MAFLD), according to a Chinese analysis that suggests the effect may be independent of obesity.

Yan Liu, PhD, from the School of Public Health at Sun Yat-sen University in Guangzhou, China, and colleagues studied data on over 5,000 individuals who self-reported sleep behaviors and underwent liver ultrasound.

Late bedtimes, snoring, and prolonged daytime napping were significantly associated with MAFLD, increasing the risk by 37%, 59%, and 17%, respectively, whereas people with both poor nighttime sleep and prolonged daytime napping had the “highest risk for developing fatty liver disease,” said Dr. Liu in a press release.

In contrast, having any of six healthy sleep behaviors decreased the risk by 16% each, and even a “moderate improvement in sleep quality was related to a 29% reduction in the risk for fatty liver disease,” he added.

The research, published online in the Journal of Clinical Endocrinology & Metabolism, also indicated that obesity accounted for only one fifth of the effect of sleep quality on MAFLD risk.

Rise in unhealthy lifestyles leads to increase in MALFD

The authors write that MAFLD is the “leading chronic liver disease worldwide,” affecting around a quarter of the adult population, and may lead to end-stage liver diseases and extrahepatic complications, thus “posing a major health and economic burden.”

Moreover, the disease prevalence is “soaring at an unanticipated rate,” increasing from 18% to 29% in China over the past decade, because of a “rapid rise in unhealthy lifestyles,” the authors note.

Sleep disturbance is increasingly prevalent, “and an emerging contributor to multiple metabolic disorders,” with insomnia and habitual snoring, for example, positively correlated with hypertension, impaired glucose metabolism, and dyslipidemia, report the authors.

However, whether sleep quality, which includes “several metabolic-related sleep behaviors,” constitutes an independent risk for MAFLD “over and above” the effect of obesity remains unclear.

To investigate further, the researchers examined data from the baseline survey of the community-based, prospective South China Cohort study, which was conducted in four regions of Southern China and involved 5,430 individuals aged 30-79 years.

Between March 2018 and October 2019, the participants self-reported sleep behaviors on the Pittsburgh Sleep Quality Index questionnaire and underwent ultrasound examination of the liver.

MAFLD was diagnosed in those with hepatic steatosis and one of the following:

• Overweight/obesity, defined by this study as a body mass index greater than or equal to 23 kg/m².
• Presence of diabetes.
• Evidence of metabolic dysregulation.

After excluding patients with insufficient data, and those with a history of liver cirrhosis, hepatectomy, or liver cancer, among others, the team included 5,011 individuals with an average age of 64 years and a mean body mass index of 24.31 kg/m². Forty percent were male.

Obesity was present in 13% of participants, whereas 15% had diabetes, 58% hypertension, and 35% metabolic syndrome.

MAFLD was diagnosed in 28% of the study population. They were older, more likely to be female with a higher education, and had a higher prevalence of preexisting metabolic disorders and worse metabolic profiles, than those without the disease.

Turning to the associations between sleep and the risk of MAFLD, the researchers say that “in contrast to previous reports, neither shorter nor longer sleep duration was found to be associated with the risk for MAFLD.”

However, after adjusting for demographics, lifestyles, medication, and preexisting metabolic comorbidities including hypertension, diabetes, and obesity, they found that the risk of MAFLD was significantly associated with late bedtime (defined as after 10 p.m.), at an odds ratio of 1.37 (P < .05).

MAFLD was also linked to snoring, at an odds ratio of 1.59, and to daytime napping for longer than 30 minutes, at an odds ratio of 1.17 (P < .05 for both).

When the team compared low-risk and high-risk sleep factors, they found that participants who had an early bedtime, slept 7-8 hours per night, never or rarely had insomnia or snoring, had infrequent daytime sleepiness, and daytime napping of half-hour or less had an odds ratio for MAFLD vs. other participants of 0.64 (P < .05).

Combining those factors into a healthy sleep score, the team found that each additional increase of healthy sleep score was associated with a fully adjusted odds ratio for MAFLD of 0.84 (P < .05).

In contrast, individuals with poor nocturnal sleep patterns and prolonged daytime napping had a higher risk for developing MAFLD, compared with those with a healthy nocturnal sleep pattern and daytime napping of half-hour or less, at an odds ratio of 2.38 (P < .05).

Further analysis indicated that individuals with a sedentary lifestyle and central obesity had a higher risk of MAFLD, but that the presence of obesity accounted for only 20.8% of the total effect of sleep quality on the risk of MAFLD.

“Taken together, our results suggests that obesity only partially mediates the effect of overall sleep quality on MAFLD,” the authors write.

“Given that large proportions of subjects suffering from poor sleep quality are underdiagnosed and undertreated, our study calls for more research into this field and strategies to improve sleep quality,” Dr. Liu said.

The study was supported by the “National Key R&D Program” of China, the Fundamental Research Funds for the Central Universities (Sun Yat-sen University), Natural Science Foundation of Guangdong Province, the Key Project of Medicine Discipline of Guangzhou, and Basic Research Project of Key Laboratory of Guangzhou.

The authors report no relevant financial relationships.

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

In a case-control study, atherosclerotic risk factors were uncommon in childhood and did not appear to be associated with the pathogenesis of arterial ischemic stroke in children or in early young adulthood.

But by the fourth and fifth decades of life, these risk factors were strongly associated with a significant risk for stroke, heightening that risk almost tenfold.

“While strokes in childhood and very early adulthood are not likely caused by atherosclerotic risk factors, it does look like these risk factors increase throughout early and young adulthood and become significant risk factors for stroke in the 30s and 40s,” lead author Sharon N. Poisson, MD, MAS, associate professor of neurology at the University of Colorado at Denver, Aurora, said in an interview.

The findings were published online in JAMA Neurology.

In this study, the researchers focused on arterial ischemic stroke, not hemorrhagic stroke. “We know that high blood pressure, diabetes, smoking, obesity, all of these are risk factors for ischemic stroke, but what we didn’t know is at what age do those atherosclerotic risk factors actually start to cause stroke,” Dr. Poisson said.

To find out more, she and her team did a case control study of data in the Kaiser Permanente Northern California system, which had been accumulating relevant data over a period of 14 years, from Jan. 1, 2000, through Dec. 31, 2014.

The analysis included 141 children and 455 young adults with arterial ischemic stroke and 1,382 age-matched controls.

The children were divided into two age categories: ages 29 days to 9 years and ages 10-19 years.

In the younger group, there were 69 cases of arterial ischemic stroke. In the older age group, there were 72 cases.

Young adults were divided into three age categories: 20-29 years (n = 71 cases), 30-39 years (144 cases), and 40-49 years (240 cases).

Among pediatric controls, 168 children aged 29 days to 9 years (46.5%) and 196 children aged 10-19 years (53.8%) developed arterial ischemic stroke.

There were 121 cases of ischemic stroke among young adult controls aged 20-29 years, 298 cases among controls aged 30-39 years, and 599 cases in those aged 40-49 years.

Both childhood cases and controls had a low prevalence of documented diagnoses of atherosclerotic risk factors (ARFs). The odds ratio of having any ARFs on arterial ischemic stroke was 1.87 for ages 0-9 years, and 1.00 for ages 10-19.

However, cases rose with age.

The OR was 2.3 for age range 20-29 years, 3.57 for age range 30-39 years, and 4.91 for age range 40-49 years.

The analysis also showed that the OR associated with multiple ARFs was 5.29 for age range 0-9 years, 2.75 for age range 10-19 years, 7.33 for age range 20-29 years, 9.86 for age range 30-39 years, and 9.35 for age range 40-49 years.

Multiple risk factors were rare in children but became more prevalent with each decade of young adult life.

The presumed cause of arterial ischemic stroke was atherosclerosis. Evidence of atherosclerosis was present in 1.4% of those aged 10-19 years, 8.5% of those aged 20-29 years, 21.5% of those aged 30-39 years, and 42.5% of those aged 40-49 years.

“This study tells us that, while stroke in adolescence and very early adulthood may not be caused by atherosclerotic risk factors, starting to accumulate those risk factors early in life clearly increases the risk of stroke in the 30s and 40s. I hope we can get this message across, because the sooner we can treat the risk factors, the better the outcome,” Dr. Poisson said.
 

Prevention starts in childhood

Prevention of cardiovascular disease begins in childhood, which is a paradigm shift from the way cardiovascular disease was thought of a couple of decades ago, noted pediatric cardiologist Guilherme Baptista de Faia, MD, from the Ann & Robert H. Lurie Children’s Hospital in Chicago.

“Our guidelines for risk factor reduction in children aim to address how or when do we screen for these risk factors, how or when do we intervene, and do these interventions impact cardiovascular outcomes later in life? This article is part of the mounting research that aims to understand the relationship between childhood cardiovascular risk factors and early cardiovascular disease,” Dr. Baptista de Faia said.

“There has been an interesting progression in our understanding of the impact of CV risk factors early in life. Large cohorts such as Bogalusa Heart Study, Risk in Young Finns Study, Muscatine Study, the Childhood Determinants of Adult Health, CARDIA, and the International Childhood Cardiovascular Cohorts (i3C) have been instrumental in evaluating this question,” he said.

The knowledge that atherosclerotic risk factors in children can lead to acceleration of atherosclerosis in later life opens the door to preventive medicine, said Dr. Baptista de Faia, who was not part of the study.

“This is where preventive medicine comes in. If we can identify the children at increased risk, can we intervene to improve outcomes later in life?” he said. Familial hypercholesterolemia is “a great example of this. We can screen children early in life, there is an effective treatment, and we know from populations studies that early treatment significantly decreases the risk for cardiovascular disease later in life.”

Dr. Poisson reported that she received grants from the National Institutes of Health during the conduct of this study, which was supported by the NIH.

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

In a case-control study, atherosclerotic risk factors were uncommon in childhood and did not appear to be associated with the pathogenesis of arterial ischemic stroke in children or in early young adulthood.

But by the fourth and fifth decades of life, these risk factors were strongly associated with a significant risk for stroke, heightening that risk almost tenfold.

“While strokes in childhood and very early adulthood are not likely caused by atherosclerotic risk factors, it does look like these risk factors increase throughout early and young adulthood and become significant risk factors for stroke in the 30s and 40s,” lead author Sharon N. Poisson, MD, MAS, associate professor of neurology at the University of Colorado at Denver, Aurora, said in an interview.

The findings were published online in JAMA Neurology.

In this study, the researchers focused on arterial ischemic stroke, not hemorrhagic stroke. “We know that high blood pressure, diabetes, smoking, obesity, all of these are risk factors for ischemic stroke, but what we didn’t know is at what age do those atherosclerotic risk factors actually start to cause stroke,” Dr. Poisson said.

To find out more, she and her team did a case control study of data in the Kaiser Permanente Northern California system, which had been accumulating relevant data over a period of 14 years, from Jan. 1, 2000, through Dec. 31, 2014.

The analysis included 141 children and 455 young adults with arterial ischemic stroke and 1,382 age-matched controls.

The children were divided into two age categories: ages 29 days to 9 years and ages 10-19 years.

In the younger group, there were 69 cases of arterial ischemic stroke. In the older age group, there were 72 cases.

Young adults were divided into three age categories: 20-29 years (n = 71 cases), 30-39 years (144 cases), and 40-49 years (240 cases).

Among pediatric controls, 168 children aged 29 days to 9 years (46.5%) and 196 children aged 10-19 years (53.8%) developed arterial ischemic stroke.

There were 121 cases of ischemic stroke among young adult controls aged 20-29 years, 298 cases among controls aged 30-39 years, and 599 cases in those aged 40-49 years.

Both childhood cases and controls had a low prevalence of documented diagnoses of atherosclerotic risk factors (ARFs). The odds ratio of having any ARFs on arterial ischemic stroke was 1.87 for ages 0-9 years, and 1.00 for ages 10-19.

However, cases rose with age.

The OR was 2.3 for age range 20-29 years, 3.57 for age range 30-39 years, and 4.91 for age range 40-49 years.

The analysis also showed that the OR associated with multiple ARFs was 5.29 for age range 0-9 years, 2.75 for age range 10-19 years, 7.33 for age range 20-29 years, 9.86 for age range 30-39 years, and 9.35 for age range 40-49 years.

Multiple risk factors were rare in children but became more prevalent with each decade of young adult life.

The presumed cause of arterial ischemic stroke was atherosclerosis. Evidence of atherosclerosis was present in 1.4% of those aged 10-19 years, 8.5% of those aged 20-29 years, 21.5% of those aged 30-39 years, and 42.5% of those aged 40-49 years.

“This study tells us that, while stroke in adolescence and very early adulthood may not be caused by atherosclerotic risk factors, starting to accumulate those risk factors early in life clearly increases the risk of stroke in the 30s and 40s. I hope we can get this message across, because the sooner we can treat the risk factors, the better the outcome,” Dr. Poisson said.
 

Prevention starts in childhood

Prevention of cardiovascular disease begins in childhood, which is a paradigm shift from the way cardiovascular disease was thought of a couple of decades ago, noted pediatric cardiologist Guilherme Baptista de Faia, MD, from the Ann & Robert H. Lurie Children’s Hospital in Chicago.

“Our guidelines for risk factor reduction in children aim to address how or when do we screen for these risk factors, how or when do we intervene, and do these interventions impact cardiovascular outcomes later in life? This article is part of the mounting research that aims to understand the relationship between childhood cardiovascular risk factors and early cardiovascular disease,” Dr. Baptista de Faia said.

“There has been an interesting progression in our understanding of the impact of CV risk factors early in life. Large cohorts such as Bogalusa Heart Study, Risk in Young Finns Study, Muscatine Study, the Childhood Determinants of Adult Health, CARDIA, and the International Childhood Cardiovascular Cohorts (i3C) have been instrumental in evaluating this question,” he said.

The knowledge that atherosclerotic risk factors in children can lead to acceleration of atherosclerosis in later life opens the door to preventive medicine, said Dr. Baptista de Faia, who was not part of the study.

“This is where preventive medicine comes in. If we can identify the children at increased risk, can we intervene to improve outcomes later in life?” he said. Familial hypercholesterolemia is “a great example of this. We can screen children early in life, there is an effective treatment, and we know from populations studies that early treatment significantly decreases the risk for cardiovascular disease later in life.”

Dr. Poisson reported that she received grants from the National Institutes of Health during the conduct of this study, which was supported by the NIH.

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

In a case-control study, atherosclerotic risk factors were uncommon in childhood and did not appear to be associated with the pathogenesis of arterial ischemic stroke in children or in early young adulthood.

But by the fourth and fifth decades of life, these risk factors were strongly associated with a significant risk for stroke, heightening that risk almost tenfold.

“While strokes in childhood and very early adulthood are not likely caused by atherosclerotic risk factors, it does look like these risk factors increase throughout early and young adulthood and become significant risk factors for stroke in the 30s and 40s,” lead author Sharon N. Poisson, MD, MAS, associate professor of neurology at the University of Colorado at Denver, Aurora, said in an interview.

The findings were published online in JAMA Neurology.

In this study, the researchers focused on arterial ischemic stroke, not hemorrhagic stroke. “We know that high blood pressure, diabetes, smoking, obesity, all of these are risk factors for ischemic stroke, but what we didn’t know is at what age do those atherosclerotic risk factors actually start to cause stroke,” Dr. Poisson said.

To find out more, she and her team did a case control study of data in the Kaiser Permanente Northern California system, which had been accumulating relevant data over a period of 14 years, from Jan. 1, 2000, through Dec. 31, 2014.

The analysis included 141 children and 455 young adults with arterial ischemic stroke and 1,382 age-matched controls.

The children were divided into two age categories: ages 29 days to 9 years and ages 10-19 years.

In the younger group, there were 69 cases of arterial ischemic stroke. In the older age group, there were 72 cases.

Young adults were divided into three age categories: 20-29 years (n = 71 cases), 30-39 years (144 cases), and 40-49 years (240 cases).

Among pediatric controls, 168 children aged 29 days to 9 years (46.5%) and 196 children aged 10-19 years (53.8%) developed arterial ischemic stroke.

There were 121 cases of ischemic stroke among young adult controls aged 20-29 years, 298 cases among controls aged 30-39 years, and 599 cases in those aged 40-49 years.

Both childhood cases and controls had a low prevalence of documented diagnoses of atherosclerotic risk factors (ARFs). The odds ratio of having any ARFs on arterial ischemic stroke was 1.87 for ages 0-9 years, and 1.00 for ages 10-19.

However, cases rose with age.

The OR was 2.3 for age range 20-29 years, 3.57 for age range 30-39 years, and 4.91 for age range 40-49 years.

The analysis also showed that the OR associated with multiple ARFs was 5.29 for age range 0-9 years, 2.75 for age range 10-19 years, 7.33 for age range 20-29 years, 9.86 for age range 30-39 years, and 9.35 for age range 40-49 years.

Multiple risk factors were rare in children but became more prevalent with each decade of young adult life.

The presumed cause of arterial ischemic stroke was atherosclerosis. Evidence of atherosclerosis was present in 1.4% of those aged 10-19 years, 8.5% of those aged 20-29 years, 21.5% of those aged 30-39 years, and 42.5% of those aged 40-49 years.

“This study tells us that, while stroke in adolescence and very early adulthood may not be caused by atherosclerotic risk factors, starting to accumulate those risk factors early in life clearly increases the risk of stroke in the 30s and 40s. I hope we can get this message across, because the sooner we can treat the risk factors, the better the outcome,” Dr. Poisson said.
 

Prevention starts in childhood

Prevention of cardiovascular disease begins in childhood, which is a paradigm shift from the way cardiovascular disease was thought of a couple of decades ago, noted pediatric cardiologist Guilherme Baptista de Faia, MD, from the Ann & Robert H. Lurie Children’s Hospital in Chicago.

“Our guidelines for risk factor reduction in children aim to address how or when do we screen for these risk factors, how or when do we intervene, and do these interventions impact cardiovascular outcomes later in life? This article is part of the mounting research that aims to understand the relationship between childhood cardiovascular risk factors and early cardiovascular disease,” Dr. Baptista de Faia said.

“There has been an interesting progression in our understanding of the impact of CV risk factors early in life. Large cohorts such as Bogalusa Heart Study, Risk in Young Finns Study, Muscatine Study, the Childhood Determinants of Adult Health, CARDIA, and the International Childhood Cardiovascular Cohorts (i3C) have been instrumental in evaluating this question,” he said.

The knowledge that atherosclerotic risk factors in children can lead to acceleration of atherosclerosis in later life opens the door to preventive medicine, said Dr. Baptista de Faia, who was not part of the study.

“This is where preventive medicine comes in. If we can identify the children at increased risk, can we intervene to improve outcomes later in life?” he said. Familial hypercholesterolemia is “a great example of this. We can screen children early in life, there is an effective treatment, and we know from populations studies that early treatment significantly decreases the risk for cardiovascular disease later in life.”

Dr. Poisson reported that she received grants from the National Institutes of Health during the conduct of this study, which was supported by the NIH.

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