Commentary

In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?

Researchers from the German Cancer Research Center (DKFZ) suspect that such zoonoses are possibly widespread and are therefore recommending that infants not be given dairy products until they are at least age 1 year. However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.

In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.

Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
 

Acid radicals

However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.

According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
 

Viral progeny

In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.

The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
 

‘Breast milk is healthy’

Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.

The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
 

Colon cancer

To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.

The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
 

Institutional skepticism

When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?

The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.

BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.

Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
 

Association with MS?

Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”

However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.

Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?

Researchers from the German Cancer Research Center (DKFZ) suspect that such zoonoses are possibly widespread and are therefore recommending that infants not be given dairy products until they are at least age 1 year. However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.

In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.

Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
 

Acid radicals

However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.

According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
 

Viral progeny

In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.

The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
 

‘Breast milk is healthy’

Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.

The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
 

Colon cancer

To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.

The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
 

Institutional skepticism

When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?

The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.

BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.

Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
 

Association with MS?

Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”

However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.

Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?

Researchers from the German Cancer Research Center (DKFZ) suspect that such zoonoses are possibly widespread and are therefore recommending that infants not be given dairy products until they are at least age 1 year. However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.

In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.

Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
 

Acid radicals

However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.

According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
 

Viral progeny

In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.

The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
 

‘Breast milk is healthy’

Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.

The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
 

Colon cancer

To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.

The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
 

Institutional skepticism

When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?

The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.

BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.

Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
 

Association with MS?

Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”

However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.

Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

One morning I stepped into the elevator in the lobby of the US Department of Veterans Affairs (VA) medical center where I work, holding a cup of coffee, joining another staffer, a middle-aged man, wearing a veteran’s pin on his employee badge. An older veteran slowly approached the elevator doors, shuffling with each step, and since he was at the front of the elevator, he cheerfully bellowed “Which floor?” as he offered to push the button for us.

“What’s on 12?” he asked in a jovial voice. I smiled. “Aging research,” referring to the Geriatrics Research Education and Clinical Center where I work.¹

“I definitely need that—I forgot where I’m going!” he joked, his fingers hovering over the elevator buttons.

As we reached his floor, the doors opened, he waved with a smile and unsteadily made his way out of the elevator and down the hall to his appointment. As the elevator doors closed behind him, the other staffer turned to me and said with a shrug, “That’ll be me one day,” as he got off at the next floor.

When I got off the elevator and walked toward my office, I reflected on the care that I as a geriatrician and we at the VA hope to provide to aging veterans, now and in the future: Age-Friendly care. Age-Friendly means the compassionate care that we want for those who have served our country, for our loved ones, and for ourselves as we age. Age-Friendly means person-centered, evidence-based care that as we grow older will help us to address challenges that may come with older age, such as falls, cognitive impairment, and polypharmacy. Too often the health care system remains focused on the chief concern or on a clinician’s specialty and may not focus on those important areas where we can potentially intervene to support aging veterans.

The VA has set a goal to become the largest Age-Friendly Health System (AFHS) in the country.² Led by the Institute for Healthcare Improvement and funded by the John A. Hartford Foundation, the Age-Friendly Health Systems Initiative aims to help clinicians and care settings “follow an essential set of evidence-based practices; cause no harm; and align with what matters to the older adult and their family caregivers.”³ An AFHS cares for older adults with attention to the 4Ms—What Matters, Mobility, Mentation, and Medications.⁴ Specifically, in an AFHS, older adults are asked what matters to them so we can align their health care with their goals; clinicians evaluate veterans for safe mobility and fall risk reduction, cognitive impairment and mood disorders, and identify and avoid high-risk medications.⁵ In an AFHS, the 4Ms are practiced as a set, reliably, across settings, so that there should be no wrong door or wrong floor for an older veteran to receive Age-Friendly care within the VA health care system.⁶

Too often our health care system and health professions education have left clinicians unprepared to care for older adults using an Age-Friendly framework; rather, we have been trained in problem-based or disease-based care that can miss the forest for the trees in an older adult living with multiple chronic conditions and/or frailty. We may focus on providing evidence-based care for individual medical conditions while neglecting the often practical interventions that can help an older person age in place by focusing on what matters, supporting safe mobility, addressing cognition and mood, and optimizing medications.¹⁸

The vision of the VA as the largest AFHS in America is urgently needed; nearly half of the veteran population is aged 65 ≥ years, compared with 16% of the general population.¹⁹ Building on the VA’s legacy of creativity and innovation in geriatrics, and the VA’s goal of being a high reliability organization, becoming an AFHS will ensure that for that older veteran stepping off that elevator there is no wrong floor, and no wrong door to receive the Age-Friendly care he deserves and that we all hope for as we age.^1,5,19,20

Acknowledgments

This material is the result of work supported with resources and the use of facilities at the Veterans Affairs Boston Healthcare System and the New England Geriatric Research Education and Clinical Center. 

One morning I stepped into the elevator in the lobby of the US Department of Veterans Affairs (VA) medical center where I work, holding a cup of coffee, joining another staffer, a middle-aged man, wearing a veteran’s pin on his employee badge. An older veteran slowly approached the elevator doors, shuffling with each step, and since he was at the front of the elevator, he cheerfully bellowed “Which floor?” as he offered to push the button for us.

“What’s on 12?” he asked in a jovial voice. I smiled. “Aging research,” referring to the Geriatrics Research Education and Clinical Center where I work.¹

“I definitely need that—I forgot where I’m going!” he joked, his fingers hovering over the elevator buttons.

As we reached his floor, the doors opened, he waved with a smile and unsteadily made his way out of the elevator and down the hall to his appointment. As the elevator doors closed behind him, the other staffer turned to me and said with a shrug, “That’ll be me one day,” as he got off at the next floor.

When I got off the elevator and walked toward my office, I reflected on the care that I as a geriatrician and we at the VA hope to provide to aging veterans, now and in the future: Age-Friendly care. Age-Friendly means the compassionate care that we want for those who have served our country, for our loved ones, and for ourselves as we age. Age-Friendly means person-centered, evidence-based care that as we grow older will help us to address challenges that may come with older age, such as falls, cognitive impairment, and polypharmacy. Too often the health care system remains focused on the chief concern or on a clinician’s specialty and may not focus on those important areas where we can potentially intervene to support aging veterans.

The VA has set a goal to become the largest Age-Friendly Health System (AFHS) in the country.² Led by the Institute for Healthcare Improvement and funded by the John A. Hartford Foundation, the Age-Friendly Health Systems Initiative aims to help clinicians and care settings “follow an essential set of evidence-based practices; cause no harm; and align with what matters to the older adult and their family caregivers.”³ An AFHS cares for older adults with attention to the 4Ms—What Matters, Mobility, Mentation, and Medications.⁴ Specifically, in an AFHS, older adults are asked what matters to them so we can align their health care with their goals; clinicians evaluate veterans for safe mobility and fall risk reduction, cognitive impairment and mood disorders, and identify and avoid high-risk medications.⁵ In an AFHS, the 4Ms are practiced as a set, reliably, across settings, so that there should be no wrong door or wrong floor for an older veteran to receive Age-Friendly care within the VA health care system.⁶

Too often our health care system and health professions education have left clinicians unprepared to care for older adults using an Age-Friendly framework; rather, we have been trained in problem-based or disease-based care that can miss the forest for the trees in an older adult living with multiple chronic conditions and/or frailty. We may focus on providing evidence-based care for individual medical conditions while neglecting the often practical interventions that can help an older person age in place by focusing on what matters, supporting safe mobility, addressing cognition and mood, and optimizing medications.¹⁸

The vision of the VA as the largest AFHS in America is urgently needed; nearly half of the veteran population is aged 65 ≥ years, compared with 16% of the general population.¹⁹ Building on the VA’s legacy of creativity and innovation in geriatrics, and the VA’s goal of being a high reliability organization, becoming an AFHS will ensure that for that older veteran stepping off that elevator there is no wrong floor, and no wrong door to receive the Age-Friendly care he deserves and that we all hope for as we age.^1,5,19,20

Acknowledgments

This material is the result of work supported with resources and the use of facilities at the Veterans Affairs Boston Healthcare System and the New England Geriatric Research Education and Clinical Center. 

One morning I stepped into the elevator in the lobby of the US Department of Veterans Affairs (VA) medical center where I work, holding a cup of coffee, joining another staffer, a middle-aged man, wearing a veteran’s pin on his employee badge. An older veteran slowly approached the elevator doors, shuffling with each step, and since he was at the front of the elevator, he cheerfully bellowed “Which floor?” as he offered to push the button for us.

“What’s on 12?” he asked in a jovial voice. I smiled. “Aging research,” referring to the Geriatrics Research Education and Clinical Center where I work.¹

“I definitely need that—I forgot where I’m going!” he joked, his fingers hovering over the elevator buttons.

As we reached his floor, the doors opened, he waved with a smile and unsteadily made his way out of the elevator and down the hall to his appointment. As the elevator doors closed behind him, the other staffer turned to me and said with a shrug, “That’ll be me one day,” as he got off at the next floor.

When I got off the elevator and walked toward my office, I reflected on the care that I as a geriatrician and we at the VA hope to provide to aging veterans, now and in the future: Age-Friendly care. Age-Friendly means the compassionate care that we want for those who have served our country, for our loved ones, and for ourselves as we age. Age-Friendly means person-centered, evidence-based care that as we grow older will help us to address challenges that may come with older age, such as falls, cognitive impairment, and polypharmacy. Too often the health care system remains focused on the chief concern or on a clinician’s specialty and may not focus on those important areas where we can potentially intervene to support aging veterans.

The VA has set a goal to become the largest Age-Friendly Health System (AFHS) in the country.² Led by the Institute for Healthcare Improvement and funded by the John A. Hartford Foundation, the Age-Friendly Health Systems Initiative aims to help clinicians and care settings “follow an essential set of evidence-based practices; cause no harm; and align with what matters to the older adult and their family caregivers.”³ An AFHS cares for older adults with attention to the 4Ms—What Matters, Mobility, Mentation, and Medications.⁴ Specifically, in an AFHS, older adults are asked what matters to them so we can align their health care with their goals; clinicians evaluate veterans for safe mobility and fall risk reduction, cognitive impairment and mood disorders, and identify and avoid high-risk medications.⁵ In an AFHS, the 4Ms are practiced as a set, reliably, across settings, so that there should be no wrong door or wrong floor for an older veteran to receive Age-Friendly care within the VA health care system.⁶

Too often our health care system and health professions education have left clinicians unprepared to care for older adults using an Age-Friendly framework; rather, we have been trained in problem-based or disease-based care that can miss the forest for the trees in an older adult living with multiple chronic conditions and/or frailty. We may focus on providing evidence-based care for individual medical conditions while neglecting the often practical interventions that can help an older person age in place by focusing on what matters, supporting safe mobility, addressing cognition and mood, and optimizing medications.¹⁸

The vision of the VA as the largest AFHS in America is urgently needed; nearly half of the veteran population is aged 65 ≥ years, compared with 16% of the general population.¹⁹ Building on the VA’s legacy of creativity and innovation in geriatrics, and the VA’s goal of being a high reliability organization, becoming an AFHS will ensure that for that older veteran stepping off that elevator there is no wrong floor, and no wrong door to receive the Age-Friendly care he deserves and that we all hope for as we age.^1,5,19,20

Acknowledgments

This material is the result of work supported with resources and the use of facilities at the Veterans Affairs Boston Healthcare System and the New England Geriatric Research Education and Clinical Center. 

It’s Oscars weekend, so for the second annual Meddy Awards – a very self-congratulatory and very tongue-in-cheek version of the Oscars – we celebrate outstanding medical performances and events in motion pictures throughout history. Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...

Best depiction of emergency medicine’s rollercoaster

M*A*S*H (1970)

The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.

Best ‘is there a doctor in the house?’ moment

Field of Dreams (1989)

When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.

Most unethical doctor

Elvis (2022)

No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”

Best self-use of a defibrillator

Casino Royale (2006)

We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.

Best worst patient lying about an injury

Tár (2022)

Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.

Best therapy for a speech disorder

The King’s Speech (2010)

Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”

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

It’s Oscars weekend, so for the second annual Meddy Awards – a very self-congratulatory and very tongue-in-cheek version of the Oscars – we celebrate outstanding medical performances and events in motion pictures throughout history. Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...

Best depiction of emergency medicine’s rollercoaster

M*A*S*H (1970)

The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.

Best ‘is there a doctor in the house?’ moment

Field of Dreams (1989)

When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.

Most unethical doctor

Elvis (2022)

No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”

Best self-use of a defibrillator

Casino Royale (2006)

We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.

Best worst patient lying about an injury

Tár (2022)

Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.

Best therapy for a speech disorder

The King’s Speech (2010)

Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”

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

It’s Oscars weekend, so for the second annual Meddy Awards – a very self-congratulatory and very tongue-in-cheek version of the Oscars – we celebrate outstanding medical performances and events in motion pictures throughout history. Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...

Best depiction of emergency medicine’s rollercoaster

M*A*S*H (1970)

The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.

Best ‘is there a doctor in the house?’ moment

Field of Dreams (1989)

When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.

Most unethical doctor

Elvis (2022)

No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”

Best self-use of a defibrillator

Casino Royale (2006)

We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.

Best worst patient lying about an injury

Tár (2022)

Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.

Best therapy for a speech disorder

The King’s Speech (2010)

Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”

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

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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

In this issue, Regn and colleagues (page 78) have provided a concise resource for primary care professionals (PCPs) on a lesser known sleep disorder that is increasingly common in veterans.¹ Their review provides a basic understanding of central sleep apnea (CSA) and a systematic clinical approach to diagnosis and treatment in primary care. We applaud the authors for providing education on sleep disorders to the Federal Practitioner audience, since sleep disorders are prevalent among military service members and veterans, with significant implications for health, wellness, productivity, and cost. The American workforce has a long-held sense of pride in working hard, often at the expense of sleep. Early work start times are common in the military and federal government, and sleep medicine specialists have the expertise necessary to diagnose and treat the myriad of sleep disorders that have come to light recently. A massive shortage of sleep medicine specialists limits the evidence-based sleep treatment implementations in medical care.

Medicine has become increasingly complex, necessitating a highly connected web of people, resources, institutions, and processes to keep up with the demands of growing information and technology. The evolution of a systems approach to health care built momentum during the 21st century.1-3 The National Academy of Medicine has published 2 reports that raised concerns about the quality and safety of medical care.4,5 With this expansion, the potential for medical errors at individual components or relationship nodes between actors in the medical system also has grown. Medical errors encompass more than acts of commission and can also take the form of acts of omission by failing to diagnosis and appropriately treat before long-term or irrevocable health consequences occur. A systems approach seeks to aid clinical decision making to improve the quality of medical care and patient outcomes in an otherwise complex medical system that can be difficult to navigate.

Although awareness of obstructive sleep apnea (OSA) has increased, CSA has not received the same level of attention and may not be recognized by PCPs. A lack of education about CSA can contribute to acts of omission in a health care setting. Although CSA is ultimately diagnosed and managed in specialty care sleep medicine clinics, PCPs play an instrumental role in referring patients for evaluation and then collaborating with specialists to optimize care and outcomes. The multidisciplinary approach of CSA management is important because it overlaps with many conditions that are commonly seen in primary care, including obesity, chronic pain, congestive heart failure (CHF), chronic kidney disease, and hypothyroidism. These chronic conditions are also prevalent among veterans. In a national cross-sectional study, veterans had higher prevalence rates of chronic health conditions, including cardiovascular disease and kidney disease, compared with nonveterans (odds ratios, 1.4 and 1.2, respectively).⁶

It is important to understand the relationship between CSA and chronic medical conditions because recognizing the signs of CSA can lead to identification of underlying medical conditions. Likewise, the chronic medical conditions that lead to CSA may cue the PCP’s clinical suspicion for CSA and lead to specialty care referrals if needed. The clinician also serves a significant role in the management of CSA by optimizing medical care for the underlying condition prior to pursuing additional specialty care treatments like positive airway pressure (PAP). For example, PCPs are often involved in the management of atrial fibrillation and cardiac dysfunction, which can minimize or exacerbate CSA. PCPs should also be aware of which drugs are associated with the presentation of CSA as withdrawal or reduction of the medication can resolve symptoms without further evaluation by a specialist.

The review by Regn and colleagues updates readers on developments—and lack thereof—in the literature. Treatment options for CSA have been limited. For most patients, continuous PAP (CPAP), which is the gold standard treatment for OSA, is not an effective CSA treatment. Earlier specialty guidelines endorsed adaptive servo-ventilation (ASV), a more sophisticated respiratory assist device, for treating CSA. In 2015, the SERVE-HF trial examined the effects of ASV in combination with guideline-based medical treatment on survival and cardiovascular outcomes for patients who had CSA and HF with reduced ejection fraction.⁷ They found that ASV had no significant effect on the primary endpoints of first event of death from any cause, lifesaving cardiovascular intervention, or unplanned hospitalization for worsening HF. However, all-cause and cardiovascular mortality were both increased with ASV. There has not been a more recent large clinical trial that either refutes or reinforces those findings (ADVENT-HF found that ASV effectively treated CSA and OSA in patients with CHF but had no impact on the primary endpoint of mortality).^7,8 We are unlikely to see more studies soon that will put this issue to rest and change the guidance that is currently available for ASV use.

Regn and colleagues also provide an update on the use of acetazolamide as to assist in CSA treatment. This should be done cautiously and potentially deferred to subspecialists in sleep medicine, cardiology, or nephrology. The theoretical benefit of acetazolamide in CSA is based on its promotion of excretion of sodium bicarbonate, leading to metabolic acidosis, which can stimulate central respiratory drive. Since CSA is characterized by episodic loss of central respiratory drive, it seems logical that a respiratory stimulant would provide benefit. However, acetazolamide is not approved by the US Food and Drug Administration for CSA.⁹ In those with impaired respiratory mechanics, CHF, chronic obstructive pulmonary disease, and obesity hypoventilation syndrome, this medication has the potential for harm by adding metabolic acidosis to a patient with concurrent respiratory acidosis or respiratory constraints that limit their ability to compensate effectively for additional acid-base derangements.

It is worth noting that Regn and colleagues do not make claims outside the intended scope. It accomplishes the mission of providing all PCPs with an updated streamlined summary for diagnosing and treating CSA. Such tools are important in an age of growing medical information technology because it can improve the quality of medical care and ultimately, patient outcomes with timely diagnosis and treatment. This is particularly significant in a veteran population with a high burden of chronic medical conditions and polypharmacy.

In this issue, Regn and colleagues (page 78) have provided a concise resource for primary care professionals (PCPs) on a lesser known sleep disorder that is increasingly common in veterans.¹ Their review provides a basic understanding of central sleep apnea (CSA) and a systematic clinical approach to diagnosis and treatment in primary care. We applaud the authors for providing education on sleep disorders to the Federal Practitioner audience, since sleep disorders are prevalent among military service members and veterans, with significant implications for health, wellness, productivity, and cost. The American workforce has a long-held sense of pride in working hard, often at the expense of sleep. Early work start times are common in the military and federal government, and sleep medicine specialists have the expertise necessary to diagnose and treat the myriad of sleep disorders that have come to light recently. A massive shortage of sleep medicine specialists limits the evidence-based sleep treatment implementations in medical care.

Medicine has become increasingly complex, necessitating a highly connected web of people, resources, institutions, and processes to keep up with the demands of growing information and technology. The evolution of a systems approach to health care built momentum during the 21st century.1-3 The National Academy of Medicine has published 2 reports that raised concerns about the quality and safety of medical care.4,5 With this expansion, the potential for medical errors at individual components or relationship nodes between actors in the medical system also has grown. Medical errors encompass more than acts of commission and can also take the form of acts of omission by failing to diagnosis and appropriately treat before long-term or irrevocable health consequences occur. A systems approach seeks to aid clinical decision making to improve the quality of medical care and patient outcomes in an otherwise complex medical system that can be difficult to navigate.

Although awareness of obstructive sleep apnea (OSA) has increased, CSA has not received the same level of attention and may not be recognized by PCPs. A lack of education about CSA can contribute to acts of omission in a health care setting. Although CSA is ultimately diagnosed and managed in specialty care sleep medicine clinics, PCPs play an instrumental role in referring patients for evaluation and then collaborating with specialists to optimize care and outcomes. The multidisciplinary approach of CSA management is important because it overlaps with many conditions that are commonly seen in primary care, including obesity, chronic pain, congestive heart failure (CHF), chronic kidney disease, and hypothyroidism. These chronic conditions are also prevalent among veterans. In a national cross-sectional study, veterans had higher prevalence rates of chronic health conditions, including cardiovascular disease and kidney disease, compared with nonveterans (odds ratios, 1.4 and 1.2, respectively).⁶

It is important to understand the relationship between CSA and chronic medical conditions because recognizing the signs of CSA can lead to identification of underlying medical conditions. Likewise, the chronic medical conditions that lead to CSA may cue the PCP’s clinical suspicion for CSA and lead to specialty care referrals if needed. The clinician also serves a significant role in the management of CSA by optimizing medical care for the underlying condition prior to pursuing additional specialty care treatments like positive airway pressure (PAP). For example, PCPs are often involved in the management of atrial fibrillation and cardiac dysfunction, which can minimize or exacerbate CSA. PCPs should also be aware of which drugs are associated with the presentation of CSA as withdrawal or reduction of the medication can resolve symptoms without further evaluation by a specialist.

The review by Regn and colleagues updates readers on developments—and lack thereof—in the literature. Treatment options for CSA have been limited. For most patients, continuous PAP (CPAP), which is the gold standard treatment for OSA, is not an effective CSA treatment. Earlier specialty guidelines endorsed adaptive servo-ventilation (ASV), a more sophisticated respiratory assist device, for treating CSA. In 2015, the SERVE-HF trial examined the effects of ASV in combination with guideline-based medical treatment on survival and cardiovascular outcomes for patients who had CSA and HF with reduced ejection fraction.⁷ They found that ASV had no significant effect on the primary endpoints of first event of death from any cause, lifesaving cardiovascular intervention, or unplanned hospitalization for worsening HF. However, all-cause and cardiovascular mortality were both increased with ASV. There has not been a more recent large clinical trial that either refutes or reinforces those findings (ADVENT-HF found that ASV effectively treated CSA and OSA in patients with CHF but had no impact on the primary endpoint of mortality).^7,8 We are unlikely to see more studies soon that will put this issue to rest and change the guidance that is currently available for ASV use.

Regn and colleagues also provide an update on the use of acetazolamide as to assist in CSA treatment. This should be done cautiously and potentially deferred to subspecialists in sleep medicine, cardiology, or nephrology. The theoretical benefit of acetazolamide in CSA is based on its promotion of excretion of sodium bicarbonate, leading to metabolic acidosis, which can stimulate central respiratory drive. Since CSA is characterized by episodic loss of central respiratory drive, it seems logical that a respiratory stimulant would provide benefit. However, acetazolamide is not approved by the US Food and Drug Administration for CSA.⁹ In those with impaired respiratory mechanics, CHF, chronic obstructive pulmonary disease, and obesity hypoventilation syndrome, this medication has the potential for harm by adding metabolic acidosis to a patient with concurrent respiratory acidosis or respiratory constraints that limit their ability to compensate effectively for additional acid-base derangements.

It is worth noting that Regn and colleagues do not make claims outside the intended scope. It accomplishes the mission of providing all PCPs with an updated streamlined summary for diagnosing and treating CSA. Such tools are important in an age of growing medical information technology because it can improve the quality of medical care and ultimately, patient outcomes with timely diagnosis and treatment. This is particularly significant in a veteran population with a high burden of chronic medical conditions and polypharmacy.

In this issue, Regn and colleagues (page 78) have provided a concise resource for primary care professionals (PCPs) on a lesser known sleep disorder that is increasingly common in veterans.¹ Their review provides a basic understanding of central sleep apnea (CSA) and a systematic clinical approach to diagnosis and treatment in primary care. We applaud the authors for providing education on sleep disorders to the Federal Practitioner audience, since sleep disorders are prevalent among military service members and veterans, with significant implications for health, wellness, productivity, and cost. The American workforce has a long-held sense of pride in working hard, often at the expense of sleep. Early work start times are common in the military and federal government, and sleep medicine specialists have the expertise necessary to diagnose and treat the myriad of sleep disorders that have come to light recently. A massive shortage of sleep medicine specialists limits the evidence-based sleep treatment implementations in medical care.

Medicine has become increasingly complex, necessitating a highly connected web of people, resources, institutions, and processes to keep up with the demands of growing information and technology. The evolution of a systems approach to health care built momentum during the 21st century.1-3 The National Academy of Medicine has published 2 reports that raised concerns about the quality and safety of medical care.4,5 With this expansion, the potential for medical errors at individual components or relationship nodes between actors in the medical system also has grown. Medical errors encompass more than acts of commission and can also take the form of acts of omission by failing to diagnosis and appropriately treat before long-term or irrevocable health consequences occur. A systems approach seeks to aid clinical decision making to improve the quality of medical care and patient outcomes in an otherwise complex medical system that can be difficult to navigate.

Although awareness of obstructive sleep apnea (OSA) has increased, CSA has not received the same level of attention and may not be recognized by PCPs. A lack of education about CSA can contribute to acts of omission in a health care setting. Although CSA is ultimately diagnosed and managed in specialty care sleep medicine clinics, PCPs play an instrumental role in referring patients for evaluation and then collaborating with specialists to optimize care and outcomes. The multidisciplinary approach of CSA management is important because it overlaps with many conditions that are commonly seen in primary care, including obesity, chronic pain, congestive heart failure (CHF), chronic kidney disease, and hypothyroidism. These chronic conditions are also prevalent among veterans. In a national cross-sectional study, veterans had higher prevalence rates of chronic health conditions, including cardiovascular disease and kidney disease, compared with nonveterans (odds ratios, 1.4 and 1.2, respectively).⁶

It is important to understand the relationship between CSA and chronic medical conditions because recognizing the signs of CSA can lead to identification of underlying medical conditions. Likewise, the chronic medical conditions that lead to CSA may cue the PCP’s clinical suspicion for CSA and lead to specialty care referrals if needed. The clinician also serves a significant role in the management of CSA by optimizing medical care for the underlying condition prior to pursuing additional specialty care treatments like positive airway pressure (PAP). For example, PCPs are often involved in the management of atrial fibrillation and cardiac dysfunction, which can minimize or exacerbate CSA. PCPs should also be aware of which drugs are associated with the presentation of CSA as withdrawal or reduction of the medication can resolve symptoms without further evaluation by a specialist.

The review by Regn and colleagues updates readers on developments—and lack thereof—in the literature. Treatment options for CSA have been limited. For most patients, continuous PAP (CPAP), which is the gold standard treatment for OSA, is not an effective CSA treatment. Earlier specialty guidelines endorsed adaptive servo-ventilation (ASV), a more sophisticated respiratory assist device, for treating CSA. In 2015, the SERVE-HF trial examined the effects of ASV in combination with guideline-based medical treatment on survival and cardiovascular outcomes for patients who had CSA and HF with reduced ejection fraction.⁷ They found that ASV had no significant effect on the primary endpoints of first event of death from any cause, lifesaving cardiovascular intervention, or unplanned hospitalization for worsening HF. However, all-cause and cardiovascular mortality were both increased with ASV. There has not been a more recent large clinical trial that either refutes or reinforces those findings (ADVENT-HF found that ASV effectively treated CSA and OSA in patients with CHF but had no impact on the primary endpoint of mortality).^7,8 We are unlikely to see more studies soon that will put this issue to rest and change the guidance that is currently available for ASV use.

Regn and colleagues also provide an update on the use of acetazolamide as to assist in CSA treatment. This should be done cautiously and potentially deferred to subspecialists in sleep medicine, cardiology, or nephrology. The theoretical benefit of acetazolamide in CSA is based on its promotion of excretion of sodium bicarbonate, leading to metabolic acidosis, which can stimulate central respiratory drive. Since CSA is characterized by episodic loss of central respiratory drive, it seems logical that a respiratory stimulant would provide benefit. However, acetazolamide is not approved by the US Food and Drug Administration for CSA.⁹ In those with impaired respiratory mechanics, CHF, chronic obstructive pulmonary disease, and obesity hypoventilation syndrome, this medication has the potential for harm by adding metabolic acidosis to a patient with concurrent respiratory acidosis or respiratory constraints that limit their ability to compensate effectively for additional acid-base derangements.

It is worth noting that Regn and colleagues do not make claims outside the intended scope. It accomplishes the mission of providing all PCPs with an updated streamlined summary for diagnosing and treating CSA. Such tools are important in an age of growing medical information technology because it can improve the quality of medical care and ultimately, patient outcomes with timely diagnosis and treatment. This is particularly significant in a veteran population with a high burden of chronic medical conditions and polypharmacy.

This discussion was recorded on Feb. 21, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Joining me today is Gilberto Salazar, MD, an emergency physician at UT Southwestern Medical Center in Dallas, to discuss a new virtual reality tool to help health care providers deescalate workplace violence. Welcome, Dr. Salazar. It’s a pleasure to have you join us today.

Gilberto A. Salazar, MD: The pleasure is all mine, Dr. Glatter. Thank you so much for having me.

Dr. Glatter: This is such an important topic, as you can imagine. Workplace violence is affecting so many providers in hospital emergency departments but also throughout other parts of the hospital.

First, can you describe how the virtual reality (VR) program was designed that you developed and what type of situations it simulates?

Dr. Salazar: We worked in conjunction with the University of Texas at Dallas. They help people like me, subject matter experts in health care, to bring ideas to reality. I worked very closely with a group of engineers from their department in designing a module specifically designed to tackle, as you mentioned, one of our biggest threats in workplace violence.

We decided to bring in a series of competencies and proficiencies that we wanted to bring into the virtual reality space. In leveraging the technology and the expertise from UT Dallas, we were able to make that happen.

Dr. Glatter: I think it’s important to understand, in terms of virtual reality, what type of environment the program creates. Can you describe what a provider who puts the goggles on is experiencing? Do they feel anything? Is there technology that enables this?

Dr. Salazar: Yes, absolutely. We were able to bring to reality a series of scenarios very common from what you and I see in the emergency department on a daily basis. We wanted to immerse a learner into that specific environment. We didn’t feel that a module or something on a computer or a slide set could really bring the reality of what it’s like to interact with a patient who may be escalating or may be aggressive.

UT Dallas

UT Southwestern Medical Center

We were able to create our own algorithm, but it’s not brand new. We’re just borrowing what we think is the best to create something that the majority of health care personnel are going to be able to relate to and be able to really be proficient at.

This includes things like active listening, bargaining, how to respond, where to put yourself in a situation, and the best possible situation to respond to a scenario, how to prevent things – how to get out of a chokehold, for example. We’re borrowing from several different disciplines and creating something that can be very concise and organized.

Dr. Glatter: Does this program that you’ve developed allow the provider to get feedback in the sense that when they’re in such a danger, their life could be at risk? For example, if they don’t remove themselves in a certain amount of time, this could be lethal.

Dr. Salazar: Yes, 100%. Probably the one thing that differentiates our project from any others is the ability to customize the experience so that a learner who is doing the things that we ask them to do in terms of safety and response is able to get out of a situation successfully within the environment. If they don’t, they get some kind of feedback.

Not to spoil the surprise here, but we’re going to be doing things like looking at decibel meters to see what the volume in the room is doing and how you’re managing the volume and the stimulation within the room. If you are able to maintain the decibel readings at a specific level, you’re going to succeed through the module. If you don’t, we keep the patient escalation going.

Dr. Glatter: There is a debrief built into this type of approach where, in other words, learning points are emphasized – where you could have done better and such.

Dr. Salazar: Yes, absolutely. We are going to be able to get individualized data for each learner so that we can tailor the debrief to their own performance and be able to give them actionable items to work on. It’s a debrief that’s productive and individualized, and folks can walk away with something useful in the end.

Dr. Glatter: Are the data shared or confidential at present?

Dr. Salazar: At this very moment, the data are confidential. We are going to look at how to best use this. We’re hoping to eventually write this up and see how this information can be best used to train personnel.

Eventually, we may see that some of the advice that we’re giving is very common to most folks. Others may require some individualized type of feedback. That said, it remains to be seen, but right now, it’s confidential.

Dr. Glatter: Is this currently being implemented as part of your curriculum for emergency medicine residents?

Dr. Salazar: We’re going to study it first. We’re very excited to include our emergency medicine residents as one of our cohorts that’s going to be undergoing the module, and we’re going to be studying other forms of workplace violence mitigation strategies. We’re really excited about the possibility of this eventually becoming the standard of education for not only our emergency medicine residents, but also health care personnel all over the world.

Dr. Glatter: I’m glad you mentioned that, because obviously nurses, clerks in the department, and anyone who’s working in the department, for that matter, and who interfaces with patients really should undergo such training.

Dr. Salazar: Absolutely. The folks at intake, at check-in, and at kiosks. Do they go through a separate area for screening? You’re absolutely right. There are many folks who interface with patients and all of us are potential victims of workplace violence. We want to give our health care family the best opportunity to succeed in these situations.

Dr. Glatter:: Absolutely. Even EMS providers, being on the front lines and encountering patients in such situations, would benefit, in my opinion.

Dr. Salazar: Yes, absolutely. Behavioral health emergencies and organically induced altered mental status results in injury, both physical and mental, to EMS professionals as well, and there’s good evidence of that. I’ll be very glad to see this type of education make it out to our initial and continuing education efforts for EMS as well.

Dr. Glatter: I want to thank you. This has been very helpful. It’s such an important task that you’ve started to explore, and I look forward to follow-up on this. Again, thank you for your time.

Dr. Salazar: It was my pleasure. Thank you so much for having me.
 

Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, N.Y. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes. Dr. Salazar is a board-certified emergency physician and associate professor at UT Southwestern Medicine Center in Dallas. He is involved with the UTSW Emergency Medicine Education Program and serves as the medical director to teach both initial and continuing the emergency medicine education for emergency medical technicians and paramedics, which trains most of the Dallas Fire Rescue personnel and the vast majority for EMS providers in the Dallas County. In addition, he serves as an associate chief of service at Parkland’s emergency department, and liaison to surgical services. A version of this article originally appeared on Medscape.com.

This discussion was recorded on Feb. 21, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Joining me today is Gilberto Salazar, MD, an emergency physician at UT Southwestern Medical Center in Dallas, to discuss a new virtual reality tool to help health care providers deescalate workplace violence. Welcome, Dr. Salazar. It’s a pleasure to have you join us today.

Gilberto A. Salazar, MD: The pleasure is all mine, Dr. Glatter. Thank you so much for having me.

Dr. Glatter: This is such an important topic, as you can imagine. Workplace violence is affecting so many providers in hospital emergency departments but also throughout other parts of the hospital.

First, can you describe how the virtual reality (VR) program was designed that you developed and what type of situations it simulates?

Dr. Salazar: We worked in conjunction with the University of Texas at Dallas. They help people like me, subject matter experts in health care, to bring ideas to reality. I worked very closely with a group of engineers from their department in designing a module specifically designed to tackle, as you mentioned, one of our biggest threats in workplace violence.

We decided to bring in a series of competencies and proficiencies that we wanted to bring into the virtual reality space. In leveraging the technology and the expertise from UT Dallas, we were able to make that happen.

Dr. Glatter: I think it’s important to understand, in terms of virtual reality, what type of environment the program creates. Can you describe what a provider who puts the goggles on is experiencing? Do they feel anything? Is there technology that enables this?

Dr. Salazar: Yes, absolutely. We were able to bring to reality a series of scenarios very common from what you and I see in the emergency department on a daily basis. We wanted to immerse a learner into that specific environment. We didn’t feel that a module or something on a computer or a slide set could really bring the reality of what it’s like to interact with a patient who may be escalating or may be aggressive.

UT Dallas

UT Southwestern Medical Center

We were able to create our own algorithm, but it’s not brand new. We’re just borrowing what we think is the best to create something that the majority of health care personnel are going to be able to relate to and be able to really be proficient at.

This includes things like active listening, bargaining, how to respond, where to put yourself in a situation, and the best possible situation to respond to a scenario, how to prevent things – how to get out of a chokehold, for example. We’re borrowing from several different disciplines and creating something that can be very concise and organized.

Dr. Glatter: Does this program that you’ve developed allow the provider to get feedback in the sense that when they’re in such a danger, their life could be at risk? For example, if they don’t remove themselves in a certain amount of time, this could be lethal.

Dr. Salazar: Yes, 100%. Probably the one thing that differentiates our project from any others is the ability to customize the experience so that a learner who is doing the things that we ask them to do in terms of safety and response is able to get out of a situation successfully within the environment. If they don’t, they get some kind of feedback.

Not to spoil the surprise here, but we’re going to be doing things like looking at decibel meters to see what the volume in the room is doing and how you’re managing the volume and the stimulation within the room. If you are able to maintain the decibel readings at a specific level, you’re going to succeed through the module. If you don’t, we keep the patient escalation going.

Dr. Glatter: There is a debrief built into this type of approach where, in other words, learning points are emphasized – where you could have done better and such.

Dr. Salazar: Yes, absolutely. We are going to be able to get individualized data for each learner so that we can tailor the debrief to their own performance and be able to give them actionable items to work on. It’s a debrief that’s productive and individualized, and folks can walk away with something useful in the end.

Dr. Glatter: Are the data shared or confidential at present?

Dr. Salazar: At this very moment, the data are confidential. We are going to look at how to best use this. We’re hoping to eventually write this up and see how this information can be best used to train personnel.

Eventually, we may see that some of the advice that we’re giving is very common to most folks. Others may require some individualized type of feedback. That said, it remains to be seen, but right now, it’s confidential.

Dr. Glatter: Is this currently being implemented as part of your curriculum for emergency medicine residents?

Dr. Salazar: We’re going to study it first. We’re very excited to include our emergency medicine residents as one of our cohorts that’s going to be undergoing the module, and we’re going to be studying other forms of workplace violence mitigation strategies. We’re really excited about the possibility of this eventually becoming the standard of education for not only our emergency medicine residents, but also health care personnel all over the world.

Dr. Glatter: I’m glad you mentioned that, because obviously nurses, clerks in the department, and anyone who’s working in the department, for that matter, and who interfaces with patients really should undergo such training.

Dr. Salazar: Absolutely. The folks at intake, at check-in, and at kiosks. Do they go through a separate area for screening? You’re absolutely right. There are many folks who interface with patients and all of us are potential victims of workplace violence. We want to give our health care family the best opportunity to succeed in these situations.

Dr. Glatter:: Absolutely. Even EMS providers, being on the front lines and encountering patients in such situations, would benefit, in my opinion.

Dr. Salazar: Yes, absolutely. Behavioral health emergencies and organically induced altered mental status results in injury, both physical and mental, to EMS professionals as well, and there’s good evidence of that. I’ll be very glad to see this type of education make it out to our initial and continuing education efforts for EMS as well.

Dr. Glatter: I want to thank you. This has been very helpful. It’s such an important task that you’ve started to explore, and I look forward to follow-up on this. Again, thank you for your time.

Dr. Salazar: It was my pleasure. Thank you so much for having me.
 

Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, N.Y. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes. Dr. Salazar is a board-certified emergency physician and associate professor at UT Southwestern Medicine Center in Dallas. He is involved with the UTSW Emergency Medicine Education Program and serves as the medical director to teach both initial and continuing the emergency medicine education for emergency medical technicians and paramedics, which trains most of the Dallas Fire Rescue personnel and the vast majority for EMS providers in the Dallas County. In addition, he serves as an associate chief of service at Parkland’s emergency department, and liaison to surgical services. A version of this article originally appeared on Medscape.com.

This discussion was recorded on Feb. 21, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Joining me today is Gilberto Salazar, MD, an emergency physician at UT Southwestern Medical Center in Dallas, to discuss a new virtual reality tool to help health care providers deescalate workplace violence. Welcome, Dr. Salazar. It’s a pleasure to have you join us today.

Gilberto A. Salazar, MD: The pleasure is all mine, Dr. Glatter. Thank you so much for having me.

Dr. Glatter: This is such an important topic, as you can imagine. Workplace violence is affecting so many providers in hospital emergency departments but also throughout other parts of the hospital.

First, can you describe how the virtual reality (VR) program was designed that you developed and what type of situations it simulates?

Dr. Salazar: We worked in conjunction with the University of Texas at Dallas. They help people like me, subject matter experts in health care, to bring ideas to reality. I worked very closely with a group of engineers from their department in designing a module specifically designed to tackle, as you mentioned, one of our biggest threats in workplace violence.

We decided to bring in a series of competencies and proficiencies that we wanted to bring into the virtual reality space. In leveraging the technology and the expertise from UT Dallas, we were able to make that happen.

Dr. Glatter: I think it’s important to understand, in terms of virtual reality, what type of environment the program creates. Can you describe what a provider who puts the goggles on is experiencing? Do they feel anything? Is there technology that enables this?

Dr. Salazar: Yes, absolutely. We were able to bring to reality a series of scenarios very common from what you and I see in the emergency department on a daily basis. We wanted to immerse a learner into that specific environment. We didn’t feel that a module or something on a computer or a slide set could really bring the reality of what it’s like to interact with a patient who may be escalating or may be aggressive.

UT Dallas

UT Southwestern Medical Center

We were able to create our own algorithm, but it’s not brand new. We’re just borrowing what we think is the best to create something that the majority of health care personnel are going to be able to relate to and be able to really be proficient at.

This includes things like active listening, bargaining, how to respond, where to put yourself in a situation, and the best possible situation to respond to a scenario, how to prevent things – how to get out of a chokehold, for example. We’re borrowing from several different disciplines and creating something that can be very concise and organized.

Dr. Glatter: Does this program that you’ve developed allow the provider to get feedback in the sense that when they’re in such a danger, their life could be at risk? For example, if they don’t remove themselves in a certain amount of time, this could be lethal.

Dr. Salazar: Yes, 100%. Probably the one thing that differentiates our project from any others is the ability to customize the experience so that a learner who is doing the things that we ask them to do in terms of safety and response is able to get out of a situation successfully within the environment. If they don’t, they get some kind of feedback.

Not to spoil the surprise here, but we’re going to be doing things like looking at decibel meters to see what the volume in the room is doing and how you’re managing the volume and the stimulation within the room. If you are able to maintain the decibel readings at a specific level, you’re going to succeed through the module. If you don’t, we keep the patient escalation going.

Dr. Glatter: There is a debrief built into this type of approach where, in other words, learning points are emphasized – where you could have done better and such.

Dr. Salazar: Yes, absolutely. We are going to be able to get individualized data for each learner so that we can tailor the debrief to their own performance and be able to give them actionable items to work on. It’s a debrief that’s productive and individualized, and folks can walk away with something useful in the end.

Dr. Glatter: Are the data shared or confidential at present?

Dr. Salazar: At this very moment, the data are confidential. We are going to look at how to best use this. We’re hoping to eventually write this up and see how this information can be best used to train personnel.

Eventually, we may see that some of the advice that we’re giving is very common to most folks. Others may require some individualized type of feedback. That said, it remains to be seen, but right now, it’s confidential.

Dr. Glatter: Is this currently being implemented as part of your curriculum for emergency medicine residents?

Dr. Salazar: We’re going to study it first. We’re very excited to include our emergency medicine residents as one of our cohorts that’s going to be undergoing the module, and we’re going to be studying other forms of workplace violence mitigation strategies. We’re really excited about the possibility of this eventually becoming the standard of education for not only our emergency medicine residents, but also health care personnel all over the world.

Dr. Glatter: I’m glad you mentioned that, because obviously nurses, clerks in the department, and anyone who’s working in the department, for that matter, and who interfaces with patients really should undergo such training.

Dr. Salazar: Absolutely. The folks at intake, at check-in, and at kiosks. Do they go through a separate area for screening? You’re absolutely right. There are many folks who interface with patients and all of us are potential victims of workplace violence. We want to give our health care family the best opportunity to succeed in these situations.

Dr. Glatter:: Absolutely. Even EMS providers, being on the front lines and encountering patients in such situations, would benefit, in my opinion.

Dr. Salazar: Yes, absolutely. Behavioral health emergencies and organically induced altered mental status results in injury, both physical and mental, to EMS professionals as well, and there’s good evidence of that. I’ll be very glad to see this type of education make it out to our initial and continuing education efforts for EMS as well.

Dr. Glatter: I want to thank you. This has been very helpful. It’s such an important task that you’ve started to explore, and I look forward to follow-up on this. Again, thank you for your time.

Dr. Salazar: It was my pleasure. Thank you so much for having me.
 

Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, N.Y. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes. Dr. Salazar is a board-certified emergency physician and associate professor at UT Southwestern Medicine Center in Dallas. He is involved with the UTSW Emergency Medicine Education Program and serves as the medical director to teach both initial and continuing the emergency medicine education for emergency medical technicians and paramedics, which trains most of the Dallas Fire Rescue personnel and the vast majority for EMS providers in the Dallas County. In addition, he serves as an associate chief of service at Parkland’s emergency department, and liaison to surgical services. A version of this article originally appeared on Medscape.com.

Evidence from three studies in sports cardiology presented at ACC 2023 piqued my interest. Not only because I love endurance sport but because the studies reported data that upset prevailing ideas.

LIVE HCM: Surprising result No. 1

Rachel Lampert, MD, from Yale University, New Haven, Conn., presented results of the LIVE-HCM observational study of vigorous exercise in more than 1,600 patients with hypertrophic cardiomyopathy (40% female). The investigators aimed to determine whether engagement in vigorous exercise, including competitive sports, is associated with increased risk for life-threatening ventricular arrhythmia and/or mortality in patients with HCM.

Because of the myocardial disease, HCM comes with a risk for ventricular arrhythmia. Prevailing wisdom held that vigorous exercise in these patients would be hazardous. It was all expert opinion; there were no data. Now there are.

Dr. Lampert and colleagues recruited patients from 42 international HCM centers. Patients self-enrolled and the researchers created three groups based on self-reported levels of exercise – vigorous, moderate, and sedentary. The main comparison was between vigorous versus nonvigorous exercisers (including moderate and sedentary). The two groups were mostly matched on baseline characteristics and typical of patients with HCM.

The primary endpoint was a composite of death, resuscitated cardiac arrest, syncope likely caused by an arrhythmia, or an appropriate shock from an ICD.

The event rates were low in all groups and almost identical in vigorous versus nonvigorous exercisers. Sub-group analyses found no increased risk in HCM patients who identified as competitive athletes.

Dr. Lampert said these data “do not support universal restriction of vigorous exercise in patients with HCM.”
 

Return to play: Surprising result No. 2

Undergraduate student Katherine Martinez from Loyola University, Chicago, presented an observational analysis of 76 elite athletes with genetic heart disease who gained a return-to-play approval from four expert centers in the United States.

The three-step, return-to-play protocol from these specialized centers deserves emphasis. First was the initial evaluation, including two ECGs, 24-hour ECG monitor, echocardiography, and treadmill exercise testing. Second was a discussion between clinicians and patients regarding the athlete’s situation. The third step was to inform coaches and staff of the team and instruct athletes to obtain a personal AED, stay replenished with electrolytes, avoid QT-prolonging drugs, and continue with annual follow-up.

Slightly more than half of these patients had HCM and almost a third had long QT syndrome. Nearly one-third had an ICD implant and 22 were women.

Of the 76 athletes, 73 chose to return to play; however, 4 of these remained disqualified because of their team’s decision. Of the remaining 69, only 3 had one or more breakthrough cardiac events during 200 patient-years of follow-up.

These comprised one male Division I basketball player with HCM who had an ICD shock while moving furniture; another male Division 1 hockey player with long QT syndrome who was taking beta-blockers experienced syncope while coming off the bench and while cooking; and a third male professional hockey player with HCM, on beta-blockers, had syncope without exertion.

The authors concluded that when there was careful evaluation by experts and shared decision-making, a specific plan to return to sport can be put into place for the highest-level athletes.
 

Masters@Heart: Surprising result No. 3

Ruben De Bosscher MD, PhD, from KU Leuven (Belgium), presented the Masters@Heart study on behalf of a Belgian team of researchers. The question they asked was whether lifelong endurance exercise is associated with more coronary atherosclerosis than standard “normal” exercise levels.

That question brings up the paradox of exercise, which is that numerous observational studies find that exercise strongly associates with lower rates of cardiovascular events, but imaging studies also report high rates of coronary artery calcium in endurance athletes, especially in those who have run multiple marathons.

Masters@Heart investigators sought to explore this paradox by performing detailed coronary imaging in three groups – lifelong athletes, late-onset athletes (after age 30 years), and super-healthy controls. Through advertisements they obtained about 1,100 middle-aged male volunteers (mean age, 55 years). Of these, 605 men were selected at random to participate to reduce the chance of enrolling people who responded to the ads because of health concerns.

Investigators assigned those selected based on self-report of exercise. The control group was notable for their good health: they were free of any risk factors, took (almost) no meds, exercised regularly but not excessively (about 3 hours per week) and had a VO₂ max of 122% of predicted.

The groups were well matched on baseline characteristics. Cycling predominated as the exercise of choice (this is a Belgian study after all). All patients had an extensive evaluation including coronary CT imaging.

European Heart Journal published the provocative results.

• Lifelong exercisers had a significantly higher CAC burden than controls, which confirms previous work.
• Lifelong exercisers had a higher percentage of multiple coronary plaques, plaques of at least 50%, and proximal plaques.
• There were no significant differences in the mixture of plaque types in the three groups. About two thirds of the plaques in each group were calcified and the remainder were deemed noncalcified or mixed.
• When looking only at noncalcified plaques, lifelong exercisers tended to have a higher prevalence of multiple plaques, plaques of at least 50%, and proximal plaques.
• So named “vulnerable” plaques were extremely infrequent in all three groups.

The authors concluded that lifelong endurance sport relative to a generic healthy lifestyle was not associated with more favorable coronary plaque composition.
 

Comments

Each of these three studies provided data where there was none. That is always a good thing.

The major theme from the first two studies is that expert opinion was too cautious. Doctors have long held the idea that patients with genetic heart disease, especially hypertrophic cardiomyopathy, are vulnerable, fragile even, when it comes to vigorous sport.

This new evidence upends this belief, as long as return to sport occurs in the setting of robust patient education and expert evaluation and surveillance.

Paternalism in prohibiting participation in sport because of genetic heart disease has joined the long list of medical reversals.

Masters@Heart provides a slightly different message. It finds that lifelong high-level exercise does not prevent coronary atherosclerosis in men. And, more provocatively, if replicated, might even show that long-term exposure to the biochemical, inflammatory, or hormonal effects of endurance training may actually be atherogenic. Like all good science, these findings raise more questions to explore in the realm of atherogenesis.

Two of the main limitations of the Belgian study was that the control arm was quite healthy; had the comparison arm been typical of sedentary controls in say, the Southeastern United States, the coronary lesions found in longtime exercisers may have looked more favorable. The more significant limitation is the lack of outcomes. Images of coronary arteries remain a surrogate marker. It’s possible that, like statins, higher levels of exercise may stabilize plaque and actually lower the risk for events.

The Belgian authors suggest – as many have – a J-curve of exercise benefits, wherein too little exercise is clearly bad, but too much exercise may also increase risk. In other words, for maximizing health, there may be a Goldilocks amount of exercise.

The problem with this idea comes in its pragmatic translation. The number of lifelong high-level, middle-aged endurance athletes that cite heart health reasons for their affliction is ... almost zero. Nearly everyone I have met in the endurance sport fraternity harbors no notion that racing a bike or running multiple marathons per year is a healthy endeavor.

Paternalism, therefore, would also fall in the realm of limiting lifelong exercise in addicted middle-aged athletes.

Via email, sports cardiologist Michael Emery, MD, reiterated the main immediate message from Masters@Heart: “Exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear honestly).”

I for one cannot give up on endurance exercise. I won’t likely race anymore but I am like the lab rat who needs to run on the wheel. Whether this affects my coronary plaque burden matters not to me.

Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no conflicts of interest.

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

Evidence from three studies in sports cardiology presented at ACC 2023 piqued my interest. Not only because I love endurance sport but because the studies reported data that upset prevailing ideas.

LIVE HCM: Surprising result No. 1

Rachel Lampert, MD, from Yale University, New Haven, Conn., presented results of the LIVE-HCM observational study of vigorous exercise in more than 1,600 patients with hypertrophic cardiomyopathy (40% female). The investigators aimed to determine whether engagement in vigorous exercise, including competitive sports, is associated with increased risk for life-threatening ventricular arrhythmia and/or mortality in patients with HCM.

Because of the myocardial disease, HCM comes with a risk for ventricular arrhythmia. Prevailing wisdom held that vigorous exercise in these patients would be hazardous. It was all expert opinion; there were no data. Now there are.

Dr. Lampert and colleagues recruited patients from 42 international HCM centers. Patients self-enrolled and the researchers created three groups based on self-reported levels of exercise – vigorous, moderate, and sedentary. The main comparison was between vigorous versus nonvigorous exercisers (including moderate and sedentary). The two groups were mostly matched on baseline characteristics and typical of patients with HCM.

The primary endpoint was a composite of death, resuscitated cardiac arrest, syncope likely caused by an arrhythmia, or an appropriate shock from an ICD.

The event rates were low in all groups and almost identical in vigorous versus nonvigorous exercisers. Sub-group analyses found no increased risk in HCM patients who identified as competitive athletes.

Dr. Lampert said these data “do not support universal restriction of vigorous exercise in patients with HCM.”
 

Return to play: Surprising result No. 2

Undergraduate student Katherine Martinez from Loyola University, Chicago, presented an observational analysis of 76 elite athletes with genetic heart disease who gained a return-to-play approval from four expert centers in the United States.

The three-step, return-to-play protocol from these specialized centers deserves emphasis. First was the initial evaluation, including two ECGs, 24-hour ECG monitor, echocardiography, and treadmill exercise testing. Second was a discussion between clinicians and patients regarding the athlete’s situation. The third step was to inform coaches and staff of the team and instruct athletes to obtain a personal AED, stay replenished with electrolytes, avoid QT-prolonging drugs, and continue with annual follow-up.

Slightly more than half of these patients had HCM and almost a third had long QT syndrome. Nearly one-third had an ICD implant and 22 were women.

Of the 76 athletes, 73 chose to return to play; however, 4 of these remained disqualified because of their team’s decision. Of the remaining 69, only 3 had one or more breakthrough cardiac events during 200 patient-years of follow-up.

These comprised one male Division I basketball player with HCM who had an ICD shock while moving furniture; another male Division 1 hockey player with long QT syndrome who was taking beta-blockers experienced syncope while coming off the bench and while cooking; and a third male professional hockey player with HCM, on beta-blockers, had syncope without exertion.

The authors concluded that when there was careful evaluation by experts and shared decision-making, a specific plan to return to sport can be put into place for the highest-level athletes.
 

Masters@Heart: Surprising result No. 3

Ruben De Bosscher MD, PhD, from KU Leuven (Belgium), presented the Masters@Heart study on behalf of a Belgian team of researchers. The question they asked was whether lifelong endurance exercise is associated with more coronary atherosclerosis than standard “normal” exercise levels.

That question brings up the paradox of exercise, which is that numerous observational studies find that exercise strongly associates with lower rates of cardiovascular events, but imaging studies also report high rates of coronary artery calcium in endurance athletes, especially in those who have run multiple marathons.

Masters@Heart investigators sought to explore this paradox by performing detailed coronary imaging in three groups – lifelong athletes, late-onset athletes (after age 30 years), and super-healthy controls. Through advertisements they obtained about 1,100 middle-aged male volunteers (mean age, 55 years). Of these, 605 men were selected at random to participate to reduce the chance of enrolling people who responded to the ads because of health concerns.

Investigators assigned those selected based on self-report of exercise. The control group was notable for their good health: they were free of any risk factors, took (almost) no meds, exercised regularly but not excessively (about 3 hours per week) and had a VO₂ max of 122% of predicted.

The groups were well matched on baseline characteristics. Cycling predominated as the exercise of choice (this is a Belgian study after all). All patients had an extensive evaluation including coronary CT imaging.

European Heart Journal published the provocative results.

• Lifelong exercisers had a significantly higher CAC burden than controls, which confirms previous work.
• Lifelong exercisers had a higher percentage of multiple coronary plaques, plaques of at least 50%, and proximal plaques.
• There were no significant differences in the mixture of plaque types in the three groups. About two thirds of the plaques in each group were calcified and the remainder were deemed noncalcified or mixed.
• When looking only at noncalcified plaques, lifelong exercisers tended to have a higher prevalence of multiple plaques, plaques of at least 50%, and proximal plaques.
• So named “vulnerable” plaques were extremely infrequent in all three groups.

The authors concluded that lifelong endurance sport relative to a generic healthy lifestyle was not associated with more favorable coronary plaque composition.
 

Comments

Each of these three studies provided data where there was none. That is always a good thing.

The major theme from the first two studies is that expert opinion was too cautious. Doctors have long held the idea that patients with genetic heart disease, especially hypertrophic cardiomyopathy, are vulnerable, fragile even, when it comes to vigorous sport.

This new evidence upends this belief, as long as return to sport occurs in the setting of robust patient education and expert evaluation and surveillance.

Paternalism in prohibiting participation in sport because of genetic heart disease has joined the long list of medical reversals.

Masters@Heart provides a slightly different message. It finds that lifelong high-level exercise does not prevent coronary atherosclerosis in men. And, more provocatively, if replicated, might even show that long-term exposure to the biochemical, inflammatory, or hormonal effects of endurance training may actually be atherogenic. Like all good science, these findings raise more questions to explore in the realm of atherogenesis.

Two of the main limitations of the Belgian study was that the control arm was quite healthy; had the comparison arm been typical of sedentary controls in say, the Southeastern United States, the coronary lesions found in longtime exercisers may have looked more favorable. The more significant limitation is the lack of outcomes. Images of coronary arteries remain a surrogate marker. It’s possible that, like statins, higher levels of exercise may stabilize plaque and actually lower the risk for events.

The Belgian authors suggest – as many have – a J-curve of exercise benefits, wherein too little exercise is clearly bad, but too much exercise may also increase risk. In other words, for maximizing health, there may be a Goldilocks amount of exercise.

The problem with this idea comes in its pragmatic translation. The number of lifelong high-level, middle-aged endurance athletes that cite heart health reasons for their affliction is ... almost zero. Nearly everyone I have met in the endurance sport fraternity harbors no notion that racing a bike or running multiple marathons per year is a healthy endeavor.

Paternalism, therefore, would also fall in the realm of limiting lifelong exercise in addicted middle-aged athletes.

Via email, sports cardiologist Michael Emery, MD, reiterated the main immediate message from Masters@Heart: “Exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear honestly).”

I for one cannot give up on endurance exercise. I won’t likely race anymore but I am like the lab rat who needs to run on the wheel. Whether this affects my coronary plaque burden matters not to me.

Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no conflicts of interest.

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

Evidence from three studies in sports cardiology presented at ACC 2023 piqued my interest. Not only because I love endurance sport but because the studies reported data that upset prevailing ideas.

LIVE HCM: Surprising result No. 1

Rachel Lampert, MD, from Yale University, New Haven, Conn., presented results of the LIVE-HCM observational study of vigorous exercise in more than 1,600 patients with hypertrophic cardiomyopathy (40% female). The investigators aimed to determine whether engagement in vigorous exercise, including competitive sports, is associated with increased risk for life-threatening ventricular arrhythmia and/or mortality in patients with HCM.

Because of the myocardial disease, HCM comes with a risk for ventricular arrhythmia. Prevailing wisdom held that vigorous exercise in these patients would be hazardous. It was all expert opinion; there were no data. Now there are.

Dr. Lampert and colleagues recruited patients from 42 international HCM centers. Patients self-enrolled and the researchers created three groups based on self-reported levels of exercise – vigorous, moderate, and sedentary. The main comparison was between vigorous versus nonvigorous exercisers (including moderate and sedentary). The two groups were mostly matched on baseline characteristics and typical of patients with HCM.

The primary endpoint was a composite of death, resuscitated cardiac arrest, syncope likely caused by an arrhythmia, or an appropriate shock from an ICD.

The event rates were low in all groups and almost identical in vigorous versus nonvigorous exercisers. Sub-group analyses found no increased risk in HCM patients who identified as competitive athletes.

Dr. Lampert said these data “do not support universal restriction of vigorous exercise in patients with HCM.”
 

Return to play: Surprising result No. 2

Undergraduate student Katherine Martinez from Loyola University, Chicago, presented an observational analysis of 76 elite athletes with genetic heart disease who gained a return-to-play approval from four expert centers in the United States.

The three-step, return-to-play protocol from these specialized centers deserves emphasis. First was the initial evaluation, including two ECGs, 24-hour ECG monitor, echocardiography, and treadmill exercise testing. Second was a discussion between clinicians and patients regarding the athlete’s situation. The third step was to inform coaches and staff of the team and instruct athletes to obtain a personal AED, stay replenished with electrolytes, avoid QT-prolonging drugs, and continue with annual follow-up.

Slightly more than half of these patients had HCM and almost a third had long QT syndrome. Nearly one-third had an ICD implant and 22 were women.

Of the 76 athletes, 73 chose to return to play; however, 4 of these remained disqualified because of their team’s decision. Of the remaining 69, only 3 had one or more breakthrough cardiac events during 200 patient-years of follow-up.

These comprised one male Division I basketball player with HCM who had an ICD shock while moving furniture; another male Division 1 hockey player with long QT syndrome who was taking beta-blockers experienced syncope while coming off the bench and while cooking; and a third male professional hockey player with HCM, on beta-blockers, had syncope without exertion.

The authors concluded that when there was careful evaluation by experts and shared decision-making, a specific plan to return to sport can be put into place for the highest-level athletes.
 

Masters@Heart: Surprising result No. 3

Ruben De Bosscher MD, PhD, from KU Leuven (Belgium), presented the Masters@Heart study on behalf of a Belgian team of researchers. The question they asked was whether lifelong endurance exercise is associated with more coronary atherosclerosis than standard “normal” exercise levels.

That question brings up the paradox of exercise, which is that numerous observational studies find that exercise strongly associates with lower rates of cardiovascular events, but imaging studies also report high rates of coronary artery calcium in endurance athletes, especially in those who have run multiple marathons.

Masters@Heart investigators sought to explore this paradox by performing detailed coronary imaging in three groups – lifelong athletes, late-onset athletes (after age 30 years), and super-healthy controls. Through advertisements they obtained about 1,100 middle-aged male volunteers (mean age, 55 years). Of these, 605 men were selected at random to participate to reduce the chance of enrolling people who responded to the ads because of health concerns.

Investigators assigned those selected based on self-report of exercise. The control group was notable for their good health: they were free of any risk factors, took (almost) no meds, exercised regularly but not excessively (about 3 hours per week) and had a VO₂ max of 122% of predicted.

The groups were well matched on baseline characteristics. Cycling predominated as the exercise of choice (this is a Belgian study after all). All patients had an extensive evaluation including coronary CT imaging.

European Heart Journal published the provocative results.

• Lifelong exercisers had a significantly higher CAC burden than controls, which confirms previous work.
• Lifelong exercisers had a higher percentage of multiple coronary plaques, plaques of at least 50%, and proximal plaques.
• There were no significant differences in the mixture of plaque types in the three groups. About two thirds of the plaques in each group were calcified and the remainder were deemed noncalcified or mixed.
• When looking only at noncalcified plaques, lifelong exercisers tended to have a higher prevalence of multiple plaques, plaques of at least 50%, and proximal plaques.
• So named “vulnerable” plaques were extremely infrequent in all three groups.

The authors concluded that lifelong endurance sport relative to a generic healthy lifestyle was not associated with more favorable coronary plaque composition.
 

Comments

Each of these three studies provided data where there was none. That is always a good thing.

The major theme from the first two studies is that expert opinion was too cautious. Doctors have long held the idea that patients with genetic heart disease, especially hypertrophic cardiomyopathy, are vulnerable, fragile even, when it comes to vigorous sport.

This new evidence upends this belief, as long as return to sport occurs in the setting of robust patient education and expert evaluation and surveillance.

Paternalism in prohibiting participation in sport because of genetic heart disease has joined the long list of medical reversals.

Masters@Heart provides a slightly different message. It finds that lifelong high-level exercise does not prevent coronary atherosclerosis in men. And, more provocatively, if replicated, might even show that long-term exposure to the biochemical, inflammatory, or hormonal effects of endurance training may actually be atherogenic. Like all good science, these findings raise more questions to explore in the realm of atherogenesis.

Two of the main limitations of the Belgian study was that the control arm was quite healthy; had the comparison arm been typical of sedentary controls in say, the Southeastern United States, the coronary lesions found in longtime exercisers may have looked more favorable. The more significant limitation is the lack of outcomes. Images of coronary arteries remain a surrogate marker. It’s possible that, like statins, higher levels of exercise may stabilize plaque and actually lower the risk for events.

The Belgian authors suggest – as many have – a J-curve of exercise benefits, wherein too little exercise is clearly bad, but too much exercise may also increase risk. In other words, for maximizing health, there may be a Goldilocks amount of exercise.

The problem with this idea comes in its pragmatic translation. The number of lifelong high-level, middle-aged endurance athletes that cite heart health reasons for their affliction is ... almost zero. Nearly everyone I have met in the endurance sport fraternity harbors no notion that racing a bike or running multiple marathons per year is a healthy endeavor.

Paternalism, therefore, would also fall in the realm of limiting lifelong exercise in addicted middle-aged athletes.

Via email, sports cardiologist Michael Emery, MD, reiterated the main immediate message from Masters@Heart: “Exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear honestly).”

I for one cannot give up on endurance exercise. I won’t likely race anymore but I am like the lab rat who needs to run on the wheel. Whether this affects my coronary plaque burden matters not to me.

Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no conflicts of interest.

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

Two feet–one hand syndrome

Two feet–one hand syndrome is a common term used to describe tinea manuum on one hand with bilateral tinea pedis. This condition, also known as ringworm, is a fungal infection caused by a dermatophyte, and presents as a superficial annular or circular rash with a raised, scaly border.

Symptoms include dryness and itchiness, and the lesions may appear red-pink on lighter skin and gray-brown on darker skin types. Although these infections can arise in a variety of combinations, two feet–one hand syndrome occurs in about 60% of cases. Trichophyton rubrum is the most common agent.

Diagnosis is made by patient history, dermoscopic visualization, and staining of skin scraping with KOH or fungal culture. Dermatophytes prefer moist, warm environments, so this disease is prevalent in tropical conditions and associated with moist public areas such as locker rooms and showers. As a result, tinea pedis is also nicknamed “athlete’s foot” for its common presentation in athletes. The fungus spreads easily through contact and can survive on infected surfaces, so patients often self-inoculate by touching/scratching the affected area then touching another body part. Cautions that should be taken to avoid transmission include not sharing personal care products, washing the area and keeping it dry, and avoiding close, humid environments.

Dr. Donna Bilu Martin

The syndrome is highly associated with onychomycosis, which can be more difficult to treat and often requires oral antifungals. Tinea manuum is commonly misdiagnosed as hand dermatitis or eczema and treated with topical steroids, which will exacerbate or flare the tinea.

Two feet–one hand syndrome can typically be treated with over-the-counter topical antifungal medications such as miconazole or clotrimazole. Topical ketoconazole may be prescribed, and oral terbinafine or itraconazole are used in more severe cases when a larger body surface area is affected or in immunocompromised patients.

Dr. Donna Bilu Martin

This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University, Davie, Fla.; Kiran C. Patel, Tampa Bay Regional Campus; and Dr. Bilu Martin.
 

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

Cleveland Clinic. Tinea manuum: Symptoms, causes & treatment. 2022. https://my.clevelandclinic.org/health/diseases/24063-tinea-manuum.

Ugalde-Trejo NX et al. Curr Fungal Infect Rep. 2022 Nov 17. doi: 10.1007/s12281-022-00447-9.

Mizumoto J. Cureus. 2021 Dec 27;13(12):e20758.

Two feet–one hand syndrome

Two feet–one hand syndrome is a common term used to describe tinea manuum on one hand with bilateral tinea pedis. This condition, also known as ringworm, is a fungal infection caused by a dermatophyte, and presents as a superficial annular or circular rash with a raised, scaly border.

Symptoms include dryness and itchiness, and the lesions may appear red-pink on lighter skin and gray-brown on darker skin types. Although these infections can arise in a variety of combinations, two feet–one hand syndrome occurs in about 60% of cases. Trichophyton rubrum is the most common agent.

Diagnosis is made by patient history, dermoscopic visualization, and staining of skin scraping with KOH or fungal culture. Dermatophytes prefer moist, warm environments, so this disease is prevalent in tropical conditions and associated with moist public areas such as locker rooms and showers. As a result, tinea pedis is also nicknamed “athlete’s foot” for its common presentation in athletes. The fungus spreads easily through contact and can survive on infected surfaces, so patients often self-inoculate by touching/scratching the affected area then touching another body part. Cautions that should be taken to avoid transmission include not sharing personal care products, washing the area and keeping it dry, and avoiding close, humid environments.

Dr. Donna Bilu Martin

The syndrome is highly associated with onychomycosis, which can be more difficult to treat and often requires oral antifungals. Tinea manuum is commonly misdiagnosed as hand dermatitis or eczema and treated with topical steroids, which will exacerbate or flare the tinea.

Two feet–one hand syndrome can typically be treated with over-the-counter topical antifungal medications such as miconazole or clotrimazole. Topical ketoconazole may be prescribed, and oral terbinafine or itraconazole are used in more severe cases when a larger body surface area is affected or in immunocompromised patients.

Dr. Donna Bilu Martin

This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University, Davie, Fla.; Kiran C. Patel, Tampa Bay Regional Campus; and Dr. Bilu Martin.
 

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

Cleveland Clinic. Tinea manuum: Symptoms, causes & treatment. 2022. https://my.clevelandclinic.org/health/diseases/24063-tinea-manuum.

Ugalde-Trejo NX et al. Curr Fungal Infect Rep. 2022 Nov 17. doi: 10.1007/s12281-022-00447-9.

Mizumoto J. Cureus. 2021 Dec 27;13(12):e20758.

Two feet–one hand syndrome

Two feet–one hand syndrome is a common term used to describe tinea manuum on one hand with bilateral tinea pedis. This condition, also known as ringworm, is a fungal infection caused by a dermatophyte, and presents as a superficial annular or circular rash with a raised, scaly border.

Symptoms include dryness and itchiness, and the lesions may appear red-pink on lighter skin and gray-brown on darker skin types. Although these infections can arise in a variety of combinations, two feet–one hand syndrome occurs in about 60% of cases. Trichophyton rubrum is the most common agent.

Diagnosis is made by patient history, dermoscopic visualization, and staining of skin scraping with KOH or fungal culture. Dermatophytes prefer moist, warm environments, so this disease is prevalent in tropical conditions and associated with moist public areas such as locker rooms and showers. As a result, tinea pedis is also nicknamed “athlete’s foot” for its common presentation in athletes. The fungus spreads easily through contact and can survive on infected surfaces, so patients often self-inoculate by touching/scratching the affected area then touching another body part. Cautions that should be taken to avoid transmission include not sharing personal care products, washing the area and keeping it dry, and avoiding close, humid environments.

Dr. Donna Bilu Martin

The syndrome is highly associated with onychomycosis, which can be more difficult to treat and often requires oral antifungals. Tinea manuum is commonly misdiagnosed as hand dermatitis or eczema and treated with topical steroids, which will exacerbate or flare the tinea.

Two feet–one hand syndrome can typically be treated with over-the-counter topical antifungal medications such as miconazole or clotrimazole. Topical ketoconazole may be prescribed, and oral terbinafine or itraconazole are used in more severe cases when a larger body surface area is affected or in immunocompromised patients.

Dr. Donna Bilu Martin

This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University, Davie, Fla.; Kiran C. Patel, Tampa Bay Regional Campus; and Dr. Bilu Martin.
 

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

Cleveland Clinic. Tinea manuum: Symptoms, causes & treatment. 2022. https://my.clevelandclinic.org/health/diseases/24063-tinea-manuum.

Ugalde-Trejo NX et al. Curr Fungal Infect Rep. 2022 Nov 17. doi: 10.1007/s12281-022-00447-9.

Mizumoto J. Cureus. 2021 Dec 27;13(12):e20758.

With the rising popularity of weight-loss drug injections, I’ve received many questions from patients about the pros, cons, and costs. While Ozempic (semaglutide) is perhaps the best known, it’s technically an agent approved only for type 2 diabetes that has been used off label for obesity. The same substance, semaglutide, is approved for use in obesity, but at a higher dose, under the brand name Wegovy. Alternatives are available, and results will vary depending on the specific agent used and the individual.

Ultimately, I decided to try these new injections for myself. I am not a paid representative for, nor an advocate of, any of these medications; I’m here only to share my personal experience.

In my discussions with patients about weight, I sometimes felt like an imposter. While I was overweight by medical standards, I fortunately had none of the underlying health problems. I wasn’t on medications for blood pressure nor did I have diabetes, but I was counseling people to lose weight and eat better while not always following my own advice.

Since having children and turning 40, my metabolism, like many other women’s, seems to have plummeted. I tried a number of older weight-loss medications, like phentermine and phendimetrazine, under the supervision of medical professionals.

Each time, the efforts worked for a short while, particularly when I followed good portion control and practiced moderate exercise. Once the side effects (that is, tachycardia, palpitations, mood changes, constipation) became intolerable, or I became tired or fearful of being on the medications too long, I’d stop and I would regain some of the weight.

When the newer subcutaneous injectable medications arrived on the scene and I started to talk to my patients about them, I was intrigued by their novel mode of action and seeming benefits.

These medications, glucagonlike peptide–1 (GLP-1) receptor agonists, were first approved for type 2 diabetes, and it soon became apparent that patients were losing significant amounts of weight taking them, so manufacturers conducted further trials in obesity patients without type 2 diabetes.

The first of these, liraglutide, is injected daily and was first approved as Victoza for type 2 diabetes; it later received an additional approval for obesity, in December 2014, as Saxenda.

Semaglutide, another of the new GLP-1 agonists, was first approved for type 2 diabetes as Ozempic but again was found to lead to substantial weight loss, so a subsequent approval of the drug for obesity, as Wegovy, came in June 2021. Semaglutide is injected once a week.

Semaglutide was branded a “game changer” when it was licensed for obesity because the mean weight loss seen in trials was around 15%, more than for any other drug and approaching what could be achieved with bariatric surgery, some doctors said.

These medications work in a different way from the older weight loss drugs, which had focused on the use of amphetamines. The newer medications became very popular because treating obesity helps lower blood glucose, blood pressure, cholesterol, kidney disease risk, and other comorbidities that occur with diabetes. Plus, for most people, there were fewer side effects.

I first tried Saxenda when it arrived on the market, via some samples that our pharmaceutical representative brought, both out of curiosity and to see if it would help me lose the stubborn baby weight. I ended up stopping the daily injections after my second or third week because of nausea and vomiting. I took a break, got a prescription for antinausea medicine, and tried again because it did indeed decrease my appetite. However, when I took my prescription to the pharmacy, my insurance wouldn’t cover it. It happens to doctors, too.

Fast-forward to 2017-2018. The baby weight was still holding on despite lifestyle changes, diet, and exercising. The newer drug classes hit the market, and again we had samples from our reps. When our rep explained the potential for weight loss in patients without diabetes, I tried Ozempic off label. Within the first 2 weeks, I noticed a 3- to- 5-lb weight loss.

When Ozempic was on backorder, I switched to a low dose of Mounjaro (tirzepatide), a new dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, approved for type 2 diabetes in May 2022, again using it off label as a weekly injection, as it isn’t currently approved for weight loss. However, it does produce significant weight loss and is awaiting approval for obesity.

With these new medications, I noticed that both my patients and I didn’t complain as much about nausea and vomiting, but I did experience stomach upset, constipation, and acid reflux.

The appetite suppression is effective. It slows down the emptying of the gut so I feel full longer. I’ve lost 30 lb with these weekly injections and would like to lose another 20 lb. I follow a routine of reasonable, portion-controlled eating and moderate exercise (30 minutes of cardiovascular activity at least two to three times a week).

Discontinuing the medications may cause rebound weight gain, especially if I’m no longer following a routine of healthy eating and/or moderate exercise. I deal with minimal constipation by taking stool softeners, and I take antacids for acid reflux.

Here’s what I recommend applying when working with patients who have obesity: First, explain how these medications work. Then conduct a health history to make sure these injections are right for them. Patients with a family history of pancreatic cancer can’t take these medications. You also want to monitor use in patients with a history of hypoglycemia so their blood sugar doesn’t drop too low. It’s also important to make sure your patients are able to afford the medication. My husband takes Ozempic for diabetes, and recently we were told that a refill would cost about $1,500 a month, even with insurance. “Covered” doesn’t necessarily mean affordable.

Take a baseline hemoglobin A1c and repeat it after the patient has been on the medication for 2-3 weeks. Also remind them that they can’t rely solely on the medication but need to practice portion control and healthier eating and to exercise more.

For myself, I want to lose those remaining 20 lb or so by eating healthy and being physically active without having to rely on medication for the rest of my life. Research on these medications is still early so we don’t know the long-term effects yet.

As clinicians, I feel it’s okay to be honest with our patients about our own personal struggles to help them understand that they are not alone and that losing weight is a challenge for everyone.

Dr. Swiner is a family physician in Durham, N.C. She reported no conflicts of interest.

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

With the rising popularity of weight-loss drug injections, I’ve received many questions from patients about the pros, cons, and costs. While Ozempic (semaglutide) is perhaps the best known, it’s technically an agent approved only for type 2 diabetes that has been used off label for obesity. The same substance, semaglutide, is approved for use in obesity, but at a higher dose, under the brand name Wegovy. Alternatives are available, and results will vary depending on the specific agent used and the individual.

Ultimately, I decided to try these new injections for myself. I am not a paid representative for, nor an advocate of, any of these medications; I’m here only to share my personal experience.

In my discussions with patients about weight, I sometimes felt like an imposter. While I was overweight by medical standards, I fortunately had none of the underlying health problems. I wasn’t on medications for blood pressure nor did I have diabetes, but I was counseling people to lose weight and eat better while not always following my own advice.

Since having children and turning 40, my metabolism, like many other women’s, seems to have plummeted. I tried a number of older weight-loss medications, like phentermine and phendimetrazine, under the supervision of medical professionals.

Each time, the efforts worked for a short while, particularly when I followed good portion control and practiced moderate exercise. Once the side effects (that is, tachycardia, palpitations, mood changes, constipation) became intolerable, or I became tired or fearful of being on the medications too long, I’d stop and I would regain some of the weight.

When the newer subcutaneous injectable medications arrived on the scene and I started to talk to my patients about them, I was intrigued by their novel mode of action and seeming benefits.

These medications, glucagonlike peptide–1 (GLP-1) receptor agonists, were first approved for type 2 diabetes, and it soon became apparent that patients were losing significant amounts of weight taking them, so manufacturers conducted further trials in obesity patients without type 2 diabetes.

The first of these, liraglutide, is injected daily and was first approved as Victoza for type 2 diabetes; it later received an additional approval for obesity, in December 2014, as Saxenda.

Semaglutide, another of the new GLP-1 agonists, was first approved for type 2 diabetes as Ozempic but again was found to lead to substantial weight loss, so a subsequent approval of the drug for obesity, as Wegovy, came in June 2021. Semaglutide is injected once a week.

Semaglutide was branded a “game changer” when it was licensed for obesity because the mean weight loss seen in trials was around 15%, more than for any other drug and approaching what could be achieved with bariatric surgery, some doctors said.

These medications work in a different way from the older weight loss drugs, which had focused on the use of amphetamines. The newer medications became very popular because treating obesity helps lower blood glucose, blood pressure, cholesterol, kidney disease risk, and other comorbidities that occur with diabetes. Plus, for most people, there were fewer side effects.

I first tried Saxenda when it arrived on the market, via some samples that our pharmaceutical representative brought, both out of curiosity and to see if it would help me lose the stubborn baby weight. I ended up stopping the daily injections after my second or third week because of nausea and vomiting. I took a break, got a prescription for antinausea medicine, and tried again because it did indeed decrease my appetite. However, when I took my prescription to the pharmacy, my insurance wouldn’t cover it. It happens to doctors, too.

Fast-forward to 2017-2018. The baby weight was still holding on despite lifestyle changes, diet, and exercising. The newer drug classes hit the market, and again we had samples from our reps. When our rep explained the potential for weight loss in patients without diabetes, I tried Ozempic off label. Within the first 2 weeks, I noticed a 3- to- 5-lb weight loss.

When Ozempic was on backorder, I switched to a low dose of Mounjaro (tirzepatide), a new dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, approved for type 2 diabetes in May 2022, again using it off label as a weekly injection, as it isn’t currently approved for weight loss. However, it does produce significant weight loss and is awaiting approval for obesity.

With these new medications, I noticed that both my patients and I didn’t complain as much about nausea and vomiting, but I did experience stomach upset, constipation, and acid reflux.

The appetite suppression is effective. It slows down the emptying of the gut so I feel full longer. I’ve lost 30 lb with these weekly injections and would like to lose another 20 lb. I follow a routine of reasonable, portion-controlled eating and moderate exercise (30 minutes of cardiovascular activity at least two to three times a week).

Discontinuing the medications may cause rebound weight gain, especially if I’m no longer following a routine of healthy eating and/or moderate exercise. I deal with minimal constipation by taking stool softeners, and I take antacids for acid reflux.

Here’s what I recommend applying when working with patients who have obesity: First, explain how these medications work. Then conduct a health history to make sure these injections are right for them. Patients with a family history of pancreatic cancer can’t take these medications. You also want to monitor use in patients with a history of hypoglycemia so their blood sugar doesn’t drop too low. It’s also important to make sure your patients are able to afford the medication. My husband takes Ozempic for diabetes, and recently we were told that a refill would cost about $1,500 a month, even with insurance. “Covered” doesn’t necessarily mean affordable.

Take a baseline hemoglobin A1c and repeat it after the patient has been on the medication for 2-3 weeks. Also remind them that they can’t rely solely on the medication but need to practice portion control and healthier eating and to exercise more.

For myself, I want to lose those remaining 20 lb or so by eating healthy and being physically active without having to rely on medication for the rest of my life. Research on these medications is still early so we don’t know the long-term effects yet.

As clinicians, I feel it’s okay to be honest with our patients about our own personal struggles to help them understand that they are not alone and that losing weight is a challenge for everyone.

Dr. Swiner is a family physician in Durham, N.C. She reported no conflicts of interest.

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

With the rising popularity of weight-loss drug injections, I’ve received many questions from patients about the pros, cons, and costs. While Ozempic (semaglutide) is perhaps the best known, it’s technically an agent approved only for type 2 diabetes that has been used off label for obesity. The same substance, semaglutide, is approved for use in obesity, but at a higher dose, under the brand name Wegovy. Alternatives are available, and results will vary depending on the specific agent used and the individual.

Ultimately, I decided to try these new injections for myself. I am not a paid representative for, nor an advocate of, any of these medications; I’m here only to share my personal experience.

In my discussions with patients about weight, I sometimes felt like an imposter. While I was overweight by medical standards, I fortunately had none of the underlying health problems. I wasn’t on medications for blood pressure nor did I have diabetes, but I was counseling people to lose weight and eat better while not always following my own advice.

Since having children and turning 40, my metabolism, like many other women’s, seems to have plummeted. I tried a number of older weight-loss medications, like phentermine and phendimetrazine, under the supervision of medical professionals.

Each time, the efforts worked for a short while, particularly when I followed good portion control and practiced moderate exercise. Once the side effects (that is, tachycardia, palpitations, mood changes, constipation) became intolerable, or I became tired or fearful of being on the medications too long, I’d stop and I would regain some of the weight.

When the newer subcutaneous injectable medications arrived on the scene and I started to talk to my patients about them, I was intrigued by their novel mode of action and seeming benefits.

These medications, glucagonlike peptide–1 (GLP-1) receptor agonists, were first approved for type 2 diabetes, and it soon became apparent that patients were losing significant amounts of weight taking them, so manufacturers conducted further trials in obesity patients without type 2 diabetes.

The first of these, liraglutide, is injected daily and was first approved as Victoza for type 2 diabetes; it later received an additional approval for obesity, in December 2014, as Saxenda.

Semaglutide, another of the new GLP-1 agonists, was first approved for type 2 diabetes as Ozempic but again was found to lead to substantial weight loss, so a subsequent approval of the drug for obesity, as Wegovy, came in June 2021. Semaglutide is injected once a week.

Semaglutide was branded a “game changer” when it was licensed for obesity because the mean weight loss seen in trials was around 15%, more than for any other drug and approaching what could be achieved with bariatric surgery, some doctors said.

These medications work in a different way from the older weight loss drugs, which had focused on the use of amphetamines. The newer medications became very popular because treating obesity helps lower blood glucose, blood pressure, cholesterol, kidney disease risk, and other comorbidities that occur with diabetes. Plus, for most people, there were fewer side effects.

I first tried Saxenda when it arrived on the market, via some samples that our pharmaceutical representative brought, both out of curiosity and to see if it would help me lose the stubborn baby weight. I ended up stopping the daily injections after my second or third week because of nausea and vomiting. I took a break, got a prescription for antinausea medicine, and tried again because it did indeed decrease my appetite. However, when I took my prescription to the pharmacy, my insurance wouldn’t cover it. It happens to doctors, too.

Fast-forward to 2017-2018. The baby weight was still holding on despite lifestyle changes, diet, and exercising. The newer drug classes hit the market, and again we had samples from our reps. When our rep explained the potential for weight loss in patients without diabetes, I tried Ozempic off label. Within the first 2 weeks, I noticed a 3- to- 5-lb weight loss.

When Ozempic was on backorder, I switched to a low dose of Mounjaro (tirzepatide), a new dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, approved for type 2 diabetes in May 2022, again using it off label as a weekly injection, as it isn’t currently approved for weight loss. However, it does produce significant weight loss and is awaiting approval for obesity.

With these new medications, I noticed that both my patients and I didn’t complain as much about nausea and vomiting, but I did experience stomach upset, constipation, and acid reflux.

The appetite suppression is effective. It slows down the emptying of the gut so I feel full longer. I’ve lost 30 lb with these weekly injections and would like to lose another 20 lb. I follow a routine of reasonable, portion-controlled eating and moderate exercise (30 minutes of cardiovascular activity at least two to three times a week).

Discontinuing the medications may cause rebound weight gain, especially if I’m no longer following a routine of healthy eating and/or moderate exercise. I deal with minimal constipation by taking stool softeners, and I take antacids for acid reflux.

Here’s what I recommend applying when working with patients who have obesity: First, explain how these medications work. Then conduct a health history to make sure these injections are right for them. Patients with a family history of pancreatic cancer can’t take these medications. You also want to monitor use in patients with a history of hypoglycemia so their blood sugar doesn’t drop too low. It’s also important to make sure your patients are able to afford the medication. My husband takes Ozempic for diabetes, and recently we were told that a refill would cost about $1,500 a month, even with insurance. “Covered” doesn’t necessarily mean affordable.

Take a baseline hemoglobin A1c and repeat it after the patient has been on the medication for 2-3 weeks. Also remind them that they can’t rely solely on the medication but need to practice portion control and healthier eating and to exercise more.

For myself, I want to lose those remaining 20 lb or so by eating healthy and being physically active without having to rely on medication for the rest of my life. Research on these medications is still early so we don’t know the long-term effects yet.

As clinicians, I feel it’s okay to be honest with our patients about our own personal struggles to help them understand that they are not alone and that losing weight is a challenge for everyone.

Dr. Swiner is a family physician in Durham, N.C. She reported no conflicts of interest.

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

A 43-year-old man presents to the emergency department with dizziness and a 6-hour history of passing maroon stool. He has been in good health with the only medical problem in his history being depression.

He is taking sertraline. On exam, his blood pressure is 100/60, and his pulse is 100, both while lying down. His blood pressure while standing is 90/60 and his pulse while standing is 130. The rest of his exam is normal. His lab values include hemoglobin of 10, hematocrit of 30, white blood cell of 4.6, platelet count of 175,000, sodium of 142, chloride of 100, bicarbonate of 24, potassium of 3.8, blood urea nitrogen (BUN) of 38, and creatinine clearance (Cr) of 1.1.

What is the most likely source of his bleeding?

A. Gastric ulcer

B. Meckel’s diverticulum

C. Arteriovenous malformation

D. Diverticulosis

E. Hemorrhoids

What makes the most sense

The most likely cause of this patient’s maroon stool is an upper gastrointestinal bleed, so it would make the most sense for a gastric ulcer to be the source of his bleeding. The clue here is the very high BUN/Cr ratio.

We were all taught early in our training that a high BUN/Cr ratio represented volume depletion. This is certainly the most common cause, but very high BUN/Cr ratios (over 30) can represent causes beyond volume depletion.

Witting and colleagues studied factors that predicted upper GI bleeding in patients presenting without hematemesis. They found that the three strongest predictors were black stool (odds ratio, 16.6), BUN/Cr ratio greater than 30 (OR, 10), and age greater than 50 (OR, 8.4).¹

Srygley and colleagues reviewed high-quality studies of factors associated with upper GI bleeding.² Factors that were found to increase the likelihood of an upper gastrointestinal bleed were Melenic stool on exam (likelihood ratio, 25), blood or coffee grounds on nasogastric aspiration (LR, 9.6), and BUN/Cr ratio greater than 30 (LR, 7.5).

Very high BUN/Cr ratios can indicate problems other than UGI bleeding and volume depletion. High BUN/Cr ratios are seen in patients with heart failure.

Zhang and colleagues studied if a high BUN/Cr ratio helped distinguish heart failure from asthma and chronic obstructive pulmonary disease (COPD).³ They found that, compared with those in the asthma group, the BUN/Cr ratios were significantly increased in the heart failure group (P < .05), whereas no significant differences in BUN/Cr ratios were found between the asthma and COPD groups.

Cheang and colleagues conducted their own study, as well as a meta-analysis, looking to see if high BUN/Cr ratios predicted increased mortality in patients with acute heart failure.⁴ In the meta-analysis of 8 studies (including their own), they found that the highest BUN/Cr ratio category was associated with an 77% higher all-cause mortality than the lowest category (hazard ratio, 1.77; 95% confidence interval, 1.52-2.07).

High dose corticosteroids can raise BUN levels, especially in patients with chronic kidney disease, and cause unexpectedly high BUN/Cr ratios.
 

Pearl

Very high BUN/Cr ratios (greater than 30) can signify upper GI bleeding, heart failure, or high-dose corticosteroid use.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Am J Emerg Med. 2006 May;24(3):280-5.

2. JAMA. 2012;307(10):1072-9.

3. Comput Math Methods Med. 2022 Jul 21. doi: 10.1155/2022/4586458.

4. Cardiorenal Med. 2020;10:415-28.

A 43-year-old man presents to the emergency department with dizziness and a 6-hour history of passing maroon stool. He has been in good health with the only medical problem in his history being depression.

He is taking sertraline. On exam, his blood pressure is 100/60, and his pulse is 100, both while lying down. His blood pressure while standing is 90/60 and his pulse while standing is 130. The rest of his exam is normal. His lab values include hemoglobin of 10, hematocrit of 30, white blood cell of 4.6, platelet count of 175,000, sodium of 142, chloride of 100, bicarbonate of 24, potassium of 3.8, blood urea nitrogen (BUN) of 38, and creatinine clearance (Cr) of 1.1.

What is the most likely source of his bleeding?

A. Gastric ulcer

B. Meckel’s diverticulum

C. Arteriovenous malformation

D. Diverticulosis

E. Hemorrhoids

What makes the most sense

The most likely cause of this patient’s maroon stool is an upper gastrointestinal bleed, so it would make the most sense for a gastric ulcer to be the source of his bleeding. The clue here is the very high BUN/Cr ratio.

We were all taught early in our training that a high BUN/Cr ratio represented volume depletion. This is certainly the most common cause, but very high BUN/Cr ratios (over 30) can represent causes beyond volume depletion.

Witting and colleagues studied factors that predicted upper GI bleeding in patients presenting without hematemesis. They found that the three strongest predictors were black stool (odds ratio, 16.6), BUN/Cr ratio greater than 30 (OR, 10), and age greater than 50 (OR, 8.4).¹

Srygley and colleagues reviewed high-quality studies of factors associated with upper GI bleeding.² Factors that were found to increase the likelihood of an upper gastrointestinal bleed were Melenic stool on exam (likelihood ratio, 25), blood or coffee grounds on nasogastric aspiration (LR, 9.6), and BUN/Cr ratio greater than 30 (LR, 7.5).

Very high BUN/Cr ratios can indicate problems other than UGI bleeding and volume depletion. High BUN/Cr ratios are seen in patients with heart failure.

Zhang and colleagues studied if a high BUN/Cr ratio helped distinguish heart failure from asthma and chronic obstructive pulmonary disease (COPD).³ They found that, compared with those in the asthma group, the BUN/Cr ratios were significantly increased in the heart failure group (P < .05), whereas no significant differences in BUN/Cr ratios were found between the asthma and COPD groups.

Cheang and colleagues conducted their own study, as well as a meta-analysis, looking to see if high BUN/Cr ratios predicted increased mortality in patients with acute heart failure.⁴ In the meta-analysis of 8 studies (including their own), they found that the highest BUN/Cr ratio category was associated with an 77% higher all-cause mortality than the lowest category (hazard ratio, 1.77; 95% confidence interval, 1.52-2.07).

High dose corticosteroids can raise BUN levels, especially in patients with chronic kidney disease, and cause unexpectedly high BUN/Cr ratios.
 

Pearl

Very high BUN/Cr ratios (greater than 30) can signify upper GI bleeding, heart failure, or high-dose corticosteroid use.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Am J Emerg Med. 2006 May;24(3):280-5.

2. JAMA. 2012;307(10):1072-9.

3. Comput Math Methods Med. 2022 Jul 21. doi: 10.1155/2022/4586458.

4. Cardiorenal Med. 2020;10:415-28.

A 43-year-old man presents to the emergency department with dizziness and a 6-hour history of passing maroon stool. He has been in good health with the only medical problem in his history being depression.

He is taking sertraline. On exam, his blood pressure is 100/60, and his pulse is 100, both while lying down. His blood pressure while standing is 90/60 and his pulse while standing is 130. The rest of his exam is normal. His lab values include hemoglobin of 10, hematocrit of 30, white blood cell of 4.6, platelet count of 175,000, sodium of 142, chloride of 100, bicarbonate of 24, potassium of 3.8, blood urea nitrogen (BUN) of 38, and creatinine clearance (Cr) of 1.1.

What is the most likely source of his bleeding?

A. Gastric ulcer

B. Meckel’s diverticulum

C. Arteriovenous malformation

D. Diverticulosis

E. Hemorrhoids

What makes the most sense

The most likely cause of this patient’s maroon stool is an upper gastrointestinal bleed, so it would make the most sense for a gastric ulcer to be the source of his bleeding. The clue here is the very high BUN/Cr ratio.

We were all taught early in our training that a high BUN/Cr ratio represented volume depletion. This is certainly the most common cause, but very high BUN/Cr ratios (over 30) can represent causes beyond volume depletion.

Witting and colleagues studied factors that predicted upper GI bleeding in patients presenting without hematemesis. They found that the three strongest predictors were black stool (odds ratio, 16.6), BUN/Cr ratio greater than 30 (OR, 10), and age greater than 50 (OR, 8.4).¹

Srygley and colleagues reviewed high-quality studies of factors associated with upper GI bleeding.² Factors that were found to increase the likelihood of an upper gastrointestinal bleed were Melenic stool on exam (likelihood ratio, 25), blood or coffee grounds on nasogastric aspiration (LR, 9.6), and BUN/Cr ratio greater than 30 (LR, 7.5).

Very high BUN/Cr ratios can indicate problems other than UGI bleeding and volume depletion. High BUN/Cr ratios are seen in patients with heart failure.

Zhang and colleagues studied if a high BUN/Cr ratio helped distinguish heart failure from asthma and chronic obstructive pulmonary disease (COPD).³ They found that, compared with those in the asthma group, the BUN/Cr ratios were significantly increased in the heart failure group (P < .05), whereas no significant differences in BUN/Cr ratios were found between the asthma and COPD groups.

Cheang and colleagues conducted their own study, as well as a meta-analysis, looking to see if high BUN/Cr ratios predicted increased mortality in patients with acute heart failure.⁴ In the meta-analysis of 8 studies (including their own), they found that the highest BUN/Cr ratio category was associated with an 77% higher all-cause mortality than the lowest category (hazard ratio, 1.77; 95% confidence interval, 1.52-2.07).

High dose corticosteroids can raise BUN levels, especially in patients with chronic kidney disease, and cause unexpectedly high BUN/Cr ratios.
 

Pearl

Very high BUN/Cr ratios (greater than 30) can signify upper GI bleeding, heart failure, or high-dose corticosteroid use.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Am J Emerg Med. 2006 May;24(3):280-5.

2. JAMA. 2012;307(10):1072-9.

3. Comput Math Methods Med. 2022 Jul 21. doi: 10.1155/2022/4586458.

4. Cardiorenal Med. 2020;10:415-28.