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When patient autonomy gets in the way
“Why didn’t you see that patient?”
The hospitalist on the phone was angry. He’d wanted the patient seen by neurology and cleared for discharge. Apparently, I hadn’t complied.
Actually, that isn’t true. I was on call, so I had dutifully dragged myself in (with the help of some coffee), reviewed the chart, and gone in to see the fellow.
The patient, however, had other ideas. He said he was sick of doctors, didn’t like them, didn’t want to see me, and asked me to leave. So I did.
This threw off the hospitalist’s well-choreographed day of admissions and discharges. Without me seeing the patient, he had to either discharge him on his own decision or find another neurologist who would do it.
Sorry, but I’m not going to force this issue. If a patient doesn’t want to see me, it’s not worth fighting over. Believe me, I get paid to see patients, so I don’t have much incentive to just walk away.
But at the same time I have to respect patients’ decisions. While a neurology consult is pretty noninvasive, it’s still a part of medicine. If a patient doesn’t want to see me, I’m not going to force them to.
Granted, there are exceptions. Obviously, if the patient is fairly demented or otherwise not mentally competent to make such a decision, I’ll see them. In those cases, their deteriorating mental status is likely the reason for the consult.
But the fellow that day seemed alert and reasonable, and there was nothing in the chart about confusion. So I’m going to assume he knew what he was doing when he told me to go away.
The hospitalist didn’t see this as an issue, but I did. I’m sorry if it messes up the discharge planning, but that’s not my fault. It’s the patient’s decision.
While I may disagree at times with patients’ decisions, their autonomy is still central to medicine. I respect and believe in that, even if it makes things more difficult for those around them.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
“Why didn’t you see that patient?”
The hospitalist on the phone was angry. He’d wanted the patient seen by neurology and cleared for discharge. Apparently, I hadn’t complied.
Actually, that isn’t true. I was on call, so I had dutifully dragged myself in (with the help of some coffee), reviewed the chart, and gone in to see the fellow.
The patient, however, had other ideas. He said he was sick of doctors, didn’t like them, didn’t want to see me, and asked me to leave. So I did.
This threw off the hospitalist’s well-choreographed day of admissions and discharges. Without me seeing the patient, he had to either discharge him on his own decision or find another neurologist who would do it.
Sorry, but I’m not going to force this issue. If a patient doesn’t want to see me, it’s not worth fighting over. Believe me, I get paid to see patients, so I don’t have much incentive to just walk away.
But at the same time I have to respect patients’ decisions. While a neurology consult is pretty noninvasive, it’s still a part of medicine. If a patient doesn’t want to see me, I’m not going to force them to.
Granted, there are exceptions. Obviously, if the patient is fairly demented or otherwise not mentally competent to make such a decision, I’ll see them. In those cases, their deteriorating mental status is likely the reason for the consult.
But the fellow that day seemed alert and reasonable, and there was nothing in the chart about confusion. So I’m going to assume he knew what he was doing when he told me to go away.
The hospitalist didn’t see this as an issue, but I did. I’m sorry if it messes up the discharge planning, but that’s not my fault. It’s the patient’s decision.
While I may disagree at times with patients’ decisions, their autonomy is still central to medicine. I respect and believe in that, even if it makes things more difficult for those around them.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
“Why didn’t you see that patient?”
The hospitalist on the phone was angry. He’d wanted the patient seen by neurology and cleared for discharge. Apparently, I hadn’t complied.
Actually, that isn’t true. I was on call, so I had dutifully dragged myself in (with the help of some coffee), reviewed the chart, and gone in to see the fellow.
The patient, however, had other ideas. He said he was sick of doctors, didn’t like them, didn’t want to see me, and asked me to leave. So I did.
This threw off the hospitalist’s well-choreographed day of admissions and discharges. Without me seeing the patient, he had to either discharge him on his own decision or find another neurologist who would do it.
Sorry, but I’m not going to force this issue. If a patient doesn’t want to see me, it’s not worth fighting over. Believe me, I get paid to see patients, so I don’t have much incentive to just walk away.
But at the same time I have to respect patients’ decisions. While a neurology consult is pretty noninvasive, it’s still a part of medicine. If a patient doesn’t want to see me, I’m not going to force them to.
Granted, there are exceptions. Obviously, if the patient is fairly demented or otherwise not mentally competent to make such a decision, I’ll see them. In those cases, their deteriorating mental status is likely the reason for the consult.
But the fellow that day seemed alert and reasonable, and there was nothing in the chart about confusion. So I’m going to assume he knew what he was doing when he told me to go away.
The hospitalist didn’t see this as an issue, but I did. I’m sorry if it messes up the discharge planning, but that’s not my fault. It’s the patient’s decision.
While I may disagree at times with patients’ decisions, their autonomy is still central to medicine. I respect and believe in that, even if it makes things more difficult for those around them.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Supporting elimination of nonmedical vaccine exemptions
Let’s suppose your first patient of the morning is a 2-month-old you have never seen before. The family arrives 10 minutes late because they are still getting the dressing-undressing-diaper change-car seat–adjusting thing worked out. Father is a computer programmer. Mother lists her occupation as nutrition counselor. The child is gaining. Breastfeeding seems to come naturally to the dyad.
As the visit draws to a close, you take the matter-of-fact approach and say, “The nurse will be in shortly with the vaccines do you have any questions.” Well ... it turns out the parents don’t feel comfortable with vaccines. They claim to understand the science and feel that vaccines make sense for some families. But they feel that for themselves, with a healthy lifestyle and God’s benevolence their son will be protected without having to introduce a host of foreign substances into his body.
What word best describes your reaction? Anger? Frustration? Disappointment (in our education system)? Maybe you’re angry at yourself for failing to make it clear in your office pamphlet and social media feeds that to protect your other patients, you no longer accept families who refuse immunizations for the common childhood diseases.
The American Academy of Pediatrics says it feels your pain, and its Annual Leadership Forum made eliminating nonmedical vaccine exemption laws its top priority in 2019. As part of its effort to help, the AAP Board of Directors was asked to advocate for the creation of a toolkit of strategies for Academy chapters facing the challenge of nonmedical exemptions. As an initial step to this process, three physicians in the department of pediatrics at the Denver Health Medical Center have begun interviewing religious leaders in hopes of developing “clergy-specific vaccine educational materials and deriv[ing] best practices for engaging them as vaccination advocates.” The investigators describe their plan and initial findings in Pediatrics (2019 Oct. doi: 10.1542/peds.2019-0933). Although they acknowledged that their efforts may not provide a quick solution to the nonmedical exemption problem, they hope that including more stakeholders and engendering trust will help future discussions.
Fourteen pages deeper into that issue of Pediatrics is the runner-up submission of this year’s Section on Pediatric Trainees essay competition titled “What I Learned From the Antivaccine Movement” (2019 Oct. doi: 10.1542/peds.2019-2384). Alana C. Ju, MD, describes the 2-hour ordeal she endured to testify at the California State Capitol in support of a state Senate bill aimed at tightening the regulations for vaccine medical exemptions. Totally unprepared for the “level of vitriol” aimed at her and other supporters of the bill, she was “accused of violating her duty as” a pediatrician because she was failing to protect children. The supporters were called “greedy, ignorant, and negligent.”
To her credit, Dr. Ju was able to step back from this assault and began looking at the faces of her accusers and learned that, “they too, felt strongly about children’s health.” She realized that “focusing on perceived ignorance is counterproductive.” She now hopes that by focusing on the shared goal of what is best for children, “we can all be better advocates.”
Both of these articles have a warm sort of kumbaya feel about them. It never is a bad idea to learn more about those with whom we disagree. But before huddling up too close to the campfire, we must realize that there is good evidence that sharing the scientific data with vaccine-hesitant parents doesn’t convert them into vaccine acceptors. In fact, it may strengthen their resolve to resist (Nyhan et al. “Effective Messages in Vaccine Promotion: A Randomized Trial,” Pediatrics. 2014 Apr;133[4] e835-42).
We are unlikely to convert many anti-vaxxers by sitting down together. Our target audience needs to be legislators and the majority of people who do vaccinate their children. These are the voters who will support legislation to eliminate nonmedical vaccine exemptions. To characterize anti-vaxxers as despicable ignorants is untrue and serves no purpose. We all do care about the health of children. However,
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
*This article has been updated 1/22/2020.
Let’s suppose your first patient of the morning is a 2-month-old you have never seen before. The family arrives 10 minutes late because they are still getting the dressing-undressing-diaper change-car seat–adjusting thing worked out. Father is a computer programmer. Mother lists her occupation as nutrition counselor. The child is gaining. Breastfeeding seems to come naturally to the dyad.
As the visit draws to a close, you take the matter-of-fact approach and say, “The nurse will be in shortly with the vaccines do you have any questions.” Well ... it turns out the parents don’t feel comfortable with vaccines. They claim to understand the science and feel that vaccines make sense for some families. But they feel that for themselves, with a healthy lifestyle and God’s benevolence their son will be protected without having to introduce a host of foreign substances into his body.
What word best describes your reaction? Anger? Frustration? Disappointment (in our education system)? Maybe you’re angry at yourself for failing to make it clear in your office pamphlet and social media feeds that to protect your other patients, you no longer accept families who refuse immunizations for the common childhood diseases.
The American Academy of Pediatrics says it feels your pain, and its Annual Leadership Forum made eliminating nonmedical vaccine exemption laws its top priority in 2019. As part of its effort to help, the AAP Board of Directors was asked to advocate for the creation of a toolkit of strategies for Academy chapters facing the challenge of nonmedical exemptions. As an initial step to this process, three physicians in the department of pediatrics at the Denver Health Medical Center have begun interviewing religious leaders in hopes of developing “clergy-specific vaccine educational materials and deriv[ing] best practices for engaging them as vaccination advocates.” The investigators describe their plan and initial findings in Pediatrics (2019 Oct. doi: 10.1542/peds.2019-0933). Although they acknowledged that their efforts may not provide a quick solution to the nonmedical exemption problem, they hope that including more stakeholders and engendering trust will help future discussions.
Fourteen pages deeper into that issue of Pediatrics is the runner-up submission of this year’s Section on Pediatric Trainees essay competition titled “What I Learned From the Antivaccine Movement” (2019 Oct. doi: 10.1542/peds.2019-2384). Alana C. Ju, MD, describes the 2-hour ordeal she endured to testify at the California State Capitol in support of a state Senate bill aimed at tightening the regulations for vaccine medical exemptions. Totally unprepared for the “level of vitriol” aimed at her and other supporters of the bill, she was “accused of violating her duty as” a pediatrician because she was failing to protect children. The supporters were called “greedy, ignorant, and negligent.”
To her credit, Dr. Ju was able to step back from this assault and began looking at the faces of her accusers and learned that, “they too, felt strongly about children’s health.” She realized that “focusing on perceived ignorance is counterproductive.” She now hopes that by focusing on the shared goal of what is best for children, “we can all be better advocates.”
Both of these articles have a warm sort of kumbaya feel about them. It never is a bad idea to learn more about those with whom we disagree. But before huddling up too close to the campfire, we must realize that there is good evidence that sharing the scientific data with vaccine-hesitant parents doesn’t convert them into vaccine acceptors. In fact, it may strengthen their resolve to resist (Nyhan et al. “Effective Messages in Vaccine Promotion: A Randomized Trial,” Pediatrics. 2014 Apr;133[4] e835-42).
We are unlikely to convert many anti-vaxxers by sitting down together. Our target audience needs to be legislators and the majority of people who do vaccinate their children. These are the voters who will support legislation to eliminate nonmedical vaccine exemptions. To characterize anti-vaxxers as despicable ignorants is untrue and serves no purpose. We all do care about the health of children. However,
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
*This article has been updated 1/22/2020.
Let’s suppose your first patient of the morning is a 2-month-old you have never seen before. The family arrives 10 minutes late because they are still getting the dressing-undressing-diaper change-car seat–adjusting thing worked out. Father is a computer programmer. Mother lists her occupation as nutrition counselor. The child is gaining. Breastfeeding seems to come naturally to the dyad.
As the visit draws to a close, you take the matter-of-fact approach and say, “The nurse will be in shortly with the vaccines do you have any questions.” Well ... it turns out the parents don’t feel comfortable with vaccines. They claim to understand the science and feel that vaccines make sense for some families. But they feel that for themselves, with a healthy lifestyle and God’s benevolence their son will be protected without having to introduce a host of foreign substances into his body.
What word best describes your reaction? Anger? Frustration? Disappointment (in our education system)? Maybe you’re angry at yourself for failing to make it clear in your office pamphlet and social media feeds that to protect your other patients, you no longer accept families who refuse immunizations for the common childhood diseases.
The American Academy of Pediatrics says it feels your pain, and its Annual Leadership Forum made eliminating nonmedical vaccine exemption laws its top priority in 2019. As part of its effort to help, the AAP Board of Directors was asked to advocate for the creation of a toolkit of strategies for Academy chapters facing the challenge of nonmedical exemptions. As an initial step to this process, three physicians in the department of pediatrics at the Denver Health Medical Center have begun interviewing religious leaders in hopes of developing “clergy-specific vaccine educational materials and deriv[ing] best practices for engaging them as vaccination advocates.” The investigators describe their plan and initial findings in Pediatrics (2019 Oct. doi: 10.1542/peds.2019-0933). Although they acknowledged that their efforts may not provide a quick solution to the nonmedical exemption problem, they hope that including more stakeholders and engendering trust will help future discussions.
Fourteen pages deeper into that issue of Pediatrics is the runner-up submission of this year’s Section on Pediatric Trainees essay competition titled “What I Learned From the Antivaccine Movement” (2019 Oct. doi: 10.1542/peds.2019-2384). Alana C. Ju, MD, describes the 2-hour ordeal she endured to testify at the California State Capitol in support of a state Senate bill aimed at tightening the regulations for vaccine medical exemptions. Totally unprepared for the “level of vitriol” aimed at her and other supporters of the bill, she was “accused of violating her duty as” a pediatrician because she was failing to protect children. The supporters were called “greedy, ignorant, and negligent.”
To her credit, Dr. Ju was able to step back from this assault and began looking at the faces of her accusers and learned that, “they too, felt strongly about children’s health.” She realized that “focusing on perceived ignorance is counterproductive.” She now hopes that by focusing on the shared goal of what is best for children, “we can all be better advocates.”
Both of these articles have a warm sort of kumbaya feel about them. It never is a bad idea to learn more about those with whom we disagree. But before huddling up too close to the campfire, we must realize that there is good evidence that sharing the scientific data with vaccine-hesitant parents doesn’t convert them into vaccine acceptors. In fact, it may strengthen their resolve to resist (Nyhan et al. “Effective Messages in Vaccine Promotion: A Randomized Trial,” Pediatrics. 2014 Apr;133[4] e835-42).
We are unlikely to convert many anti-vaxxers by sitting down together. Our target audience needs to be legislators and the majority of people who do vaccinate their children. These are the voters who will support legislation to eliminate nonmedical vaccine exemptions. To characterize anti-vaxxers as despicable ignorants is untrue and serves no purpose. We all do care about the health of children. However,
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
*This article has been updated 1/22/2020.
Climate change, health systems, and hospital medicine
Working toward carbon neutrality
I have always enjoyed talking with my patients from coastal Louisiana. They enjoy life, embrace their environment, and give me a perspective which is both similar and different than that of residents of New Orleans where I practice hospital medicine.
Their hospitalization is often a reflective moment in their lives. Lately I have been asking them about their advice to their children concerning the future of southern Louisiana in reference to sea rise, global warming, and increasing climatic events. More often than not, they have been telling their children it is time to move away.
These are a people who have strong devotion to family, but they are also practical. More than anything they would like their children to stay and preserve their heritage, but concern for their children’s future outweighs that. They have not come to this conclusion by scientific reports, but rather by what is happening before them. This group of people doesn’t alarm easily, but they see the unrelenting evidence of land loss and sea rise before them with little reason to believe it will change.
I am normally not one to speak out about climate change. Like most I have listened to the continuous alarms sounded by experts but have always assumed someone more qualified than myself should lead the efforts. But when I see the tangible effects of climate change both in my own life and the lives of my patients, I feel a sense of urgency.
12 years
Twelve years. That is the time we have to significantly reduce carbon emissions before catastrophic and potentially irreversible events will occur. This evidence is according to the authors of the landmark report by the UN Intergovernmental Panel on Climate Change released in October 2018. The report states urgent and unprecedented changes are needed to limit temperature elevations of 1.5°C and 2°C, as compared with the preindustrial era. Exceeding a 2°C elevation will likely lead to global adverse events at an unprecedented level.1
The events forecast by the U.N. report are not abstract, particularly as they relate to public health. With high confidence, the report outlines with high specificity: increases in extreme heat, floods, crop failures, and a multitude of economic and social stressors which will affect the care of our most vulnerable patients.1
This statement by Dr. Dana Hanson, president of the World Medical Association, summarizes the effects of climate change on the delivery of health care: “Climate change represents an inevitable massive threat to global health that will likely eclipse the major pandemics as a leading cause of death in the 21st century.”
So, what does the health care system have to do with climate change and its primary driver, carbon emissions? More than I realized, as the U.S. health care industry produces 10% of the nation’s carbon emissions.2 If the U.S. health care system was a country it would be ranked seventh, ahead of the United Kingdom; 10% of all smog and 9% of all particulate-related respiratory disease can be attributed to the carbon emissions of the health care industry. This breaks down to possibly 20,000 premature deaths per year.2 Our current health care industry is a significant driver of environmentally related disease and will continue to be so, unless major change occurs.
Although much of it is behind the scenes, providing health care 24/7 is a highly energy-intensive and waste-producing endeavor. Many of the innovations to reduce carbon emissions that have been seen in other industries have lagged behind in health care, as we have focused on other issues.
But the health care system is transitioning. It strives to address the whole person, including where they live, work, and play. A key component of this will be addressing our impact on the environments we serve. How can we make that argument if we don’t first address our own impact on the climate?
Carbon-neutral health care
Health care is one of the few industries that has the economic clout, the scientific basis, the community engagement, and perhaps most importantly the motivations to “first, do no harm” that could lead a national (if not a global) transformation in environmental stewardship among all industries.
Many agree that action is needed, but is essential that we set specific meaningful goals that take into account the urgency of the situation. One possible solution is to encourage every health care system to begin the process of becoming carbon neutral. Simply defined, carbon neutrality is balancing the activities that result in carbon emissions with activities that reduce carbon emissions. Carbon neutrality has become the standard by which an industry’s commitment to reducing carbon emissions is measured. The measurement is standardized and achievable, and the basic concept is understood by most. It results not only in long-term benefits to climate change, but immediate improvement of air quality in the local community. In addition, achieving carbon neutrality serves as a catalyst of new desired industries, improves employee morale, and aids in recruitment.3
So, what would a carbon-neutral health care system look like? In short, sustainability should be considered in all of its actions. Risks and benefits would be contemplated, as we do with all treatments, except now environmental risks would be brought into the equation. This includes the obvious, such as purchasing and supporting the development of renewable energy, but also transportation of patients and employees, food supply chains, and even the use of virtual visits to reduce the environmental impact of patient transportation.
I am optimistic that carbon neutrality is achievable in the health care sector. It can drive economic development and engage the community in environmental stewardship efforts. But time is of the essence and leaders for these efforts are needed now. As hospitalists, we are on the front lines of the health care system. We see the direct impact of social, economic, and environmental issues on our patients. We have credibility with both our patients and hospital administration. Among all industries, there need to be champions of environmental sustainability efforts. Hospitalists are uniquely positioned to fill that role.
My concern is that 12 years is right around the corner. We are at an inflection point on our efforts to reduce carbon emissions and that is good, but time has become our enemy. The difference between terrible and unlivable will be our, and the world’s, response to reducing carbon emissions.
It is time for bold action from us, the health care community. It is our moment and our place to lead those efforts, so let’s take advantage of both this challenge and this opportunity. Consider leading those efforts in your health care system.
Dr. Conrad is medical director of community affairs and health policy at Ochsner Health Systems in New Orleans.
References
1. Special Report on Global Warming of 1.5°C. Incheon [Republic of Korea]: Intergovernmental Panel on Climate Change. 7 Oct 2018.
2. Eckelman MJ, Sherman J. Environmental Impacts of the U.S. Health Care System and Effects on Public Health. PLoS ONE. 11(6):e0157014.
3. McCunn LJ, Gifford R. Do green offices affect employee engagement and environmental attitudes? Archit Sci Rev. 55:2;128-34. doi: 10.1080/00038628.2012.667939.
Working toward carbon neutrality
Working toward carbon neutrality
I have always enjoyed talking with my patients from coastal Louisiana. They enjoy life, embrace their environment, and give me a perspective which is both similar and different than that of residents of New Orleans where I practice hospital medicine.
Their hospitalization is often a reflective moment in their lives. Lately I have been asking them about their advice to their children concerning the future of southern Louisiana in reference to sea rise, global warming, and increasing climatic events. More often than not, they have been telling their children it is time to move away.
These are a people who have strong devotion to family, but they are also practical. More than anything they would like their children to stay and preserve their heritage, but concern for their children’s future outweighs that. They have not come to this conclusion by scientific reports, but rather by what is happening before them. This group of people doesn’t alarm easily, but they see the unrelenting evidence of land loss and sea rise before them with little reason to believe it will change.
I am normally not one to speak out about climate change. Like most I have listened to the continuous alarms sounded by experts but have always assumed someone more qualified than myself should lead the efforts. But when I see the tangible effects of climate change both in my own life and the lives of my patients, I feel a sense of urgency.
12 years
Twelve years. That is the time we have to significantly reduce carbon emissions before catastrophic and potentially irreversible events will occur. This evidence is according to the authors of the landmark report by the UN Intergovernmental Panel on Climate Change released in October 2018. The report states urgent and unprecedented changes are needed to limit temperature elevations of 1.5°C and 2°C, as compared with the preindustrial era. Exceeding a 2°C elevation will likely lead to global adverse events at an unprecedented level.1
The events forecast by the U.N. report are not abstract, particularly as they relate to public health. With high confidence, the report outlines with high specificity: increases in extreme heat, floods, crop failures, and a multitude of economic and social stressors which will affect the care of our most vulnerable patients.1
This statement by Dr. Dana Hanson, president of the World Medical Association, summarizes the effects of climate change on the delivery of health care: “Climate change represents an inevitable massive threat to global health that will likely eclipse the major pandemics as a leading cause of death in the 21st century.”
So, what does the health care system have to do with climate change and its primary driver, carbon emissions? More than I realized, as the U.S. health care industry produces 10% of the nation’s carbon emissions.2 If the U.S. health care system was a country it would be ranked seventh, ahead of the United Kingdom; 10% of all smog and 9% of all particulate-related respiratory disease can be attributed to the carbon emissions of the health care industry. This breaks down to possibly 20,000 premature deaths per year.2 Our current health care industry is a significant driver of environmentally related disease and will continue to be so, unless major change occurs.
Although much of it is behind the scenes, providing health care 24/7 is a highly energy-intensive and waste-producing endeavor. Many of the innovations to reduce carbon emissions that have been seen in other industries have lagged behind in health care, as we have focused on other issues.
But the health care system is transitioning. It strives to address the whole person, including where they live, work, and play. A key component of this will be addressing our impact on the environments we serve. How can we make that argument if we don’t first address our own impact on the climate?
Carbon-neutral health care
Health care is one of the few industries that has the economic clout, the scientific basis, the community engagement, and perhaps most importantly the motivations to “first, do no harm” that could lead a national (if not a global) transformation in environmental stewardship among all industries.
Many agree that action is needed, but is essential that we set specific meaningful goals that take into account the urgency of the situation. One possible solution is to encourage every health care system to begin the process of becoming carbon neutral. Simply defined, carbon neutrality is balancing the activities that result in carbon emissions with activities that reduce carbon emissions. Carbon neutrality has become the standard by which an industry’s commitment to reducing carbon emissions is measured. The measurement is standardized and achievable, and the basic concept is understood by most. It results not only in long-term benefits to climate change, but immediate improvement of air quality in the local community. In addition, achieving carbon neutrality serves as a catalyst of new desired industries, improves employee morale, and aids in recruitment.3
So, what would a carbon-neutral health care system look like? In short, sustainability should be considered in all of its actions. Risks and benefits would be contemplated, as we do with all treatments, except now environmental risks would be brought into the equation. This includes the obvious, such as purchasing and supporting the development of renewable energy, but also transportation of patients and employees, food supply chains, and even the use of virtual visits to reduce the environmental impact of patient transportation.
I am optimistic that carbon neutrality is achievable in the health care sector. It can drive economic development and engage the community in environmental stewardship efforts. But time is of the essence and leaders for these efforts are needed now. As hospitalists, we are on the front lines of the health care system. We see the direct impact of social, economic, and environmental issues on our patients. We have credibility with both our patients and hospital administration. Among all industries, there need to be champions of environmental sustainability efforts. Hospitalists are uniquely positioned to fill that role.
My concern is that 12 years is right around the corner. We are at an inflection point on our efforts to reduce carbon emissions and that is good, but time has become our enemy. The difference between terrible and unlivable will be our, and the world’s, response to reducing carbon emissions.
It is time for bold action from us, the health care community. It is our moment and our place to lead those efforts, so let’s take advantage of both this challenge and this opportunity. Consider leading those efforts in your health care system.
Dr. Conrad is medical director of community affairs and health policy at Ochsner Health Systems in New Orleans.
References
1. Special Report on Global Warming of 1.5°C. Incheon [Republic of Korea]: Intergovernmental Panel on Climate Change. 7 Oct 2018.
2. Eckelman MJ, Sherman J. Environmental Impacts of the U.S. Health Care System and Effects on Public Health. PLoS ONE. 11(6):e0157014.
3. McCunn LJ, Gifford R. Do green offices affect employee engagement and environmental attitudes? Archit Sci Rev. 55:2;128-34. doi: 10.1080/00038628.2012.667939.
I have always enjoyed talking with my patients from coastal Louisiana. They enjoy life, embrace their environment, and give me a perspective which is both similar and different than that of residents of New Orleans where I practice hospital medicine.
Their hospitalization is often a reflective moment in their lives. Lately I have been asking them about their advice to their children concerning the future of southern Louisiana in reference to sea rise, global warming, and increasing climatic events. More often than not, they have been telling their children it is time to move away.
These are a people who have strong devotion to family, but they are also practical. More than anything they would like their children to stay and preserve their heritage, but concern for their children’s future outweighs that. They have not come to this conclusion by scientific reports, but rather by what is happening before them. This group of people doesn’t alarm easily, but they see the unrelenting evidence of land loss and sea rise before them with little reason to believe it will change.
I am normally not one to speak out about climate change. Like most I have listened to the continuous alarms sounded by experts but have always assumed someone more qualified than myself should lead the efforts. But when I see the tangible effects of climate change both in my own life and the lives of my patients, I feel a sense of urgency.
12 years
Twelve years. That is the time we have to significantly reduce carbon emissions before catastrophic and potentially irreversible events will occur. This evidence is according to the authors of the landmark report by the UN Intergovernmental Panel on Climate Change released in October 2018. The report states urgent and unprecedented changes are needed to limit temperature elevations of 1.5°C and 2°C, as compared with the preindustrial era. Exceeding a 2°C elevation will likely lead to global adverse events at an unprecedented level.1
The events forecast by the U.N. report are not abstract, particularly as they relate to public health. With high confidence, the report outlines with high specificity: increases in extreme heat, floods, crop failures, and a multitude of economic and social stressors which will affect the care of our most vulnerable patients.1
This statement by Dr. Dana Hanson, president of the World Medical Association, summarizes the effects of climate change on the delivery of health care: “Climate change represents an inevitable massive threat to global health that will likely eclipse the major pandemics as a leading cause of death in the 21st century.”
So, what does the health care system have to do with climate change and its primary driver, carbon emissions? More than I realized, as the U.S. health care industry produces 10% of the nation’s carbon emissions.2 If the U.S. health care system was a country it would be ranked seventh, ahead of the United Kingdom; 10% of all smog and 9% of all particulate-related respiratory disease can be attributed to the carbon emissions of the health care industry. This breaks down to possibly 20,000 premature deaths per year.2 Our current health care industry is a significant driver of environmentally related disease and will continue to be so, unless major change occurs.
Although much of it is behind the scenes, providing health care 24/7 is a highly energy-intensive and waste-producing endeavor. Many of the innovations to reduce carbon emissions that have been seen in other industries have lagged behind in health care, as we have focused on other issues.
But the health care system is transitioning. It strives to address the whole person, including where they live, work, and play. A key component of this will be addressing our impact on the environments we serve. How can we make that argument if we don’t first address our own impact on the climate?
Carbon-neutral health care
Health care is one of the few industries that has the economic clout, the scientific basis, the community engagement, and perhaps most importantly the motivations to “first, do no harm” that could lead a national (if not a global) transformation in environmental stewardship among all industries.
Many agree that action is needed, but is essential that we set specific meaningful goals that take into account the urgency of the situation. One possible solution is to encourage every health care system to begin the process of becoming carbon neutral. Simply defined, carbon neutrality is balancing the activities that result in carbon emissions with activities that reduce carbon emissions. Carbon neutrality has become the standard by which an industry’s commitment to reducing carbon emissions is measured. The measurement is standardized and achievable, and the basic concept is understood by most. It results not only in long-term benefits to climate change, but immediate improvement of air quality in the local community. In addition, achieving carbon neutrality serves as a catalyst of new desired industries, improves employee morale, and aids in recruitment.3
So, what would a carbon-neutral health care system look like? In short, sustainability should be considered in all of its actions. Risks and benefits would be contemplated, as we do with all treatments, except now environmental risks would be brought into the equation. This includes the obvious, such as purchasing and supporting the development of renewable energy, but also transportation of patients and employees, food supply chains, and even the use of virtual visits to reduce the environmental impact of patient transportation.
I am optimistic that carbon neutrality is achievable in the health care sector. It can drive economic development and engage the community in environmental stewardship efforts. But time is of the essence and leaders for these efforts are needed now. As hospitalists, we are on the front lines of the health care system. We see the direct impact of social, economic, and environmental issues on our patients. We have credibility with both our patients and hospital administration. Among all industries, there need to be champions of environmental sustainability efforts. Hospitalists are uniquely positioned to fill that role.
My concern is that 12 years is right around the corner. We are at an inflection point on our efforts to reduce carbon emissions and that is good, but time has become our enemy. The difference between terrible and unlivable will be our, and the world’s, response to reducing carbon emissions.
It is time for bold action from us, the health care community. It is our moment and our place to lead those efforts, so let’s take advantage of both this challenge and this opportunity. Consider leading those efforts in your health care system.
Dr. Conrad is medical director of community affairs and health policy at Ochsner Health Systems in New Orleans.
References
1. Special Report on Global Warming of 1.5°C. Incheon [Republic of Korea]: Intergovernmental Panel on Climate Change. 7 Oct 2018.
2. Eckelman MJ, Sherman J. Environmental Impacts of the U.S. Health Care System and Effects on Public Health. PLoS ONE. 11(6):e0157014.
3. McCunn LJ, Gifford R. Do green offices affect employee engagement and environmental attitudes? Archit Sci Rev. 55:2;128-34. doi: 10.1080/00038628.2012.667939.
Antituberculosis drugs in pregnancy and lactation
Tuberculosis is one of the top ten causes of death worldwide and the leading cause from a single infectious agent. In the 2012-2017 period, there were more than 9,000 cases of TB each year in the United States. The Centers for Disease Control and Prevention states that untreated TB is a greater hazard to a pregnant woman and her fetus than its treatment.
In the material below, the molecular weights, rounded to the nearest whole number, are shown in parentheses after the drug name. Those less than 1,000 or so suggest that the drug will cross the placenta throughout pregnancy. In the second half of pregnancy, especially in the third trimester, nearly all drugs will cross regardless of their molecular weight.
Para-aminosalicylic acid (Paser) (153) is most frequently used in combination with other agents for the treatment of multidrug-resistant tuberculosis; multidrug-resistant TB (MDR TB) is defined as being caused by TB bacteria that is resistant to at least isoniazid and rifampin, the two most potent TB drugs. The drug has been associated with a marked increased risk of birth defects in some, but not all, studies. Because of this potential risk, the drug is best avoided in the first trimester. The drug is excreted into breast milk, but there are no reports of its use during breastfeeding.
Bedaquiline (Sirturo) (556) is used in combination therapy for patents with multidrug-resistant tuberculosis. One report describing the use of this drug during human pregnancy has been located. Treatment was started in the last 3 weeks of pregnancy and no abnormalities were noted in the child at birth and for 2 years after birth (Emerg Infect Dis. 2017. doi: 10.3201/eid2310.161398). The CDC states that the drug should be used only in a minimum four-drug treatment regimen and administered by direct observation (MMWR Recomm Rep. 2013 Oct 25;62[RR-09]:1-12). The drug probably is excreted into breast milk, but there are no reports of its use during breastfeeding.
Capreomycin (Capastat) (653-669) is a polypeptide antibiotic isolated from Streptomyces capreolus that is given intramuscularly. The human pregnancy data are limited to three reports. The toxicity of capreomycin is similar to aminoglycosides (e.g., cranial nerve VIII and renal) and it should not be used with these agents. The CDC has classified the drug as contraindicated in pregnancy. The drug probably is excreted into breast milk, but there are no reports of its use during breastfeeding.
Cycloserine (Seromycin) (102) is a broad spectrum antibiotic. The human pregnancy data are limited but have not shown embryo-fetal harm. Although the best course is to avoid the drug during gestation, it should not be withheld because of pregnancy if the maternal condition requires the antibiotic. The American Academy of Pediatrics classified cycloserine as compatible with breastfeeding.
Ethambutol (Myambutol) (205) should be used in conjunction with other antituberculosis drugs. The human pregnancy data do not suggest an embryo-fetal risk. A frequently used regimen is ethambutol + isoniazid + rifampin. The American Academy of Pediatrics classified ethambutol as compatible with breastfeeding.
Ethionamide (Trecator) (166) is indicated when Mycobacterium tuberculosis is resistant to isoniazid or rifampin, or when the patient is intolerant to other drugs. Although the animal reproductive data suggest risk, the limited human data suggest that the risk is probably low. If indicated, the drug should not be withheld because of pregnancy. Although the molecular weight suggests that the drug will be excreted into breast milk, no reports describing the amount in milk have been located.
Isoniazid (137) is compatible in pregnancy, even though the molecular weight suggests that it will cross the placenta, because the maternal benefit is much greater than the potential embryo-fetal risk. Although the human data are limited, the molecular weight also suggests that the drug will be excreted into breast milk, but it can be considered probably compatible during breastfeeding. No reports of isoniazid-induced effects in the nursing infant have been located, but the potential for interference with nucleic acid function and for hepatotoxicity may exist.
Pyrazinamide (123) is metabolized to an active metabolite. The molecular weight, low plasma protein binding (10%), and prolonged elimination half-life (9-10 hours) suggest that the drug will cross the placenta throughout pregnancy. The drug has been used in human pregnancy without causing embryo-fetal harm. Similar results, although limited, were reported when the drug was used during breastfeeding.
Rifabutin (Mycobutin) (847) has no reported human pregnancy data, but the animal data suggest low risk. The drug probably crosses the placenta throughout pregnancy. The maternal benefit appears to outweigh the unknown risk to the embryo-fetus, so therapy should not be withheld because of pregnancy. The drug probably is excreted into breast milk.
Rifampin (Rifadin) (823) appears to be compatible in pregnancy. Several reviews and reports have concluded that the drug was not a teratogen and recommended use of the drug with isoniazid and ethambutol. However, prophylactic vitamin K1 has been recommended to prevent drug-induced hemorrhagic disease of the newborn. There are no data regarding its use during breastfeeding, but it is probably compatible.
Rifapentine (Priftin) (877) was toxic and teratogenic in two animal species at doses close to those used in humans. In a 2018 study, however, the rates of fetal loss in pregnancies of less than 20 weeks (8/54, 15%) and congenital anomalies in live births (1/37, 3%) were within the expected background rates (Ann Am Thorac Soc. 2018 May;15[4]:570-80). There are no data regarding its use during breastfeeding, but it is probably compatible.
The CDC classifies four antituberculosis and one class of drugs as contraindicated in pregnancy. In addition to capreomycin mentioned above, they are amikacin, fluoroquinolones (ciprofloxacin, gemifloxacin, levofloxacin, lomefloxacin, moxifloxacin, ofloxacin), kanamycin, and streptomycin. These ten agents are discussed in the 11th edition of my book “Drugs in Pregnancy and Lactation,” (Wolters Kluwer Health: Riverwood, Il., 2017). If they have to be used, checking this source will provide information that has to be discussed with the patient.
Mr. Briggs is clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs had no disclosures, except for his book. Email him at obnews@mdedge.com.
Tuberculosis is one of the top ten causes of death worldwide and the leading cause from a single infectious agent. In the 2012-2017 period, there were more than 9,000 cases of TB each year in the United States. The Centers for Disease Control and Prevention states that untreated TB is a greater hazard to a pregnant woman and her fetus than its treatment.
In the material below, the molecular weights, rounded to the nearest whole number, are shown in parentheses after the drug name. Those less than 1,000 or so suggest that the drug will cross the placenta throughout pregnancy. In the second half of pregnancy, especially in the third trimester, nearly all drugs will cross regardless of their molecular weight.
Para-aminosalicylic acid (Paser) (153) is most frequently used in combination with other agents for the treatment of multidrug-resistant tuberculosis; multidrug-resistant TB (MDR TB) is defined as being caused by TB bacteria that is resistant to at least isoniazid and rifampin, the two most potent TB drugs. The drug has been associated with a marked increased risk of birth defects in some, but not all, studies. Because of this potential risk, the drug is best avoided in the first trimester. The drug is excreted into breast milk, but there are no reports of its use during breastfeeding.
Bedaquiline (Sirturo) (556) is used in combination therapy for patents with multidrug-resistant tuberculosis. One report describing the use of this drug during human pregnancy has been located. Treatment was started in the last 3 weeks of pregnancy and no abnormalities were noted in the child at birth and for 2 years after birth (Emerg Infect Dis. 2017. doi: 10.3201/eid2310.161398). The CDC states that the drug should be used only in a minimum four-drug treatment regimen and administered by direct observation (MMWR Recomm Rep. 2013 Oct 25;62[RR-09]:1-12). The drug probably is excreted into breast milk, but there are no reports of its use during breastfeeding.
Capreomycin (Capastat) (653-669) is a polypeptide antibiotic isolated from Streptomyces capreolus that is given intramuscularly. The human pregnancy data are limited to three reports. The toxicity of capreomycin is similar to aminoglycosides (e.g., cranial nerve VIII and renal) and it should not be used with these agents. The CDC has classified the drug as contraindicated in pregnancy. The drug probably is excreted into breast milk, but there are no reports of its use during breastfeeding.
Cycloserine (Seromycin) (102) is a broad spectrum antibiotic. The human pregnancy data are limited but have not shown embryo-fetal harm. Although the best course is to avoid the drug during gestation, it should not be withheld because of pregnancy if the maternal condition requires the antibiotic. The American Academy of Pediatrics classified cycloserine as compatible with breastfeeding.
Ethambutol (Myambutol) (205) should be used in conjunction with other antituberculosis drugs. The human pregnancy data do not suggest an embryo-fetal risk. A frequently used regimen is ethambutol + isoniazid + rifampin. The American Academy of Pediatrics classified ethambutol as compatible with breastfeeding.
Ethionamide (Trecator) (166) is indicated when Mycobacterium tuberculosis is resistant to isoniazid or rifampin, or when the patient is intolerant to other drugs. Although the animal reproductive data suggest risk, the limited human data suggest that the risk is probably low. If indicated, the drug should not be withheld because of pregnancy. Although the molecular weight suggests that the drug will be excreted into breast milk, no reports describing the amount in milk have been located.
Isoniazid (137) is compatible in pregnancy, even though the molecular weight suggests that it will cross the placenta, because the maternal benefit is much greater than the potential embryo-fetal risk. Although the human data are limited, the molecular weight also suggests that the drug will be excreted into breast milk, but it can be considered probably compatible during breastfeeding. No reports of isoniazid-induced effects in the nursing infant have been located, but the potential for interference with nucleic acid function and for hepatotoxicity may exist.
Pyrazinamide (123) is metabolized to an active metabolite. The molecular weight, low plasma protein binding (10%), and prolonged elimination half-life (9-10 hours) suggest that the drug will cross the placenta throughout pregnancy. The drug has been used in human pregnancy without causing embryo-fetal harm. Similar results, although limited, were reported when the drug was used during breastfeeding.
Rifabutin (Mycobutin) (847) has no reported human pregnancy data, but the animal data suggest low risk. The drug probably crosses the placenta throughout pregnancy. The maternal benefit appears to outweigh the unknown risk to the embryo-fetus, so therapy should not be withheld because of pregnancy. The drug probably is excreted into breast milk.
Rifampin (Rifadin) (823) appears to be compatible in pregnancy. Several reviews and reports have concluded that the drug was not a teratogen and recommended use of the drug with isoniazid and ethambutol. However, prophylactic vitamin K1 has been recommended to prevent drug-induced hemorrhagic disease of the newborn. There are no data regarding its use during breastfeeding, but it is probably compatible.
Rifapentine (Priftin) (877) was toxic and teratogenic in two animal species at doses close to those used in humans. In a 2018 study, however, the rates of fetal loss in pregnancies of less than 20 weeks (8/54, 15%) and congenital anomalies in live births (1/37, 3%) were within the expected background rates (Ann Am Thorac Soc. 2018 May;15[4]:570-80). There are no data regarding its use during breastfeeding, but it is probably compatible.
The CDC classifies four antituberculosis and one class of drugs as contraindicated in pregnancy. In addition to capreomycin mentioned above, they are amikacin, fluoroquinolones (ciprofloxacin, gemifloxacin, levofloxacin, lomefloxacin, moxifloxacin, ofloxacin), kanamycin, and streptomycin. These ten agents are discussed in the 11th edition of my book “Drugs in Pregnancy and Lactation,” (Wolters Kluwer Health: Riverwood, Il., 2017). If they have to be used, checking this source will provide information that has to be discussed with the patient.
Mr. Briggs is clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs had no disclosures, except for his book. Email him at obnews@mdedge.com.
Tuberculosis is one of the top ten causes of death worldwide and the leading cause from a single infectious agent. In the 2012-2017 period, there were more than 9,000 cases of TB each year in the United States. The Centers for Disease Control and Prevention states that untreated TB is a greater hazard to a pregnant woman and her fetus than its treatment.
In the material below, the molecular weights, rounded to the nearest whole number, are shown in parentheses after the drug name. Those less than 1,000 or so suggest that the drug will cross the placenta throughout pregnancy. In the second half of pregnancy, especially in the third trimester, nearly all drugs will cross regardless of their molecular weight.
Para-aminosalicylic acid (Paser) (153) is most frequently used in combination with other agents for the treatment of multidrug-resistant tuberculosis; multidrug-resistant TB (MDR TB) is defined as being caused by TB bacteria that is resistant to at least isoniazid and rifampin, the two most potent TB drugs. The drug has been associated with a marked increased risk of birth defects in some, but not all, studies. Because of this potential risk, the drug is best avoided in the first trimester. The drug is excreted into breast milk, but there are no reports of its use during breastfeeding.
Bedaquiline (Sirturo) (556) is used in combination therapy for patents with multidrug-resistant tuberculosis. One report describing the use of this drug during human pregnancy has been located. Treatment was started in the last 3 weeks of pregnancy and no abnormalities were noted in the child at birth and for 2 years after birth (Emerg Infect Dis. 2017. doi: 10.3201/eid2310.161398). The CDC states that the drug should be used only in a minimum four-drug treatment regimen and administered by direct observation (MMWR Recomm Rep. 2013 Oct 25;62[RR-09]:1-12). The drug probably is excreted into breast milk, but there are no reports of its use during breastfeeding.
Capreomycin (Capastat) (653-669) is a polypeptide antibiotic isolated from Streptomyces capreolus that is given intramuscularly. The human pregnancy data are limited to three reports. The toxicity of capreomycin is similar to aminoglycosides (e.g., cranial nerve VIII and renal) and it should not be used with these agents. The CDC has classified the drug as contraindicated in pregnancy. The drug probably is excreted into breast milk, but there are no reports of its use during breastfeeding.
Cycloserine (Seromycin) (102) is a broad spectrum antibiotic. The human pregnancy data are limited but have not shown embryo-fetal harm. Although the best course is to avoid the drug during gestation, it should not be withheld because of pregnancy if the maternal condition requires the antibiotic. The American Academy of Pediatrics classified cycloserine as compatible with breastfeeding.
Ethambutol (Myambutol) (205) should be used in conjunction with other antituberculosis drugs. The human pregnancy data do not suggest an embryo-fetal risk. A frequently used regimen is ethambutol + isoniazid + rifampin. The American Academy of Pediatrics classified ethambutol as compatible with breastfeeding.
Ethionamide (Trecator) (166) is indicated when Mycobacterium tuberculosis is resistant to isoniazid or rifampin, or when the patient is intolerant to other drugs. Although the animal reproductive data suggest risk, the limited human data suggest that the risk is probably low. If indicated, the drug should not be withheld because of pregnancy. Although the molecular weight suggests that the drug will be excreted into breast milk, no reports describing the amount in milk have been located.
Isoniazid (137) is compatible in pregnancy, even though the molecular weight suggests that it will cross the placenta, because the maternal benefit is much greater than the potential embryo-fetal risk. Although the human data are limited, the molecular weight also suggests that the drug will be excreted into breast milk, but it can be considered probably compatible during breastfeeding. No reports of isoniazid-induced effects in the nursing infant have been located, but the potential for interference with nucleic acid function and for hepatotoxicity may exist.
Pyrazinamide (123) is metabolized to an active metabolite. The molecular weight, low plasma protein binding (10%), and prolonged elimination half-life (9-10 hours) suggest that the drug will cross the placenta throughout pregnancy. The drug has been used in human pregnancy without causing embryo-fetal harm. Similar results, although limited, were reported when the drug was used during breastfeeding.
Rifabutin (Mycobutin) (847) has no reported human pregnancy data, but the animal data suggest low risk. The drug probably crosses the placenta throughout pregnancy. The maternal benefit appears to outweigh the unknown risk to the embryo-fetus, so therapy should not be withheld because of pregnancy. The drug probably is excreted into breast milk.
Rifampin (Rifadin) (823) appears to be compatible in pregnancy. Several reviews and reports have concluded that the drug was not a teratogen and recommended use of the drug with isoniazid and ethambutol. However, prophylactic vitamin K1 has been recommended to prevent drug-induced hemorrhagic disease of the newborn. There are no data regarding its use during breastfeeding, but it is probably compatible.
Rifapentine (Priftin) (877) was toxic and teratogenic in two animal species at doses close to those used in humans. In a 2018 study, however, the rates of fetal loss in pregnancies of less than 20 weeks (8/54, 15%) and congenital anomalies in live births (1/37, 3%) were within the expected background rates (Ann Am Thorac Soc. 2018 May;15[4]:570-80). There are no data regarding its use during breastfeeding, but it is probably compatible.
The CDC classifies four antituberculosis and one class of drugs as contraindicated in pregnancy. In addition to capreomycin mentioned above, they are amikacin, fluoroquinolones (ciprofloxacin, gemifloxacin, levofloxacin, lomefloxacin, moxifloxacin, ofloxacin), kanamycin, and streptomycin. These ten agents are discussed in the 11th edition of my book “Drugs in Pregnancy and Lactation,” (Wolters Kluwer Health: Riverwood, Il., 2017). If they have to be used, checking this source will provide information that has to be discussed with the patient.
Mr. Briggs is clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs had no disclosures, except for his book. Email him at obnews@mdedge.com.
‘Joker’ filled with mental illness misconceptions
The Batman characters have been cultural icons for generations – spanning more than three-quarters of a century. How many of us had Batman (or the Joker) on our school lunch box or watched reruns of Adam West’s campy televised rendition of Batman? The October release of “Joker” has been breaking contemporary box office records.
(Spoiler alert!) The Todd Phillips film associates mental illness with violent acts, spurring a slew of articles explaining that this association is uncommon and may promote stigmatization and public fear of people with obvious symptoms of mental illness. The protagonist, Arthur Fleck (Joaquin Phoenix), suffers from a condition in which his affect and facial expressions are not appropriate to his emotions or to the situation. He laughs uncontrollably when a situation is sad or upsetting. Sometimes he laughs and cries at the same time. As a result, he often is misunderstood, ridiculed, and victimized – like many people with obvious mental illness.
Arthur Fleck is a loner who has difficulty with relationships and self-esteem, and is beaten severely while at work as a clown. Shortly after the incident, he is given a gun by one of his coworkers. He keeps it with him even when working as a clown in a children’s hospital – where it is accidentally revealed, and he is subsequently fired. Still in his clown garb, he later uses the gun when he is mocked and assaulted on the subway by three Gotham City bankers.
In an unusual tone, his mental health worker reminds him early in the film that he is prescribed seven different psychotropic medications, helping to cement for the viewer that mental illness is the cause of Arthur’s problems and the Joker’s origin story. Then the funding for Arthur’s mental health treatment (even if it was not good treatment) was cut – a problem not just in Gotham.
While some of Arthur Fleck’s symptoms are consistent with real mental illness, the combination of symptoms is unusual. Although he is being treated with a variety of medications, it is unclear whether any of them are helping him or what exactly they are helping him with. (Ironically, once he is off of his medications, he becomes a better dresser and a better dancer.) He writes in a disorganized way in his journal; the only intelligible sentence that is focused on is, “The worst part about having mental illness is people expect you to behave as if you DONT.” A smiley face in the ‘O’ suggests that his affect is inappropriate even in his writing. Arthur’s condition of uncontrollable laughing and/or crying, associated with head trauma, appears more consistent with the neurologic condition pseudobulbar affect rather than a mental illness. In addition to pseudobulbar affect, Arthur demonstrates a constellation of symptoms of different kinds of mental illness, including erotomanic delusions, ideas of reference, and disorganized thinking. He also does not appear to take social cues, such as knowing when he is being mocked. He appears to believe that his neighbor is his girlfriend (as the viewer was similarly led to believe), eventually breaking into her apartment where he thought he belonged, much to her horror when she finds him there. Some of his symptoms may run in his family (whether it be his biological or adoptive family).
Penny (Arthur’s mother) strongly believes (perhaps a delusion, perhaps not) that her previous employer Thomas Wayne (the future Batman’s father) is the father of her love-child, Arthur. When Arthur obtains Penny’s mental health records (through his own violent devices), he finds that she had been diagnosed with narcissistic personality disorder and a psychotic disorder. She had been found guilty of endangering the welfare of her (perhaps adopted, perhaps not) child Arthur, who had been malnourished, with severe head trauma, and tied to a radiator.
Arthur’s smothering of his mother with a pillow in her hospital bed, after he was devastated by both her stroke and this newfound data, occurred in a perfect storm. The killing is not portrayed as an act of euthanasia. We know that schizophrenia is overrepresented among matricide perpetrators and that long-term dysfunctional relationships between mother and (grown) child usually precede matricides. Mothers are often seen as controlling, fathers are often absent (as in Arthur’s case), and the child is often overly dependent. The mother and child (as seen here) often have a relationship marked by love and hate – mutual dependence and hostility. But Arthur is not the only character in the Batman universe to commit matricide. Recall that the Batman’s psychiatrist Amadeus Arkham himself killed his own mentally ill mother during his young adulthood.
Pop culture can give the public negative impressions of mental illness. While filmmakers need not portray actual mental illnesses or their symptoms in moving their stories forward, their portrayals have an impact on what the public sees as mental illness. This is similar to the current American president and others in political power asserting that mental illness causes mass shootings, and those in the public taking their word for it rather than the word of psychiatry.
In actuality, what felt the most true to life in the film was the early scene in which Arthur was seriously assaulted while waving the going-out-of-business sign on the sidewalk, just trying to make a living. As psychiatrists know, people with mental illness are more likely to be victimized by others in society than to be perpetrators of violence. To be sure, some of Arthur’s characteristics are dynamic risk factors, such as his unemployment and social isolation. However, society often conflates mental illness with dangerousness, but most people with mental illness are not violent.
In the final scenes, Arthur Fleck (who is now the Joker) is apparently back in the white-walled Arkham State Hospital, with an implication that he has gotten away with the murders, either found incompetent or insane. This, too, has negative implications for the public viewing the film – and further perpetuates the misunderstanding that people with mental illness “get away” with their crimes. In reality, depending on the study, approximately one-quarter of those who pleaded insanity were found insane, and those facing jury trials (and public perception) are less likely to be found insane than those with bench trials. Public misinterpretations and outrage over the idea that a mentally unwell person might be found insane rather than guilty have existed for centuries, perhaps most memorably when John Hinckley Jr. attempted to assassinate former President Ronald Reagan, after identifying with a character in the film “Taxi Driver.” Let’s presume that Gotham has an insanity defense similar to other places in America. Then, in order to be found insane, Arthur’s pseudobulbar affect or his (unclear) mental illness would have either caused him not to know the nature and consequences of his acts, and/or to appreciate the wrongfulness of his acts (if we are fairly certain that Gotham is actually New York City). Neither of these appear to be true from the film. He knew that he was killing. No delusions or hallucinations made him think his acts were not wrong. Rather, he had an arguably rational motive – certainly the multitudes wearing clown masks in the subsequent uprisings against the powerful also believed his motive to be rational. He deliberately killed the bankers who mocked and beat him. He was also able to defer his killings until what he calculated was the right time to have the most impact – for example, on live television, or when he was alone with his mother in the hospital.
In closing, unrealistic portrayals of the link between mental illness, violence, and forensic hospitalization are seen on the silver screen in “Joker.” We hope that others who feign mental illness symptoms to evade criminal responsibility will emulate Joaquin Phoenix’s Joker as it will make it much easier for forensic psychiatrists to ferret out malingerers!
Dr. Hatters Friedman serves as the Phillip Resnick Professor of Forensic Psychiatry at Case Western Reserve University, Cleveland. She is also editor of Family Murder: Pathologies of Love and Hate (Washington, D.C.: American Psychiatric Association Publishing [2019]), which was written by the Group for the Advancement of Psychiatry’s Committee on Psychiatry & Law. Dr. Rosenbaum is a clinical and forensic psychiatrist in private practice in New York. She is an assistant clinical professor at New York University Langone Medical Center and on the faculty at Weill-Cornell Medical Center.
The Batman characters have been cultural icons for generations – spanning more than three-quarters of a century. How many of us had Batman (or the Joker) on our school lunch box or watched reruns of Adam West’s campy televised rendition of Batman? The October release of “Joker” has been breaking contemporary box office records.
(Spoiler alert!) The Todd Phillips film associates mental illness with violent acts, spurring a slew of articles explaining that this association is uncommon and may promote stigmatization and public fear of people with obvious symptoms of mental illness. The protagonist, Arthur Fleck (Joaquin Phoenix), suffers from a condition in which his affect and facial expressions are not appropriate to his emotions or to the situation. He laughs uncontrollably when a situation is sad or upsetting. Sometimes he laughs and cries at the same time. As a result, he often is misunderstood, ridiculed, and victimized – like many people with obvious mental illness.
Arthur Fleck is a loner who has difficulty with relationships and self-esteem, and is beaten severely while at work as a clown. Shortly after the incident, he is given a gun by one of his coworkers. He keeps it with him even when working as a clown in a children’s hospital – where it is accidentally revealed, and he is subsequently fired. Still in his clown garb, he later uses the gun when he is mocked and assaulted on the subway by three Gotham City bankers.
In an unusual tone, his mental health worker reminds him early in the film that he is prescribed seven different psychotropic medications, helping to cement for the viewer that mental illness is the cause of Arthur’s problems and the Joker’s origin story. Then the funding for Arthur’s mental health treatment (even if it was not good treatment) was cut – a problem not just in Gotham.
While some of Arthur Fleck’s symptoms are consistent with real mental illness, the combination of symptoms is unusual. Although he is being treated with a variety of medications, it is unclear whether any of them are helping him or what exactly they are helping him with. (Ironically, once he is off of his medications, he becomes a better dresser and a better dancer.) He writes in a disorganized way in his journal; the only intelligible sentence that is focused on is, “The worst part about having mental illness is people expect you to behave as if you DONT.” A smiley face in the ‘O’ suggests that his affect is inappropriate even in his writing. Arthur’s condition of uncontrollable laughing and/or crying, associated with head trauma, appears more consistent with the neurologic condition pseudobulbar affect rather than a mental illness. In addition to pseudobulbar affect, Arthur demonstrates a constellation of symptoms of different kinds of mental illness, including erotomanic delusions, ideas of reference, and disorganized thinking. He also does not appear to take social cues, such as knowing when he is being mocked. He appears to believe that his neighbor is his girlfriend (as the viewer was similarly led to believe), eventually breaking into her apartment where he thought he belonged, much to her horror when she finds him there. Some of his symptoms may run in his family (whether it be his biological or adoptive family).
Penny (Arthur’s mother) strongly believes (perhaps a delusion, perhaps not) that her previous employer Thomas Wayne (the future Batman’s father) is the father of her love-child, Arthur. When Arthur obtains Penny’s mental health records (through his own violent devices), he finds that she had been diagnosed with narcissistic personality disorder and a psychotic disorder. She had been found guilty of endangering the welfare of her (perhaps adopted, perhaps not) child Arthur, who had been malnourished, with severe head trauma, and tied to a radiator.
Arthur’s smothering of his mother with a pillow in her hospital bed, after he was devastated by both her stroke and this newfound data, occurred in a perfect storm. The killing is not portrayed as an act of euthanasia. We know that schizophrenia is overrepresented among matricide perpetrators and that long-term dysfunctional relationships between mother and (grown) child usually precede matricides. Mothers are often seen as controlling, fathers are often absent (as in Arthur’s case), and the child is often overly dependent. The mother and child (as seen here) often have a relationship marked by love and hate – mutual dependence and hostility. But Arthur is not the only character in the Batman universe to commit matricide. Recall that the Batman’s psychiatrist Amadeus Arkham himself killed his own mentally ill mother during his young adulthood.
Pop culture can give the public negative impressions of mental illness. While filmmakers need not portray actual mental illnesses or their symptoms in moving their stories forward, their portrayals have an impact on what the public sees as mental illness. This is similar to the current American president and others in political power asserting that mental illness causes mass shootings, and those in the public taking their word for it rather than the word of psychiatry.
In actuality, what felt the most true to life in the film was the early scene in which Arthur was seriously assaulted while waving the going-out-of-business sign on the sidewalk, just trying to make a living. As psychiatrists know, people with mental illness are more likely to be victimized by others in society than to be perpetrators of violence. To be sure, some of Arthur’s characteristics are dynamic risk factors, such as his unemployment and social isolation. However, society often conflates mental illness with dangerousness, but most people with mental illness are not violent.
In the final scenes, Arthur Fleck (who is now the Joker) is apparently back in the white-walled Arkham State Hospital, with an implication that he has gotten away with the murders, either found incompetent or insane. This, too, has negative implications for the public viewing the film – and further perpetuates the misunderstanding that people with mental illness “get away” with their crimes. In reality, depending on the study, approximately one-quarter of those who pleaded insanity were found insane, and those facing jury trials (and public perception) are less likely to be found insane than those with bench trials. Public misinterpretations and outrage over the idea that a mentally unwell person might be found insane rather than guilty have existed for centuries, perhaps most memorably when John Hinckley Jr. attempted to assassinate former President Ronald Reagan, after identifying with a character in the film “Taxi Driver.” Let’s presume that Gotham has an insanity defense similar to other places in America. Then, in order to be found insane, Arthur’s pseudobulbar affect or his (unclear) mental illness would have either caused him not to know the nature and consequences of his acts, and/or to appreciate the wrongfulness of his acts (if we are fairly certain that Gotham is actually New York City). Neither of these appear to be true from the film. He knew that he was killing. No delusions or hallucinations made him think his acts were not wrong. Rather, he had an arguably rational motive – certainly the multitudes wearing clown masks in the subsequent uprisings against the powerful also believed his motive to be rational. He deliberately killed the bankers who mocked and beat him. He was also able to defer his killings until what he calculated was the right time to have the most impact – for example, on live television, or when he was alone with his mother in the hospital.
In closing, unrealistic portrayals of the link between mental illness, violence, and forensic hospitalization are seen on the silver screen in “Joker.” We hope that others who feign mental illness symptoms to evade criminal responsibility will emulate Joaquin Phoenix’s Joker as it will make it much easier for forensic psychiatrists to ferret out malingerers!
Dr. Hatters Friedman serves as the Phillip Resnick Professor of Forensic Psychiatry at Case Western Reserve University, Cleveland. She is also editor of Family Murder: Pathologies of Love and Hate (Washington, D.C.: American Psychiatric Association Publishing [2019]), which was written by the Group for the Advancement of Psychiatry’s Committee on Psychiatry & Law. Dr. Rosenbaum is a clinical and forensic psychiatrist in private practice in New York. She is an assistant clinical professor at New York University Langone Medical Center and on the faculty at Weill-Cornell Medical Center.
The Batman characters have been cultural icons for generations – spanning more than three-quarters of a century. How many of us had Batman (or the Joker) on our school lunch box or watched reruns of Adam West’s campy televised rendition of Batman? The October release of “Joker” has been breaking contemporary box office records.
(Spoiler alert!) The Todd Phillips film associates mental illness with violent acts, spurring a slew of articles explaining that this association is uncommon and may promote stigmatization and public fear of people with obvious symptoms of mental illness. The protagonist, Arthur Fleck (Joaquin Phoenix), suffers from a condition in which his affect and facial expressions are not appropriate to his emotions or to the situation. He laughs uncontrollably when a situation is sad or upsetting. Sometimes he laughs and cries at the same time. As a result, he often is misunderstood, ridiculed, and victimized – like many people with obvious mental illness.
Arthur Fleck is a loner who has difficulty with relationships and self-esteem, and is beaten severely while at work as a clown. Shortly after the incident, he is given a gun by one of his coworkers. He keeps it with him even when working as a clown in a children’s hospital – where it is accidentally revealed, and he is subsequently fired. Still in his clown garb, he later uses the gun when he is mocked and assaulted on the subway by three Gotham City bankers.
In an unusual tone, his mental health worker reminds him early in the film that he is prescribed seven different psychotropic medications, helping to cement for the viewer that mental illness is the cause of Arthur’s problems and the Joker’s origin story. Then the funding for Arthur’s mental health treatment (even if it was not good treatment) was cut – a problem not just in Gotham.
While some of Arthur Fleck’s symptoms are consistent with real mental illness, the combination of symptoms is unusual. Although he is being treated with a variety of medications, it is unclear whether any of them are helping him or what exactly they are helping him with. (Ironically, once he is off of his medications, he becomes a better dresser and a better dancer.) He writes in a disorganized way in his journal; the only intelligible sentence that is focused on is, “The worst part about having mental illness is people expect you to behave as if you DONT.” A smiley face in the ‘O’ suggests that his affect is inappropriate even in his writing. Arthur’s condition of uncontrollable laughing and/or crying, associated with head trauma, appears more consistent with the neurologic condition pseudobulbar affect rather than a mental illness. In addition to pseudobulbar affect, Arthur demonstrates a constellation of symptoms of different kinds of mental illness, including erotomanic delusions, ideas of reference, and disorganized thinking. He also does not appear to take social cues, such as knowing when he is being mocked. He appears to believe that his neighbor is his girlfriend (as the viewer was similarly led to believe), eventually breaking into her apartment where he thought he belonged, much to her horror when she finds him there. Some of his symptoms may run in his family (whether it be his biological or adoptive family).
Penny (Arthur’s mother) strongly believes (perhaps a delusion, perhaps not) that her previous employer Thomas Wayne (the future Batman’s father) is the father of her love-child, Arthur. When Arthur obtains Penny’s mental health records (through his own violent devices), he finds that she had been diagnosed with narcissistic personality disorder and a psychotic disorder. She had been found guilty of endangering the welfare of her (perhaps adopted, perhaps not) child Arthur, who had been malnourished, with severe head trauma, and tied to a radiator.
Arthur’s smothering of his mother with a pillow in her hospital bed, after he was devastated by both her stroke and this newfound data, occurred in a perfect storm. The killing is not portrayed as an act of euthanasia. We know that schizophrenia is overrepresented among matricide perpetrators and that long-term dysfunctional relationships between mother and (grown) child usually precede matricides. Mothers are often seen as controlling, fathers are often absent (as in Arthur’s case), and the child is often overly dependent. The mother and child (as seen here) often have a relationship marked by love and hate – mutual dependence and hostility. But Arthur is not the only character in the Batman universe to commit matricide. Recall that the Batman’s psychiatrist Amadeus Arkham himself killed his own mentally ill mother during his young adulthood.
Pop culture can give the public negative impressions of mental illness. While filmmakers need not portray actual mental illnesses or their symptoms in moving their stories forward, their portrayals have an impact on what the public sees as mental illness. This is similar to the current American president and others in political power asserting that mental illness causes mass shootings, and those in the public taking their word for it rather than the word of psychiatry.
In actuality, what felt the most true to life in the film was the early scene in which Arthur was seriously assaulted while waving the going-out-of-business sign on the sidewalk, just trying to make a living. As psychiatrists know, people with mental illness are more likely to be victimized by others in society than to be perpetrators of violence. To be sure, some of Arthur’s characteristics are dynamic risk factors, such as his unemployment and social isolation. However, society often conflates mental illness with dangerousness, but most people with mental illness are not violent.
In the final scenes, Arthur Fleck (who is now the Joker) is apparently back in the white-walled Arkham State Hospital, with an implication that he has gotten away with the murders, either found incompetent or insane. This, too, has negative implications for the public viewing the film – and further perpetuates the misunderstanding that people with mental illness “get away” with their crimes. In reality, depending on the study, approximately one-quarter of those who pleaded insanity were found insane, and those facing jury trials (and public perception) are less likely to be found insane than those with bench trials. Public misinterpretations and outrage over the idea that a mentally unwell person might be found insane rather than guilty have existed for centuries, perhaps most memorably when John Hinckley Jr. attempted to assassinate former President Ronald Reagan, after identifying with a character in the film “Taxi Driver.” Let’s presume that Gotham has an insanity defense similar to other places in America. Then, in order to be found insane, Arthur’s pseudobulbar affect or his (unclear) mental illness would have either caused him not to know the nature and consequences of his acts, and/or to appreciate the wrongfulness of his acts (if we are fairly certain that Gotham is actually New York City). Neither of these appear to be true from the film. He knew that he was killing. No delusions or hallucinations made him think his acts were not wrong. Rather, he had an arguably rational motive – certainly the multitudes wearing clown masks in the subsequent uprisings against the powerful also believed his motive to be rational. He deliberately killed the bankers who mocked and beat him. He was also able to defer his killings until what he calculated was the right time to have the most impact – for example, on live television, or when he was alone with his mother in the hospital.
In closing, unrealistic portrayals of the link between mental illness, violence, and forensic hospitalization are seen on the silver screen in “Joker.” We hope that others who feign mental illness symptoms to evade criminal responsibility will emulate Joaquin Phoenix’s Joker as it will make it much easier for forensic psychiatrists to ferret out malingerers!
Dr. Hatters Friedman serves as the Phillip Resnick Professor of Forensic Psychiatry at Case Western Reserve University, Cleveland. She is also editor of Family Murder: Pathologies of Love and Hate (Washington, D.C.: American Psychiatric Association Publishing [2019]), which was written by the Group for the Advancement of Psychiatry’s Committee on Psychiatry & Law. Dr. Rosenbaum is a clinical and forensic psychiatrist in private practice in New York. She is an assistant clinical professor at New York University Langone Medical Center and on the faculty at Weill-Cornell Medical Center.
A cigarette in one hand and a Fitbit on the other
A cardiologist friend of mine told me a story about one of his patients. The man had recently been in to see him for an office visit. He had quite a scare needing two stents after an episode of prolonged chest pain and, during the office visit, apparently had said that he had “found religion” and was going to change his ways. He showed off the Fitbit that he had gotten and shared his excitement about using a new app to track his diet on his smart phone. His blood pressure was a little elevated, so my friend added a third antihypertensive in an effort to get his blood pressure under control. He referred the patient back to his primary care physician to address his elevated hemoglobin A1c.
My friend saw the patient again a couple of weeks later – this time at the mall. As he was driving through the parking lot, he noticed his patient sitting on a bench outside the entrance. He also noticed a cigarette in his patient’s right hand and saw the Fitbit still on his wrist. Now, it’s not that there is anything wrong with wearing a Fitbit, but …
My friend is an incredibly respectful person, and very nice. He decided not to say hello and risk embarrassing his patient, so he walked to a different door far from the bench and went inside. Nonetheless, the image bothered him. It bothered him enough to repeat the story to me 2 weeks later. It bothers me too.
The other day I was talking to a healthy young nurse with whom I work. She has been trying to get into shape, and her goal is to get to the gym 5 days a week after work. She read on a popular website that she should use a heart rate monitor to keep track of her training and that, if her heart rate is too slow, she should run faster and, if her heart rate is too fast, she should slow down. She was discouraged the other day, however, because her watch indicated that her pulse was going up to 170 while she was running hard, and she had heard that could be dangerous for her heart.
When she doesn’t push hard, though, she told me that her heart rate often plateaus at about 110, sometimes 115. She has been finding it difficult to achieve her calculated target heart rate of 120-160 beats per minute. She is frustrated and was going to skip her workout that evening. I explained to her that she should stop checking her pulse and just run – if she felt she was running too slow she could run faster.
With everything that we have learned about science and technology, the reality is that we are still people, with all our weaknesses and strengths. We often set goals with ambivalence, then rush forward hoping that a technological solution will move us in the direction we think we want to move. Unfortunately, owning a Fitbit will not make us more fit, and checking our pulse every five minutes while working out will not lead to a better exercise session. With the availability of so much technology for tracking our daily exercise, vital signs, and various other measures of health, we need to be more careful than ever to determine specifically what it is that we are trying to accomplish with the use of our technology.
When it comes to good health, it is the fundamentals that matter, and achieving the fundamentals requires being mindful and making repeated efforts to master them. For almost all adults, the most important habits to develop are still related to diet and exercise. Consuming the right diet and exercising adequately requires that the correct choices be made each and every day, all day long. Technology can help but will not do it for us. We need to be thoughtful about how we use technology and explicit about how we expect it to help. After a reasonable amount of time, we should evaluate to see if it is working for us. If it is, then we should continue to use it. If it is not, then we should stop using it or make a different change, like performing a new type of exercise.
Our goal should be to have intelligent empathic integration of technological and behavioral techniques to achieve an optimal health outcome. Putting running shoes by the bed at night is a great thing to do to encourage us to run in the morning. Choosing motivational music can help us get the energy and enthusiasm to go for that run (our favorites include the Rocky theme song and “I Didn’t Come this Far to Only Come this Far”). A visual reminder over the refrigerator can “nudge” us to make good choices as we open the door.
For those who want to learn more about how to integrate behavioral management into their advice for patients we highly recommend reading “Switch: How to Change Things When Change Is Hard” by Chip Heath and “Nudge: Improving Decisions About Health, Wealth, and Happiness” by Richard Thaler. We have always been, and remain, excited about the promise of technology to help us accomplish our goals. That said, we told the nurse to stop checking her pulse, to put on some music, and to appreciate the leaves on the trees this autumn while she was running. As for the gentleman outside the mall, well …
We are interested in your thoughts. Please email us at fpnews@mdedge.com.
Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Jefferson Health. Follow him on Twitter @doctornotte. Dr. Skolnik is professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington Jefferson Health.
A cardiologist friend of mine told me a story about one of his patients. The man had recently been in to see him for an office visit. He had quite a scare needing two stents after an episode of prolonged chest pain and, during the office visit, apparently had said that he had “found religion” and was going to change his ways. He showed off the Fitbit that he had gotten and shared his excitement about using a new app to track his diet on his smart phone. His blood pressure was a little elevated, so my friend added a third antihypertensive in an effort to get his blood pressure under control. He referred the patient back to his primary care physician to address his elevated hemoglobin A1c.
My friend saw the patient again a couple of weeks later – this time at the mall. As he was driving through the parking lot, he noticed his patient sitting on a bench outside the entrance. He also noticed a cigarette in his patient’s right hand and saw the Fitbit still on his wrist. Now, it’s not that there is anything wrong with wearing a Fitbit, but …
My friend is an incredibly respectful person, and very nice. He decided not to say hello and risk embarrassing his patient, so he walked to a different door far from the bench and went inside. Nonetheless, the image bothered him. It bothered him enough to repeat the story to me 2 weeks later. It bothers me too.
The other day I was talking to a healthy young nurse with whom I work. She has been trying to get into shape, and her goal is to get to the gym 5 days a week after work. She read on a popular website that she should use a heart rate monitor to keep track of her training and that, if her heart rate is too slow, she should run faster and, if her heart rate is too fast, she should slow down. She was discouraged the other day, however, because her watch indicated that her pulse was going up to 170 while she was running hard, and she had heard that could be dangerous for her heart.
When she doesn’t push hard, though, she told me that her heart rate often plateaus at about 110, sometimes 115. She has been finding it difficult to achieve her calculated target heart rate of 120-160 beats per minute. She is frustrated and was going to skip her workout that evening. I explained to her that she should stop checking her pulse and just run – if she felt she was running too slow she could run faster.
With everything that we have learned about science and technology, the reality is that we are still people, with all our weaknesses and strengths. We often set goals with ambivalence, then rush forward hoping that a technological solution will move us in the direction we think we want to move. Unfortunately, owning a Fitbit will not make us more fit, and checking our pulse every five minutes while working out will not lead to a better exercise session. With the availability of so much technology for tracking our daily exercise, vital signs, and various other measures of health, we need to be more careful than ever to determine specifically what it is that we are trying to accomplish with the use of our technology.
When it comes to good health, it is the fundamentals that matter, and achieving the fundamentals requires being mindful and making repeated efforts to master them. For almost all adults, the most important habits to develop are still related to diet and exercise. Consuming the right diet and exercising adequately requires that the correct choices be made each and every day, all day long. Technology can help but will not do it for us. We need to be thoughtful about how we use technology and explicit about how we expect it to help. After a reasonable amount of time, we should evaluate to see if it is working for us. If it is, then we should continue to use it. If it is not, then we should stop using it or make a different change, like performing a new type of exercise.
Our goal should be to have intelligent empathic integration of technological and behavioral techniques to achieve an optimal health outcome. Putting running shoes by the bed at night is a great thing to do to encourage us to run in the morning. Choosing motivational music can help us get the energy and enthusiasm to go for that run (our favorites include the Rocky theme song and “I Didn’t Come this Far to Only Come this Far”). A visual reminder over the refrigerator can “nudge” us to make good choices as we open the door.
For those who want to learn more about how to integrate behavioral management into their advice for patients we highly recommend reading “Switch: How to Change Things When Change Is Hard” by Chip Heath and “Nudge: Improving Decisions About Health, Wealth, and Happiness” by Richard Thaler. We have always been, and remain, excited about the promise of technology to help us accomplish our goals. That said, we told the nurse to stop checking her pulse, to put on some music, and to appreciate the leaves on the trees this autumn while she was running. As for the gentleman outside the mall, well …
We are interested in your thoughts. Please email us at fpnews@mdedge.com.
Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Jefferson Health. Follow him on Twitter @doctornotte. Dr. Skolnik is professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington Jefferson Health.
A cardiologist friend of mine told me a story about one of his patients. The man had recently been in to see him for an office visit. He had quite a scare needing two stents after an episode of prolonged chest pain and, during the office visit, apparently had said that he had “found religion” and was going to change his ways. He showed off the Fitbit that he had gotten and shared his excitement about using a new app to track his diet on his smart phone. His blood pressure was a little elevated, so my friend added a third antihypertensive in an effort to get his blood pressure under control. He referred the patient back to his primary care physician to address his elevated hemoglobin A1c.
My friend saw the patient again a couple of weeks later – this time at the mall. As he was driving through the parking lot, he noticed his patient sitting on a bench outside the entrance. He also noticed a cigarette in his patient’s right hand and saw the Fitbit still on his wrist. Now, it’s not that there is anything wrong with wearing a Fitbit, but …
My friend is an incredibly respectful person, and very nice. He decided not to say hello and risk embarrassing his patient, so he walked to a different door far from the bench and went inside. Nonetheless, the image bothered him. It bothered him enough to repeat the story to me 2 weeks later. It bothers me too.
The other day I was talking to a healthy young nurse with whom I work. She has been trying to get into shape, and her goal is to get to the gym 5 days a week after work. She read on a popular website that she should use a heart rate monitor to keep track of her training and that, if her heart rate is too slow, she should run faster and, if her heart rate is too fast, she should slow down. She was discouraged the other day, however, because her watch indicated that her pulse was going up to 170 while she was running hard, and she had heard that could be dangerous for her heart.
When she doesn’t push hard, though, she told me that her heart rate often plateaus at about 110, sometimes 115. She has been finding it difficult to achieve her calculated target heart rate of 120-160 beats per minute. She is frustrated and was going to skip her workout that evening. I explained to her that she should stop checking her pulse and just run – if she felt she was running too slow she could run faster.
With everything that we have learned about science and technology, the reality is that we are still people, with all our weaknesses and strengths. We often set goals with ambivalence, then rush forward hoping that a technological solution will move us in the direction we think we want to move. Unfortunately, owning a Fitbit will not make us more fit, and checking our pulse every five minutes while working out will not lead to a better exercise session. With the availability of so much technology for tracking our daily exercise, vital signs, and various other measures of health, we need to be more careful than ever to determine specifically what it is that we are trying to accomplish with the use of our technology.
When it comes to good health, it is the fundamentals that matter, and achieving the fundamentals requires being mindful and making repeated efforts to master them. For almost all adults, the most important habits to develop are still related to diet and exercise. Consuming the right diet and exercising adequately requires that the correct choices be made each and every day, all day long. Technology can help but will not do it for us. We need to be thoughtful about how we use technology and explicit about how we expect it to help. After a reasonable amount of time, we should evaluate to see if it is working for us. If it is, then we should continue to use it. If it is not, then we should stop using it or make a different change, like performing a new type of exercise.
Our goal should be to have intelligent empathic integration of technological and behavioral techniques to achieve an optimal health outcome. Putting running shoes by the bed at night is a great thing to do to encourage us to run in the morning. Choosing motivational music can help us get the energy and enthusiasm to go for that run (our favorites include the Rocky theme song and “I Didn’t Come this Far to Only Come this Far”). A visual reminder over the refrigerator can “nudge” us to make good choices as we open the door.
For those who want to learn more about how to integrate behavioral management into their advice for patients we highly recommend reading “Switch: How to Change Things When Change Is Hard” by Chip Heath and “Nudge: Improving Decisions About Health, Wealth, and Happiness” by Richard Thaler. We have always been, and remain, excited about the promise of technology to help us accomplish our goals. That said, we told the nurse to stop checking her pulse, to put on some music, and to appreciate the leaves on the trees this autumn while she was running. As for the gentleman outside the mall, well …
We are interested in your thoughts. Please email us at fpnews@mdedge.com.
Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Jefferson Health. Follow him on Twitter @doctornotte. Dr. Skolnik is professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington Jefferson Health.
Will changing the names of psychiatric medications lead to better treatment?
Back in 1980, the American Psychiatric Association dropped the word “neurosis” from the DSM-III, so that if you had been neurotic, after 1980, you were neurotic no longer.
At the time, I discussed this on my daily radio show. For those folks who were nervous, worried, fearful, and full of anxieties about themselves, their families, welfare, health, and the environment around them, a new set of labels was introduced to more specifically describe one or more problems related to anxiety.
For codification, and at times, a clearer understanding of a specific problem, the change was made to be helpful. Certainly, for insurers and pharmacologic treatments, it worked. However, it’s interesting that the word and concept, neurosis, which still is used by some psychiatrists and psychologists – although not scientific – does offer a clear overall picture of a suffering, anxiety-ridden person who might have a combination of an anxiety disorder, panic attacks, somatic symptoms, and endless worry. This overlapping picture often is seen in clinical practice more than the multiple one-dimensional labels that are currently used. So be it.
This all leads me to what I’ve recently learned about the Neuroscience-based Nomenclature (NbN) Project. According to a recent article in the APA’s Psychiatric News, the group’s board of trustees has endorsed a proposal that would change or revise the names of psychiatric medications so that the names reflect their mechanism of action – a move seemingly focused on a pure biological model.
For example, according to the article, the medication perphenazine would be renamed a “D2 receptor antagonist” rather than an antipsychotic. For depression, we might have a serotonergic reuptake inhibitor, according to the report, and of course, the list of changes would go on – based on current knowledge of biological activity. It’s true that in general medicine, there are examples where mode of action is discussed. For example, in cardiology we have beta-blockers and alpha-blockers, which are descriptive of their actions. As doctors who have trained for years and know the mechanism of action of various medications, we will understand all this. But in patient care, both doctors and their patients often understand and feel comfortable using descriptive terms indicating the treatment modality, such as antibiotics, antivirals, antifungals, anti-inflammatory medications, as well as anti-itching, antiaging, and antispasmodic drugs.
So, I am concerned about these proposed changes. In an era focused on patient-centered care, where we seek to make it simpler for the patient/health care consumer, we might make it harder for the patient to grasp what’s going on.
It’s very important to keep in mind that we as physicians know the ins and outs of medications, and that even the most educated and bright patients who are not in medicine do not know what our education has taught us. For example, regardless of specialty, we all know the difference between left-sided and right-sided heart failure. Those outside of medicine, however, rarely know the difference. They understand heart disease as a rule. People in general might understand some general concepts, such as RBC, WBC, and platelets. A patient will speak of taking a blood thinner but rarely know or understand the differences between antiplatelets and anticoagulants. And why should they know this?
The point here is that I believe good patient care is keeping it simple and taking the time to explain what’s being treated, aiming to inform patients using down-to-earth, accessible language rather than the language of biochemistry.
It’s true that in psychiatry, wider use of certain medications than originally indicated has grown tremendously as well as off-label use. In light of that, the NbN idea is laudable. However, it would seem more practical to leave the traditional modes of action in place and expand our discussions with patients as to why we are using a specific medication. I have found a very simple and even rewarding way to explain to patients, for example, that yes, this is an antiseizure medication but it is now used in psychiatry as a mood stabilizer.
Another important point is the question of whether using nomenclature that describes the exact location of the problem is all that accurate. Currently, we know we still have a lot to learn about brain chemistry and neuronal transmission in mental disorders, just as in many medical disorders, there are gaps in our understanding of many illnesses and subsequent molecular changes.
Just as the DSM-III left behind the all-encompassing and descriptive word neurosis and the APA has changed labels in the DSM-IV and DSM-5, so the NbN project would change the nomenclature of current psychotropic medications. The intentions are good, but the idea that those changes will foster better patient understanding defies common sense. A better idea might be to continue use of both scientific names and names of commonly used actions of the medications, leaving both in place and letting clinicians decide what nomenclature best suits each patient.
It will be a sad day when psychiatrists become so medically and “scientifically” driven that we cannot explain to a patient, “I’m prescribing this antidepressant because it’s now used to treat anxiety,” or “Yes, this medicine is labeled ‘antipsychotic,’ but you’re not psychotic. It may help your mood swings and may even help you sleep better.” Now, is that hard? Is talking to a person and explaining the treatment no longer part of care? The take-home messages from the recent APA/Institute of Psychiatric Services meeting I attended seemed to suggest that human attention and care have great value. My father, a surgeon, always said that you learn a lot by simply talking to patients – and they learn from you.
Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019).
Back in 1980, the American Psychiatric Association dropped the word “neurosis” from the DSM-III, so that if you had been neurotic, after 1980, you were neurotic no longer.
At the time, I discussed this on my daily radio show. For those folks who were nervous, worried, fearful, and full of anxieties about themselves, their families, welfare, health, and the environment around them, a new set of labels was introduced to more specifically describe one or more problems related to anxiety.
For codification, and at times, a clearer understanding of a specific problem, the change was made to be helpful. Certainly, for insurers and pharmacologic treatments, it worked. However, it’s interesting that the word and concept, neurosis, which still is used by some psychiatrists and psychologists – although not scientific – does offer a clear overall picture of a suffering, anxiety-ridden person who might have a combination of an anxiety disorder, panic attacks, somatic symptoms, and endless worry. This overlapping picture often is seen in clinical practice more than the multiple one-dimensional labels that are currently used. So be it.
This all leads me to what I’ve recently learned about the Neuroscience-based Nomenclature (NbN) Project. According to a recent article in the APA’s Psychiatric News, the group’s board of trustees has endorsed a proposal that would change or revise the names of psychiatric medications so that the names reflect their mechanism of action – a move seemingly focused on a pure biological model.
For example, according to the article, the medication perphenazine would be renamed a “D2 receptor antagonist” rather than an antipsychotic. For depression, we might have a serotonergic reuptake inhibitor, according to the report, and of course, the list of changes would go on – based on current knowledge of biological activity. It’s true that in general medicine, there are examples where mode of action is discussed. For example, in cardiology we have beta-blockers and alpha-blockers, which are descriptive of their actions. As doctors who have trained for years and know the mechanism of action of various medications, we will understand all this. But in patient care, both doctors and their patients often understand and feel comfortable using descriptive terms indicating the treatment modality, such as antibiotics, antivirals, antifungals, anti-inflammatory medications, as well as anti-itching, antiaging, and antispasmodic drugs.
So, I am concerned about these proposed changes. In an era focused on patient-centered care, where we seek to make it simpler for the patient/health care consumer, we might make it harder for the patient to grasp what’s going on.
It’s very important to keep in mind that we as physicians know the ins and outs of medications, and that even the most educated and bright patients who are not in medicine do not know what our education has taught us. For example, regardless of specialty, we all know the difference between left-sided and right-sided heart failure. Those outside of medicine, however, rarely know the difference. They understand heart disease as a rule. People in general might understand some general concepts, such as RBC, WBC, and platelets. A patient will speak of taking a blood thinner but rarely know or understand the differences between antiplatelets and anticoagulants. And why should they know this?
The point here is that I believe good patient care is keeping it simple and taking the time to explain what’s being treated, aiming to inform patients using down-to-earth, accessible language rather than the language of biochemistry.
It’s true that in psychiatry, wider use of certain medications than originally indicated has grown tremendously as well as off-label use. In light of that, the NbN idea is laudable. However, it would seem more practical to leave the traditional modes of action in place and expand our discussions with patients as to why we are using a specific medication. I have found a very simple and even rewarding way to explain to patients, for example, that yes, this is an antiseizure medication but it is now used in psychiatry as a mood stabilizer.
Another important point is the question of whether using nomenclature that describes the exact location of the problem is all that accurate. Currently, we know we still have a lot to learn about brain chemistry and neuronal transmission in mental disorders, just as in many medical disorders, there are gaps in our understanding of many illnesses and subsequent molecular changes.
Just as the DSM-III left behind the all-encompassing and descriptive word neurosis and the APA has changed labels in the DSM-IV and DSM-5, so the NbN project would change the nomenclature of current psychotropic medications. The intentions are good, but the idea that those changes will foster better patient understanding defies common sense. A better idea might be to continue use of both scientific names and names of commonly used actions of the medications, leaving both in place and letting clinicians decide what nomenclature best suits each patient.
It will be a sad day when psychiatrists become so medically and “scientifically” driven that we cannot explain to a patient, “I’m prescribing this antidepressant because it’s now used to treat anxiety,” or “Yes, this medicine is labeled ‘antipsychotic,’ but you’re not psychotic. It may help your mood swings and may even help you sleep better.” Now, is that hard? Is talking to a person and explaining the treatment no longer part of care? The take-home messages from the recent APA/Institute of Psychiatric Services meeting I attended seemed to suggest that human attention and care have great value. My father, a surgeon, always said that you learn a lot by simply talking to patients – and they learn from you.
Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019).
Back in 1980, the American Psychiatric Association dropped the word “neurosis” from the DSM-III, so that if you had been neurotic, after 1980, you were neurotic no longer.
At the time, I discussed this on my daily radio show. For those folks who were nervous, worried, fearful, and full of anxieties about themselves, their families, welfare, health, and the environment around them, a new set of labels was introduced to more specifically describe one or more problems related to anxiety.
For codification, and at times, a clearer understanding of a specific problem, the change was made to be helpful. Certainly, for insurers and pharmacologic treatments, it worked. However, it’s interesting that the word and concept, neurosis, which still is used by some psychiatrists and psychologists – although not scientific – does offer a clear overall picture of a suffering, anxiety-ridden person who might have a combination of an anxiety disorder, panic attacks, somatic symptoms, and endless worry. This overlapping picture often is seen in clinical practice more than the multiple one-dimensional labels that are currently used. So be it.
This all leads me to what I’ve recently learned about the Neuroscience-based Nomenclature (NbN) Project. According to a recent article in the APA’s Psychiatric News, the group’s board of trustees has endorsed a proposal that would change or revise the names of psychiatric medications so that the names reflect their mechanism of action – a move seemingly focused on a pure biological model.
For example, according to the article, the medication perphenazine would be renamed a “D2 receptor antagonist” rather than an antipsychotic. For depression, we might have a serotonergic reuptake inhibitor, according to the report, and of course, the list of changes would go on – based on current knowledge of biological activity. It’s true that in general medicine, there are examples where mode of action is discussed. For example, in cardiology we have beta-blockers and alpha-blockers, which are descriptive of their actions. As doctors who have trained for years and know the mechanism of action of various medications, we will understand all this. But in patient care, both doctors and their patients often understand and feel comfortable using descriptive terms indicating the treatment modality, such as antibiotics, antivirals, antifungals, anti-inflammatory medications, as well as anti-itching, antiaging, and antispasmodic drugs.
So, I am concerned about these proposed changes. In an era focused on patient-centered care, where we seek to make it simpler for the patient/health care consumer, we might make it harder for the patient to grasp what’s going on.
It’s very important to keep in mind that we as physicians know the ins and outs of medications, and that even the most educated and bright patients who are not in medicine do not know what our education has taught us. For example, regardless of specialty, we all know the difference between left-sided and right-sided heart failure. Those outside of medicine, however, rarely know the difference. They understand heart disease as a rule. People in general might understand some general concepts, such as RBC, WBC, and platelets. A patient will speak of taking a blood thinner but rarely know or understand the differences between antiplatelets and anticoagulants. And why should they know this?
The point here is that I believe good patient care is keeping it simple and taking the time to explain what’s being treated, aiming to inform patients using down-to-earth, accessible language rather than the language of biochemistry.
It’s true that in psychiatry, wider use of certain medications than originally indicated has grown tremendously as well as off-label use. In light of that, the NbN idea is laudable. However, it would seem more practical to leave the traditional modes of action in place and expand our discussions with patients as to why we are using a specific medication. I have found a very simple and even rewarding way to explain to patients, for example, that yes, this is an antiseizure medication but it is now used in psychiatry as a mood stabilizer.
Another important point is the question of whether using nomenclature that describes the exact location of the problem is all that accurate. Currently, we know we still have a lot to learn about brain chemistry and neuronal transmission in mental disorders, just as in many medical disorders, there are gaps in our understanding of many illnesses and subsequent molecular changes.
Just as the DSM-III left behind the all-encompassing and descriptive word neurosis and the APA has changed labels in the DSM-IV and DSM-5, so the NbN project would change the nomenclature of current psychotropic medications. The intentions are good, but the idea that those changes will foster better patient understanding defies common sense. A better idea might be to continue use of both scientific names and names of commonly used actions of the medications, leaving both in place and letting clinicians decide what nomenclature best suits each patient.
It will be a sad day when psychiatrists become so medically and “scientifically” driven that we cannot explain to a patient, “I’m prescribing this antidepressant because it’s now used to treat anxiety,” or “Yes, this medicine is labeled ‘antipsychotic,’ but you’re not psychotic. It may help your mood swings and may even help you sleep better.” Now, is that hard? Is talking to a person and explaining the treatment no longer part of care? The take-home messages from the recent APA/Institute of Psychiatric Services meeting I attended seemed to suggest that human attention and care have great value. My father, a surgeon, always said that you learn a lot by simply talking to patients – and they learn from you.
Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019).
Is carpal tunnel syndrome the tip of the iceberg?
He takes the following medications: felodipine and atorvastatin. On exam, his blood pressure is 110/60 mm Hg, and his pulse is 90 beats per minute.
A cardiac examination found normal heart sounds with no murmurs.
A chest examination found dullness to percussion at both bases and rales.
A chest x-ray showed bilateral effusions and mild pulmonary edema.
The brain natriuretic peptide test found a level of 1,300 picograms/mL.
An ECG found increased ventricular wall thickness, an ejection fraction of 32%, and normal aortic and mitral valves.
What history would be the most helpful in making a diagnosis?
A. History of prostate cancer
B. History of carpal tunnel syndrome
C. History of playing professional football
D. History of hyperlipidemia
E. History of ulcerative colitis
The correct answer here would be B. history of carpal tunnel syndrome (CTS). This patient has clinical heart failure, without a history of clinical ischemic disease. The differential diagnosis for causes of heart failure is long, with the most common causes being chronic hypertension and ischemic heart disease. Other common causes include chronic untreated sleep apnea and valvular heart disease.
This patient really does not have clear reasons for having clinical heart failure. His cardiovascular risk factors have been well controlled, and no valvular disease was found on ECG.
Several recent reports have raised the importance of a history of CTS significantly increasing the likelihood of amyloidosis being the cause of underlying heart failure.
CTS is such a common clinical entity that it is easy to not appreciate its presence as a clue to possible amyloid cardiomyopathy. Fosbøl et al. reported that a diagnosis of CTS was associated with a higher incidence of heart failure (hazard ratio, 1.54; CI, 1.45-1.64).1 They found a highly increased risk of amyloid (HR, 12.2) in patients who had surgery for CTS.
Sperry et al. found that over 10% of patients who underwent carpal tunnel release stained for amyloid on biopsy specimens, and that concomitant cardiac evaluation identified patients with cardiac involvement.2
Pinney et al. found that 48% of patients with transthyretin amyloidosis had a history of CTS.3
In a retrospective study of patients with wild-type transthyretin amyloid (253), patients with hereditary transthyretin amyloid (136), and asymptomatic gene carriers (77), participants were screened for a history of spinal stenosis and CTS.4 Almost 60% of the patients with amyloid had a history of CTS, and 11% had a history of spinal stenosis. Patients with CTS and hereditary amyloid had thicker interventricular septums, higher left ventricular mass, and lower Karnovsky index than those without CTS.
The diagnosis of CTS, especially in those who need surgery for treatment or have bilateral disease, should make us consider the possibility of underlying amyloidosis.
Pearl: In patients who have heart failure and a history of CTS, amyloidosis should be considered as a cause.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at that university. Contact Dr. Paauw at imnews@mdedge.com.
References
1. Fosbøl EL et al. J Am Coll Cardiol. 2019;74:15-23.
2. Sperry BW et al. J Am Coll Cardiol. 2018 Oct 23;72(17):2040-50.
3. Pinney JH et al. J Am Heart Assoc. 2013 Apr 22;2(2):e000098.
4. Aus dem Siepen F et al. Clin Res Cardiol. 2019 Apr 5. doi: 10.1007/s00392-019-01467-1.
He takes the following medications: felodipine and atorvastatin. On exam, his blood pressure is 110/60 mm Hg, and his pulse is 90 beats per minute.
A cardiac examination found normal heart sounds with no murmurs.
A chest examination found dullness to percussion at both bases and rales.
A chest x-ray showed bilateral effusions and mild pulmonary edema.
The brain natriuretic peptide test found a level of 1,300 picograms/mL.
An ECG found increased ventricular wall thickness, an ejection fraction of 32%, and normal aortic and mitral valves.
What history would be the most helpful in making a diagnosis?
A. History of prostate cancer
B. History of carpal tunnel syndrome
C. History of playing professional football
D. History of hyperlipidemia
E. History of ulcerative colitis
The correct answer here would be B. history of carpal tunnel syndrome (CTS). This patient has clinical heart failure, without a history of clinical ischemic disease. The differential diagnosis for causes of heart failure is long, with the most common causes being chronic hypertension and ischemic heart disease. Other common causes include chronic untreated sleep apnea and valvular heart disease.
This patient really does not have clear reasons for having clinical heart failure. His cardiovascular risk factors have been well controlled, and no valvular disease was found on ECG.
Several recent reports have raised the importance of a history of CTS significantly increasing the likelihood of amyloidosis being the cause of underlying heart failure.
CTS is such a common clinical entity that it is easy to not appreciate its presence as a clue to possible amyloid cardiomyopathy. Fosbøl et al. reported that a diagnosis of CTS was associated with a higher incidence of heart failure (hazard ratio, 1.54; CI, 1.45-1.64).1 They found a highly increased risk of amyloid (HR, 12.2) in patients who had surgery for CTS.
Sperry et al. found that over 10% of patients who underwent carpal tunnel release stained for amyloid on biopsy specimens, and that concomitant cardiac evaluation identified patients with cardiac involvement.2
Pinney et al. found that 48% of patients with transthyretin amyloidosis had a history of CTS.3
In a retrospective study of patients with wild-type transthyretin amyloid (253), patients with hereditary transthyretin amyloid (136), and asymptomatic gene carriers (77), participants were screened for a history of spinal stenosis and CTS.4 Almost 60% of the patients with amyloid had a history of CTS, and 11% had a history of spinal stenosis. Patients with CTS and hereditary amyloid had thicker interventricular septums, higher left ventricular mass, and lower Karnovsky index than those without CTS.
The diagnosis of CTS, especially in those who need surgery for treatment or have bilateral disease, should make us consider the possibility of underlying amyloidosis.
Pearl: In patients who have heart failure and a history of CTS, amyloidosis should be considered as a cause.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at that university. Contact Dr. Paauw at imnews@mdedge.com.
References
1. Fosbøl EL et al. J Am Coll Cardiol. 2019;74:15-23.
2. Sperry BW et al. J Am Coll Cardiol. 2018 Oct 23;72(17):2040-50.
3. Pinney JH et al. J Am Heart Assoc. 2013 Apr 22;2(2):e000098.
4. Aus dem Siepen F et al. Clin Res Cardiol. 2019 Apr 5. doi: 10.1007/s00392-019-01467-1.
He takes the following medications: felodipine and atorvastatin. On exam, his blood pressure is 110/60 mm Hg, and his pulse is 90 beats per minute.
A cardiac examination found normal heart sounds with no murmurs.
A chest examination found dullness to percussion at both bases and rales.
A chest x-ray showed bilateral effusions and mild pulmonary edema.
The brain natriuretic peptide test found a level of 1,300 picograms/mL.
An ECG found increased ventricular wall thickness, an ejection fraction of 32%, and normal aortic and mitral valves.
What history would be the most helpful in making a diagnosis?
A. History of prostate cancer
B. History of carpal tunnel syndrome
C. History of playing professional football
D. History of hyperlipidemia
E. History of ulcerative colitis
The correct answer here would be B. history of carpal tunnel syndrome (CTS). This patient has clinical heart failure, without a history of clinical ischemic disease. The differential diagnosis for causes of heart failure is long, with the most common causes being chronic hypertension and ischemic heart disease. Other common causes include chronic untreated sleep apnea and valvular heart disease.
This patient really does not have clear reasons for having clinical heart failure. His cardiovascular risk factors have been well controlled, and no valvular disease was found on ECG.
Several recent reports have raised the importance of a history of CTS significantly increasing the likelihood of amyloidosis being the cause of underlying heart failure.
CTS is such a common clinical entity that it is easy to not appreciate its presence as a clue to possible amyloid cardiomyopathy. Fosbøl et al. reported that a diagnosis of CTS was associated with a higher incidence of heart failure (hazard ratio, 1.54; CI, 1.45-1.64).1 They found a highly increased risk of amyloid (HR, 12.2) in patients who had surgery for CTS.
Sperry et al. found that over 10% of patients who underwent carpal tunnel release stained for amyloid on biopsy specimens, and that concomitant cardiac evaluation identified patients with cardiac involvement.2
Pinney et al. found that 48% of patients with transthyretin amyloidosis had a history of CTS.3
In a retrospective study of patients with wild-type transthyretin amyloid (253), patients with hereditary transthyretin amyloid (136), and asymptomatic gene carriers (77), participants were screened for a history of spinal stenosis and CTS.4 Almost 60% of the patients with amyloid had a history of CTS, and 11% had a history of spinal stenosis. Patients with CTS and hereditary amyloid had thicker interventricular septums, higher left ventricular mass, and lower Karnovsky index than those without CTS.
The diagnosis of CTS, especially in those who need surgery for treatment or have bilateral disease, should make us consider the possibility of underlying amyloidosis.
Pearl: In patients who have heart failure and a history of CTS, amyloidosis should be considered as a cause.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at that university. Contact Dr. Paauw at imnews@mdedge.com.
References
1. Fosbøl EL et al. J Am Coll Cardiol. 2019;74:15-23.
2. Sperry BW et al. J Am Coll Cardiol. 2018 Oct 23;72(17):2040-50.
3. Pinney JH et al. J Am Heart Assoc. 2013 Apr 22;2(2):e000098.
4. Aus dem Siepen F et al. Clin Res Cardiol. 2019 Apr 5. doi: 10.1007/s00392-019-01467-1.
Flu vaccine: Larger impact on influenza burden than you thought?
ID Week, the annual meeting of the Infectious Disease Society of America, provided valuable insights into past season’s endemic influenza burden and the effectiveness of prevention strategies. Each year, there are from 9million to 49 million influenza cases in the United States, 140,000-960,000 hospitalized cases, and 12,000-70,000 deaths directly attributable to influenza infection. The burden disproportionately falls on infants and adults 65 years of age and older; 11,000-48,000 children are hospitalized, and as many as several hundred children may die from influenza and related complications. School age children (aged 5-19 years) and adults (aged 30-39 years) are a major part of the transmission cycle. Influenza vaccine underlies the prevention strategy for limiting the burden of disease in U.S. populations. ID Week provided new insights into critical questions about influenza vaccines.
1. What is the effectiveness of influenza vaccine against severe disease (hospitalization) in children? Does it vary by age? By type or subtype?
Angela P. Campbell, MD, MPH, of the Centers for Disease Control and Prevention, and associates presented data on influenza vaccine effectiveness from the New Vaccine Surveillance Network in children for the 2016-2017 and 2017-2018 season (ID Week session 99; Abstract 899). During both 2016-2017 and 2017-2018, H3N2 was the dominant virus and influenza B represented about one-third of cases, and H1N1 was a greater percentage of cases in 2017-2018. Influenza positivity among children younger than 18 years of age admitted to hospital with respiratory disease was 14% among unvaccinated and 8% among vaccinated children; effectiveness again hospitalization was 50%. Vaccine effectiveness (VE) was not statistically different between children younger than 8 years of age and those older that 8 years but did differ by vaccine type. VE was 76% against H1N1 disease, 59% again B disease, and only 33% against H3N2 disease.
Clearly, vaccination with influenza vaccine prevents serious respiratory disease. However, the impact of vaccine will vary by season and by which influenza stains are circulating in the community. The authors concluded that further understanding of the lower VE against H3N2 disease is needed.
2. Does the priming dose of influenza vaccine improve vaccine effectiveness?
Current recommendations call for a two-dose series for influenza vaccine in children aged 6 months through 8 years who have not had prior influenza vaccine. The recommendation is based on evidence demonstrating higher antibody responses in children receiving two doses, compared with a single dose. Using data from the U.S. Influenza Vaccine Effectiveness Network, Jessie R. Chung, MPH, of the CDC, and associates compared VE in children younger than 2 years receiving two doses in the first year of flu immunization (fully immunized), compared with those who received only one dose (partially immunized) (ID Week session 99; Abstract 900). VE was 53% for fully immunized and 23% for partially immunized children. Receipt of a single dose did not provide statistically significant protection against influenza. Surprisingly (to me), of 5,355 children aged 6 months to less than 2 years with no prior influenza vaccine, 1,870 (35%) received only one dose in the season.
The data strongly support the current recommendations for a priming dose, especially in young children, in the first season of influenza vaccine and warrants increased efforts to increase the update of second doses during the season. Hopefully we can do better in 2019!
3. Should we wait to vaccinate with influenza vaccine?
Some evidence suggests that waning immunity to influenza vaccine, primarily in those aged 65 years and older, may explain increased disease activity toward the end of influenza season. Other explanations include increasing viral diversity throughout the season, resulting in reduced effectiveness. Do such concerns warrant delaying immunization? The onset and peak of influenza season varies by year; in October 2019, 3% of tests performed on patients with respiratory illness were influenza positive. The trade-offs for delaying immunization until October are the unpredictability of onset of influenza season, the requirement for two doses in infants, the need for 2 weeks to achieve peak antibody concentrations, and the potential that fewer individuals will be vaccinated. Kathy Neuzil, MD, MPH, from the Center for Vaccine Development and Global Health, University of Maryland School of Medicine, reviewed recent modeling (for adults aged 65 years and older) and reported that delaying vaccine programs until October is associated with greater burden of hospitalization if 14% fewer individuals (who would be vaccinated in August/September) are vaccinated (ID Week; Session 940).
In response to these concerns, the CDC recommendations for 2019 are that, in children aged 6 months through 8 years who need two doses, start early so that you can achieve both doses before influenza season (MMWR 2019 Aug 23;68[3]:1-21).In older children and adults, who need only a single dose, early vaccination (August and early September) may lead to reduced protection late in the influenza season?
4. How can we optimize vaccine impact?
Vaccine impact refers to the affect on a population level and not at an individual level. Meagan C. Fitzpatrick, PhD, from the Center for Vaccine Development and Global Health, University of Maryland School of Medicine, evaluated the benefits of our moderately effective influenza vaccines (VE 40%-60%) to the population beyond those who are vaccinated. Her conclusions were that even a modestly effective vaccine prevents 21 million cases of influenza, 129,000 hospitalizations, and 62,000 deaths. And that two-thirds of the deaths prevented are from herd benefit (or indirect effects). Although both coverage and vaccine effectiveness are important, she reported that population impact was most sensitive to coverage, compared with vaccine effectiveness. Dr. Fitzpatrick found that targeting school-age children 6-19 years of age and adults 30-39 years of age maximizes the public health benefits (herd effects) of influenza vaccine. In 2018 season, influenza coverage was 63% for at least one dose in children aged 6 months through 17 years and 45% in adults aged 18 years and older; in the two target age groups 5-17 and 30-39 years, coverage was 59% and approximately 35%, respectively (ID Week; Session 939).
Clearly, even our modestly effective influenza vaccines have significant public health benefit in protecting the U.S. populations from serious disease and death. Efforts to increase vaccine uptake in school-age children, both those with and without comorbidity, and the 30- to 39-year-old adult cohort would likely further reduce the burden of serious disease from influenza.
In summary, despite a vaccine that is only moderately effective, there is clear evidence to support current recommendations of universal immunization beginning at 6 months of age. Delaying until October 1 is a good idea only if the same number of individuals will receive influenza vaccine, otherwise the hypothetical benefit is lost.
Dr. Pelton is professor of pediatrics and epidemiology at Boston University schools of medicine and public health and is senior attending physician, Boston Medical Center. Dr. Pelton has investigator-initiated research awards to Boston Medical Center from Pfizer and Merck Vaccines. He also received honorarium as an advisory board member, participation in symposium and consultation from Seqirus and Merck Vaccine, Pfizer, and Sanofi Pasteur. Email him at pdnews@mdedge.com.
ID Week, the annual meeting of the Infectious Disease Society of America, provided valuable insights into past season’s endemic influenza burden and the effectiveness of prevention strategies. Each year, there are from 9million to 49 million influenza cases in the United States, 140,000-960,000 hospitalized cases, and 12,000-70,000 deaths directly attributable to influenza infection. The burden disproportionately falls on infants and adults 65 years of age and older; 11,000-48,000 children are hospitalized, and as many as several hundred children may die from influenza and related complications. School age children (aged 5-19 years) and adults (aged 30-39 years) are a major part of the transmission cycle. Influenza vaccine underlies the prevention strategy for limiting the burden of disease in U.S. populations. ID Week provided new insights into critical questions about influenza vaccines.
1. What is the effectiveness of influenza vaccine against severe disease (hospitalization) in children? Does it vary by age? By type or subtype?
Angela P. Campbell, MD, MPH, of the Centers for Disease Control and Prevention, and associates presented data on influenza vaccine effectiveness from the New Vaccine Surveillance Network in children for the 2016-2017 and 2017-2018 season (ID Week session 99; Abstract 899). During both 2016-2017 and 2017-2018, H3N2 was the dominant virus and influenza B represented about one-third of cases, and H1N1 was a greater percentage of cases in 2017-2018. Influenza positivity among children younger than 18 years of age admitted to hospital with respiratory disease was 14% among unvaccinated and 8% among vaccinated children; effectiveness again hospitalization was 50%. Vaccine effectiveness (VE) was not statistically different between children younger than 8 years of age and those older that 8 years but did differ by vaccine type. VE was 76% against H1N1 disease, 59% again B disease, and only 33% against H3N2 disease.
Clearly, vaccination with influenza vaccine prevents serious respiratory disease. However, the impact of vaccine will vary by season and by which influenza stains are circulating in the community. The authors concluded that further understanding of the lower VE against H3N2 disease is needed.
2. Does the priming dose of influenza vaccine improve vaccine effectiveness?
Current recommendations call for a two-dose series for influenza vaccine in children aged 6 months through 8 years who have not had prior influenza vaccine. The recommendation is based on evidence demonstrating higher antibody responses in children receiving two doses, compared with a single dose. Using data from the U.S. Influenza Vaccine Effectiveness Network, Jessie R. Chung, MPH, of the CDC, and associates compared VE in children younger than 2 years receiving two doses in the first year of flu immunization (fully immunized), compared with those who received only one dose (partially immunized) (ID Week session 99; Abstract 900). VE was 53% for fully immunized and 23% for partially immunized children. Receipt of a single dose did not provide statistically significant protection against influenza. Surprisingly (to me), of 5,355 children aged 6 months to less than 2 years with no prior influenza vaccine, 1,870 (35%) received only one dose in the season.
The data strongly support the current recommendations for a priming dose, especially in young children, in the first season of influenza vaccine and warrants increased efforts to increase the update of second doses during the season. Hopefully we can do better in 2019!
3. Should we wait to vaccinate with influenza vaccine?
Some evidence suggests that waning immunity to influenza vaccine, primarily in those aged 65 years and older, may explain increased disease activity toward the end of influenza season. Other explanations include increasing viral diversity throughout the season, resulting in reduced effectiveness. Do such concerns warrant delaying immunization? The onset and peak of influenza season varies by year; in October 2019, 3% of tests performed on patients with respiratory illness were influenza positive. The trade-offs for delaying immunization until October are the unpredictability of onset of influenza season, the requirement for two doses in infants, the need for 2 weeks to achieve peak antibody concentrations, and the potential that fewer individuals will be vaccinated. Kathy Neuzil, MD, MPH, from the Center for Vaccine Development and Global Health, University of Maryland School of Medicine, reviewed recent modeling (for adults aged 65 years and older) and reported that delaying vaccine programs until October is associated with greater burden of hospitalization if 14% fewer individuals (who would be vaccinated in August/September) are vaccinated (ID Week; Session 940).
In response to these concerns, the CDC recommendations for 2019 are that, in children aged 6 months through 8 years who need two doses, start early so that you can achieve both doses before influenza season (MMWR 2019 Aug 23;68[3]:1-21).In older children and adults, who need only a single dose, early vaccination (August and early September) may lead to reduced protection late in the influenza season?
4. How can we optimize vaccine impact?
Vaccine impact refers to the affect on a population level and not at an individual level. Meagan C. Fitzpatrick, PhD, from the Center for Vaccine Development and Global Health, University of Maryland School of Medicine, evaluated the benefits of our moderately effective influenza vaccines (VE 40%-60%) to the population beyond those who are vaccinated. Her conclusions were that even a modestly effective vaccine prevents 21 million cases of influenza, 129,000 hospitalizations, and 62,000 deaths. And that two-thirds of the deaths prevented are from herd benefit (or indirect effects). Although both coverage and vaccine effectiveness are important, she reported that population impact was most sensitive to coverage, compared with vaccine effectiveness. Dr. Fitzpatrick found that targeting school-age children 6-19 years of age and adults 30-39 years of age maximizes the public health benefits (herd effects) of influenza vaccine. In 2018 season, influenza coverage was 63% for at least one dose in children aged 6 months through 17 years and 45% in adults aged 18 years and older; in the two target age groups 5-17 and 30-39 years, coverage was 59% and approximately 35%, respectively (ID Week; Session 939).
Clearly, even our modestly effective influenza vaccines have significant public health benefit in protecting the U.S. populations from serious disease and death. Efforts to increase vaccine uptake in school-age children, both those with and without comorbidity, and the 30- to 39-year-old adult cohort would likely further reduce the burden of serious disease from influenza.
In summary, despite a vaccine that is only moderately effective, there is clear evidence to support current recommendations of universal immunization beginning at 6 months of age. Delaying until October 1 is a good idea only if the same number of individuals will receive influenza vaccine, otherwise the hypothetical benefit is lost.
Dr. Pelton is professor of pediatrics and epidemiology at Boston University schools of medicine and public health and is senior attending physician, Boston Medical Center. Dr. Pelton has investigator-initiated research awards to Boston Medical Center from Pfizer and Merck Vaccines. He also received honorarium as an advisory board member, participation in symposium and consultation from Seqirus and Merck Vaccine, Pfizer, and Sanofi Pasteur. Email him at pdnews@mdedge.com.
ID Week, the annual meeting of the Infectious Disease Society of America, provided valuable insights into past season’s endemic influenza burden and the effectiveness of prevention strategies. Each year, there are from 9million to 49 million influenza cases in the United States, 140,000-960,000 hospitalized cases, and 12,000-70,000 deaths directly attributable to influenza infection. The burden disproportionately falls on infants and adults 65 years of age and older; 11,000-48,000 children are hospitalized, and as many as several hundred children may die from influenza and related complications. School age children (aged 5-19 years) and adults (aged 30-39 years) are a major part of the transmission cycle. Influenza vaccine underlies the prevention strategy for limiting the burden of disease in U.S. populations. ID Week provided new insights into critical questions about influenza vaccines.
1. What is the effectiveness of influenza vaccine against severe disease (hospitalization) in children? Does it vary by age? By type or subtype?
Angela P. Campbell, MD, MPH, of the Centers for Disease Control and Prevention, and associates presented data on influenza vaccine effectiveness from the New Vaccine Surveillance Network in children for the 2016-2017 and 2017-2018 season (ID Week session 99; Abstract 899). During both 2016-2017 and 2017-2018, H3N2 was the dominant virus and influenza B represented about one-third of cases, and H1N1 was a greater percentage of cases in 2017-2018. Influenza positivity among children younger than 18 years of age admitted to hospital with respiratory disease was 14% among unvaccinated and 8% among vaccinated children; effectiveness again hospitalization was 50%. Vaccine effectiveness (VE) was not statistically different between children younger than 8 years of age and those older that 8 years but did differ by vaccine type. VE was 76% against H1N1 disease, 59% again B disease, and only 33% against H3N2 disease.
Clearly, vaccination with influenza vaccine prevents serious respiratory disease. However, the impact of vaccine will vary by season and by which influenza stains are circulating in the community. The authors concluded that further understanding of the lower VE against H3N2 disease is needed.
2. Does the priming dose of influenza vaccine improve vaccine effectiveness?
Current recommendations call for a two-dose series for influenza vaccine in children aged 6 months through 8 years who have not had prior influenza vaccine. The recommendation is based on evidence demonstrating higher antibody responses in children receiving two doses, compared with a single dose. Using data from the U.S. Influenza Vaccine Effectiveness Network, Jessie R. Chung, MPH, of the CDC, and associates compared VE in children younger than 2 years receiving two doses in the first year of flu immunization (fully immunized), compared with those who received only one dose (partially immunized) (ID Week session 99; Abstract 900). VE was 53% for fully immunized and 23% for partially immunized children. Receipt of a single dose did not provide statistically significant protection against influenza. Surprisingly (to me), of 5,355 children aged 6 months to less than 2 years with no prior influenza vaccine, 1,870 (35%) received only one dose in the season.
The data strongly support the current recommendations for a priming dose, especially in young children, in the first season of influenza vaccine and warrants increased efforts to increase the update of second doses during the season. Hopefully we can do better in 2019!
3. Should we wait to vaccinate with influenza vaccine?
Some evidence suggests that waning immunity to influenza vaccine, primarily in those aged 65 years and older, may explain increased disease activity toward the end of influenza season. Other explanations include increasing viral diversity throughout the season, resulting in reduced effectiveness. Do such concerns warrant delaying immunization? The onset and peak of influenza season varies by year; in October 2019, 3% of tests performed on patients with respiratory illness were influenza positive. The trade-offs for delaying immunization until October are the unpredictability of onset of influenza season, the requirement for two doses in infants, the need for 2 weeks to achieve peak antibody concentrations, and the potential that fewer individuals will be vaccinated. Kathy Neuzil, MD, MPH, from the Center for Vaccine Development and Global Health, University of Maryland School of Medicine, reviewed recent modeling (for adults aged 65 years and older) and reported that delaying vaccine programs until October is associated with greater burden of hospitalization if 14% fewer individuals (who would be vaccinated in August/September) are vaccinated (ID Week; Session 940).
In response to these concerns, the CDC recommendations for 2019 are that, in children aged 6 months through 8 years who need two doses, start early so that you can achieve both doses before influenza season (MMWR 2019 Aug 23;68[3]:1-21).In older children and adults, who need only a single dose, early vaccination (August and early September) may lead to reduced protection late in the influenza season?
4. How can we optimize vaccine impact?
Vaccine impact refers to the affect on a population level and not at an individual level. Meagan C. Fitzpatrick, PhD, from the Center for Vaccine Development and Global Health, University of Maryland School of Medicine, evaluated the benefits of our moderately effective influenza vaccines (VE 40%-60%) to the population beyond those who are vaccinated. Her conclusions were that even a modestly effective vaccine prevents 21 million cases of influenza, 129,000 hospitalizations, and 62,000 deaths. And that two-thirds of the deaths prevented are from herd benefit (or indirect effects). Although both coverage and vaccine effectiveness are important, she reported that population impact was most sensitive to coverage, compared with vaccine effectiveness. Dr. Fitzpatrick found that targeting school-age children 6-19 years of age and adults 30-39 years of age maximizes the public health benefits (herd effects) of influenza vaccine. In 2018 season, influenza coverage was 63% for at least one dose in children aged 6 months through 17 years and 45% in adults aged 18 years and older; in the two target age groups 5-17 and 30-39 years, coverage was 59% and approximately 35%, respectively (ID Week; Session 939).
Clearly, even our modestly effective influenza vaccines have significant public health benefit in protecting the U.S. populations from serious disease and death. Efforts to increase vaccine uptake in school-age children, both those with and without comorbidity, and the 30- to 39-year-old adult cohort would likely further reduce the burden of serious disease from influenza.
In summary, despite a vaccine that is only moderately effective, there is clear evidence to support current recommendations of universal immunization beginning at 6 months of age. Delaying until October 1 is a good idea only if the same number of individuals will receive influenza vaccine, otherwise the hypothetical benefit is lost.
Dr. Pelton is professor of pediatrics and epidemiology at Boston University schools of medicine and public health and is senior attending physician, Boston Medical Center. Dr. Pelton has investigator-initiated research awards to Boston Medical Center from Pfizer and Merck Vaccines. He also received honorarium as an advisory board member, participation in symposium and consultation from Seqirus and Merck Vaccine, Pfizer, and Sanofi Pasteur. Email him at pdnews@mdedge.com.
Sixty-five roses
Like many of you, my wife and I took the DNA plunge for fun and spit in the cup. She is genetically perfect, but I, however, am a carrier for alpha-1 anti-trypsin deficiency, hemochromatosis, and like 1 in 19 Irish people, cystic fibrosis. Plus, I was in the top 20% for Neanderthal genes.
My Y chromosome had traveled to the United States from Europe, where it had spent several hundred years in Ireland (in the house of Neal); wandering to Ireland from the Middle East, and originating in Siberia! Fascinating stuff.
away. It is hypothesized that the very-high-frequency deleterious genes have a survival advantage in the heterozygous state, coined the “heterozygote advantage.”
Alpha-1 antitrypsin deficiency allows the body to concentrate an inflammatory response in the lungs and liver, perhaps providing protection against tuberculosis (Am J Respir Crit Care Med. 2006 May 15;173[10]:1072-7).
Hemochromatosis allows for increased iron absorption attributable to decreased iron in a grain-based diet, and facilitates thyroid-stimulating hormone release in cold environments (Am J Phys Anthropol. 2016 May;160[1]:86-101).
Cystic fibrosis carriers are more resistant to diarrheal illness, particularly cholera and typhoid fever since they have only one exudative chloride channel to switch on. Their sputum is also thicker, interfering with microdroplet generation and spread of the bacilli to others.
This topic and learning of my CF carrier status bring to mind one of my patients. When doing skin exams, I sometimes ask patients about elaborate tattoos (not the obvious youthful misadventures). “Nice ink” I will say, and I wait and see if they want to elaborate. This particular patient was enthusiastic and explained that the elaborate floral design with roses on his right leg was in memory of his daughter. I asked what had happened, expecting a tragic car wreck, or perhaps cancer or a drug overdose. He cheerfully explained she had died of cystic fibrosis at age 21, a year after a lung transplant.
My eyes started to water. My patient was upbeat and said she had lived with gusto and survived long enough to buy him a triple gin and tonic at bar. She had always had a bright outlook, despite her debilitating and eventually fatal disease.
I had to ask more about the memorial tattoo. He explained that her initials were linked with his at the bottom of the bouquet of many, many roses. “Why roses?” I asked. “Well,” he said, “when she was little, she could not pronounce cystic fibrosis, so she always said, ‘My daddy says I have 65 roses.’ ”*
Oh boy. I had to go sit in my office, turn out the lights, and cry.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com.
* This is in fact, what many children with the disease call it, and is the symbol of the Cystic Fibrosis Foundation, a story originating in 1965, when a 4-year-old with cystic fibrosis asked his mother about “65 Roses” after he heard her talking on the phone raising funds for research.
Like many of you, my wife and I took the DNA plunge for fun and spit in the cup. She is genetically perfect, but I, however, am a carrier for alpha-1 anti-trypsin deficiency, hemochromatosis, and like 1 in 19 Irish people, cystic fibrosis. Plus, I was in the top 20% for Neanderthal genes.
My Y chromosome had traveled to the United States from Europe, where it had spent several hundred years in Ireland (in the house of Neal); wandering to Ireland from the Middle East, and originating in Siberia! Fascinating stuff.
away. It is hypothesized that the very-high-frequency deleterious genes have a survival advantage in the heterozygous state, coined the “heterozygote advantage.”
Alpha-1 antitrypsin deficiency allows the body to concentrate an inflammatory response in the lungs and liver, perhaps providing protection against tuberculosis (Am J Respir Crit Care Med. 2006 May 15;173[10]:1072-7).
Hemochromatosis allows for increased iron absorption attributable to decreased iron in a grain-based diet, and facilitates thyroid-stimulating hormone release in cold environments (Am J Phys Anthropol. 2016 May;160[1]:86-101).
Cystic fibrosis carriers are more resistant to diarrheal illness, particularly cholera and typhoid fever since they have only one exudative chloride channel to switch on. Their sputum is also thicker, interfering with microdroplet generation and spread of the bacilli to others.
This topic and learning of my CF carrier status bring to mind one of my patients. When doing skin exams, I sometimes ask patients about elaborate tattoos (not the obvious youthful misadventures). “Nice ink” I will say, and I wait and see if they want to elaborate. This particular patient was enthusiastic and explained that the elaborate floral design with roses on his right leg was in memory of his daughter. I asked what had happened, expecting a tragic car wreck, or perhaps cancer or a drug overdose. He cheerfully explained she had died of cystic fibrosis at age 21, a year after a lung transplant.
My eyes started to water. My patient was upbeat and said she had lived with gusto and survived long enough to buy him a triple gin and tonic at bar. She had always had a bright outlook, despite her debilitating and eventually fatal disease.
I had to ask more about the memorial tattoo. He explained that her initials were linked with his at the bottom of the bouquet of many, many roses. “Why roses?” I asked. “Well,” he said, “when she was little, she could not pronounce cystic fibrosis, so she always said, ‘My daddy says I have 65 roses.’ ”*
Oh boy. I had to go sit in my office, turn out the lights, and cry.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com.
* This is in fact, what many children with the disease call it, and is the symbol of the Cystic Fibrosis Foundation, a story originating in 1965, when a 4-year-old with cystic fibrosis asked his mother about “65 Roses” after he heard her talking on the phone raising funds for research.
Like many of you, my wife and I took the DNA plunge for fun and spit in the cup. She is genetically perfect, but I, however, am a carrier for alpha-1 anti-trypsin deficiency, hemochromatosis, and like 1 in 19 Irish people, cystic fibrosis. Plus, I was in the top 20% for Neanderthal genes.
My Y chromosome had traveled to the United States from Europe, where it had spent several hundred years in Ireland (in the house of Neal); wandering to Ireland from the Middle East, and originating in Siberia! Fascinating stuff.
away. It is hypothesized that the very-high-frequency deleterious genes have a survival advantage in the heterozygous state, coined the “heterozygote advantage.”
Alpha-1 antitrypsin deficiency allows the body to concentrate an inflammatory response in the lungs and liver, perhaps providing protection against tuberculosis (Am J Respir Crit Care Med. 2006 May 15;173[10]:1072-7).
Hemochromatosis allows for increased iron absorption attributable to decreased iron in a grain-based diet, and facilitates thyroid-stimulating hormone release in cold environments (Am J Phys Anthropol. 2016 May;160[1]:86-101).
Cystic fibrosis carriers are more resistant to diarrheal illness, particularly cholera and typhoid fever since they have only one exudative chloride channel to switch on. Their sputum is also thicker, interfering with microdroplet generation and spread of the bacilli to others.
This topic and learning of my CF carrier status bring to mind one of my patients. When doing skin exams, I sometimes ask patients about elaborate tattoos (not the obvious youthful misadventures). “Nice ink” I will say, and I wait and see if they want to elaborate. This particular patient was enthusiastic and explained that the elaborate floral design with roses on his right leg was in memory of his daughter. I asked what had happened, expecting a tragic car wreck, or perhaps cancer or a drug overdose. He cheerfully explained she had died of cystic fibrosis at age 21, a year after a lung transplant.
My eyes started to water. My patient was upbeat and said she had lived with gusto and survived long enough to buy him a triple gin and tonic at bar. She had always had a bright outlook, despite her debilitating and eventually fatal disease.
I had to ask more about the memorial tattoo. He explained that her initials were linked with his at the bottom of the bouquet of many, many roses. “Why roses?” I asked. “Well,” he said, “when she was little, she could not pronounce cystic fibrosis, so she always said, ‘My daddy says I have 65 roses.’ ”*
Oh boy. I had to go sit in my office, turn out the lights, and cry.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com.
* This is in fact, what many children with the disease call it, and is the symbol of the Cystic Fibrosis Foundation, a story originating in 1965, when a 4-year-old with cystic fibrosis asked his mother about “65 Roses” after he heard her talking on the phone raising funds for research.