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Obesity: A Social Vulnerability
Sometime in the last year or 2 I wrote that, despite my considerable reservations, I had finally come to the conclusion that the American Medical Association’s decision to designate obesity as a disease was appropriate. My rationalization was that the disease label would open more opportunities for funding obesity treatments. However, the explosive growth and popularity of glucagon-like peptide 1 (GLP-1) agonists over the last year has had me rethinking my decision to suppress my long-held reservations about the disease designation.
So, if it’s not a disease, then what should we call it? How do we explain its surge in high-income countries that began in the 1980s? While there are still some folks who see obesity as a character flaw, I think you and I as healthcare providers have difficulty explaining the increase prevalence of obesity as either global breakdown of willpower or a widespread genetic shift as the result of burst of radiation from solar flares.
However, if we want to continue our search and finger-pointing we need to have a better definition of exactly what obesity is. If we’re going to continue calling it a disease we have done a pretty sloppy job of creating diagnostic criteria. To be honest, we aren’t doing such a hot job with “long COVID” either.
A recent article in the New York Times makes it clear that I’m not the only physician who is feeling uncomfortable with this lack of diagnostic specificity.
We know that using body mass index (BMI) as a criteria is imprecise. There are healthy individuals with elevated BMIs and there are others who are carrying an unhealthy amount of fat who have normal BMIs. And, there are individuals who have what might appear to be an excess amount of fat who are fit and healthy by other criteria.
Some investigators feel that a set of measurements that includes a waist and/or hip measurement may be a more accurate way of determining visceral adipose tissue. However, this body roundness index (BRI) currently relies on a tape measurement. Until the technique can be preformed by an inexpensive and readily available scanner, the BRI cannot be considered a practical tool for determining obesity.
Dr. Francisco Rubino, the chair of metabolic and bariatric surgery at Kings College in London, England, has been quoted as saying that, “if one defines a disease inaccurately, everything that stems from that – from diagnosis to treatment to policies – will be distorted and biased.”
Denmark has been forced to relabel obesity as a risk factor because the disease designation was stressing the financial viability of their healthcare system as more and more patients were being prescribe GLP-1 agonists, sometimes off label. A rationing strategy was resulting in suboptimal treatment of a significant portion of the obese population.
Spearheaded by Dr. Rubino, a Lancet Commission composed of physicians has tasked itself to define an “evidence-based diagnosis for obesity. Instead of relying on a single metric such as the BMI or BRI, diagnosing “clinical obesity” would involve a broad array of observations including a history, physical examination, standard laboratory and additional testing, “naming signs and symptoms, organ by organ, tissue by tissue, with plausible mechanisms for each one.” In other words, treating each patient as an individual using evidence-based criteria to make a diagnosis. While likely to be time consuming, this strategy feels like a more scientific approach. I suspect once clinical obesity is more rigorously defined it could be divided into several subtypes. For example, there would be a few conditions that were genetic; Prader-Willi syndrome being the best known.
However, I think the Lancet Commission’s strategy will find that the majority of individuals who make up this half-century global surge have become clinically obese because they have been unable to adapt to the obeseogenic forces in our society, which include diet, autocentricity, and attractive sedentary forms of entertainment, to name just three.
In some cases these unfortunate individuals are more vulnerable because there were born into an economically disadvantaged situation. In other scenarios a lack of foresight and/or political will may have left individuals with no other choice but to rely on automobiles to get around. Still others may find themselves living in a nutritional desert because all of the grocery stores have closed.
I recently encountered a descriptor in a story about the Federal Emergency Management Agency which could easily be adapted to describe this large and growing subtype of individuals with clinical obesity. “Social vulnerability” is measure of how well a community can withstand external stressors that impact human health. For example, the emergency management folks are thinking in terms of natural disaster such as hurricanes, floods, and tornadoes and are asking how well a given community can meet the challenges one would create.
But, the term social vulnerability can easily be applied to individuals living in a society in which unhealthy food is abundant, an infrastructure that discourages or outright prevents non-motorized travel, and the temptation of sedentary entertainment options is unavoidable. Fortunately, not every citizen living in an obesogenic society becomes obese. What factors have protected the non-obese individuals from these obeseogenic stressors? What are the characteristics of the unfortunate “vulnerables” living in the same society who end up being obese?
It is time to shift our focus away from a poorly defined disease model to one in which we begin looking at our society to find out why we have so many socially vulnerable individuals. The toll of obesity as it is currently defined is many order of magnitudes greater than any natural disaster. We have become communities that can no longer withstand the its obesogenic stressors many of which we have created and/or allowed to accumulate over the last century.
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.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Sometime in the last year or 2 I wrote that, despite my considerable reservations, I had finally come to the conclusion that the American Medical Association’s decision to designate obesity as a disease was appropriate. My rationalization was that the disease label would open more opportunities for funding obesity treatments. However, the explosive growth and popularity of glucagon-like peptide 1 (GLP-1) agonists over the last year has had me rethinking my decision to suppress my long-held reservations about the disease designation.
So, if it’s not a disease, then what should we call it? How do we explain its surge in high-income countries that began in the 1980s? While there are still some folks who see obesity as a character flaw, I think you and I as healthcare providers have difficulty explaining the increase prevalence of obesity as either global breakdown of willpower or a widespread genetic shift as the result of burst of radiation from solar flares.
However, if we want to continue our search and finger-pointing we need to have a better definition of exactly what obesity is. If we’re going to continue calling it a disease we have done a pretty sloppy job of creating diagnostic criteria. To be honest, we aren’t doing such a hot job with “long COVID” either.
A recent article in the New York Times makes it clear that I’m not the only physician who is feeling uncomfortable with this lack of diagnostic specificity.
We know that using body mass index (BMI) as a criteria is imprecise. There are healthy individuals with elevated BMIs and there are others who are carrying an unhealthy amount of fat who have normal BMIs. And, there are individuals who have what might appear to be an excess amount of fat who are fit and healthy by other criteria.
Some investigators feel that a set of measurements that includes a waist and/or hip measurement may be a more accurate way of determining visceral adipose tissue. However, this body roundness index (BRI) currently relies on a tape measurement. Until the technique can be preformed by an inexpensive and readily available scanner, the BRI cannot be considered a practical tool for determining obesity.
Dr. Francisco Rubino, the chair of metabolic and bariatric surgery at Kings College in London, England, has been quoted as saying that, “if one defines a disease inaccurately, everything that stems from that – from diagnosis to treatment to policies – will be distorted and biased.”
Denmark has been forced to relabel obesity as a risk factor because the disease designation was stressing the financial viability of their healthcare system as more and more patients were being prescribe GLP-1 agonists, sometimes off label. A rationing strategy was resulting in suboptimal treatment of a significant portion of the obese population.
Spearheaded by Dr. Rubino, a Lancet Commission composed of physicians has tasked itself to define an “evidence-based diagnosis for obesity. Instead of relying on a single metric such as the BMI or BRI, diagnosing “clinical obesity” would involve a broad array of observations including a history, physical examination, standard laboratory and additional testing, “naming signs and symptoms, organ by organ, tissue by tissue, with plausible mechanisms for each one.” In other words, treating each patient as an individual using evidence-based criteria to make a diagnosis. While likely to be time consuming, this strategy feels like a more scientific approach. I suspect once clinical obesity is more rigorously defined it could be divided into several subtypes. For example, there would be a few conditions that were genetic; Prader-Willi syndrome being the best known.
However, I think the Lancet Commission’s strategy will find that the majority of individuals who make up this half-century global surge have become clinically obese because they have been unable to adapt to the obeseogenic forces in our society, which include diet, autocentricity, and attractive sedentary forms of entertainment, to name just three.
In some cases these unfortunate individuals are more vulnerable because there were born into an economically disadvantaged situation. In other scenarios a lack of foresight and/or political will may have left individuals with no other choice but to rely on automobiles to get around. Still others may find themselves living in a nutritional desert because all of the grocery stores have closed.
I recently encountered a descriptor in a story about the Federal Emergency Management Agency which could easily be adapted to describe this large and growing subtype of individuals with clinical obesity. “Social vulnerability” is measure of how well a community can withstand external stressors that impact human health. For example, the emergency management folks are thinking in terms of natural disaster such as hurricanes, floods, and tornadoes and are asking how well a given community can meet the challenges one would create.
But, the term social vulnerability can easily be applied to individuals living in a society in which unhealthy food is abundant, an infrastructure that discourages or outright prevents non-motorized travel, and the temptation of sedentary entertainment options is unavoidable. Fortunately, not every citizen living in an obesogenic society becomes obese. What factors have protected the non-obese individuals from these obeseogenic stressors? What are the characteristics of the unfortunate “vulnerables” living in the same society who end up being obese?
It is time to shift our focus away from a poorly defined disease model to one in which we begin looking at our society to find out why we have so many socially vulnerable individuals. The toll of obesity as it is currently defined is many order of magnitudes greater than any natural disaster. We have become communities that can no longer withstand the its obesogenic stressors many of which we have created and/or allowed to accumulate over the last century.
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.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Sometime in the last year or 2 I wrote that, despite my considerable reservations, I had finally come to the conclusion that the American Medical Association’s decision to designate obesity as a disease was appropriate. My rationalization was that the disease label would open more opportunities for funding obesity treatments. However, the explosive growth and popularity of glucagon-like peptide 1 (GLP-1) agonists over the last year has had me rethinking my decision to suppress my long-held reservations about the disease designation.
So, if it’s not a disease, then what should we call it? How do we explain its surge in high-income countries that began in the 1980s? While there are still some folks who see obesity as a character flaw, I think you and I as healthcare providers have difficulty explaining the increase prevalence of obesity as either global breakdown of willpower or a widespread genetic shift as the result of burst of radiation from solar flares.
However, if we want to continue our search and finger-pointing we need to have a better definition of exactly what obesity is. If we’re going to continue calling it a disease we have done a pretty sloppy job of creating diagnostic criteria. To be honest, we aren’t doing such a hot job with “long COVID” either.
A recent article in the New York Times makes it clear that I’m not the only physician who is feeling uncomfortable with this lack of diagnostic specificity.
We know that using body mass index (BMI) as a criteria is imprecise. There are healthy individuals with elevated BMIs and there are others who are carrying an unhealthy amount of fat who have normal BMIs. And, there are individuals who have what might appear to be an excess amount of fat who are fit and healthy by other criteria.
Some investigators feel that a set of measurements that includes a waist and/or hip measurement may be a more accurate way of determining visceral adipose tissue. However, this body roundness index (BRI) currently relies on a tape measurement. Until the technique can be preformed by an inexpensive and readily available scanner, the BRI cannot be considered a practical tool for determining obesity.
Dr. Francisco Rubino, the chair of metabolic and bariatric surgery at Kings College in London, England, has been quoted as saying that, “if one defines a disease inaccurately, everything that stems from that – from diagnosis to treatment to policies – will be distorted and biased.”
Denmark has been forced to relabel obesity as a risk factor because the disease designation was stressing the financial viability of their healthcare system as more and more patients were being prescribe GLP-1 agonists, sometimes off label. A rationing strategy was resulting in suboptimal treatment of a significant portion of the obese population.
Spearheaded by Dr. Rubino, a Lancet Commission composed of physicians has tasked itself to define an “evidence-based diagnosis for obesity. Instead of relying on a single metric such as the BMI or BRI, diagnosing “clinical obesity” would involve a broad array of observations including a history, physical examination, standard laboratory and additional testing, “naming signs and symptoms, organ by organ, tissue by tissue, with plausible mechanisms for each one.” In other words, treating each patient as an individual using evidence-based criteria to make a diagnosis. While likely to be time consuming, this strategy feels like a more scientific approach. I suspect once clinical obesity is more rigorously defined it could be divided into several subtypes. For example, there would be a few conditions that were genetic; Prader-Willi syndrome being the best known.
However, I think the Lancet Commission’s strategy will find that the majority of individuals who make up this half-century global surge have become clinically obese because they have been unable to adapt to the obeseogenic forces in our society, which include diet, autocentricity, and attractive sedentary forms of entertainment, to name just three.
In some cases these unfortunate individuals are more vulnerable because there were born into an economically disadvantaged situation. In other scenarios a lack of foresight and/or political will may have left individuals with no other choice but to rely on automobiles to get around. Still others may find themselves living in a nutritional desert because all of the grocery stores have closed.
I recently encountered a descriptor in a story about the Federal Emergency Management Agency which could easily be adapted to describe this large and growing subtype of individuals with clinical obesity. “Social vulnerability” is measure of how well a community can withstand external stressors that impact human health. For example, the emergency management folks are thinking in terms of natural disaster such as hurricanes, floods, and tornadoes and are asking how well a given community can meet the challenges one would create.
But, the term social vulnerability can easily be applied to individuals living in a society in which unhealthy food is abundant, an infrastructure that discourages or outright prevents non-motorized travel, and the temptation of sedentary entertainment options is unavoidable. Fortunately, not every citizen living in an obesogenic society becomes obese. What factors have protected the non-obese individuals from these obeseogenic stressors? What are the characteristics of the unfortunate “vulnerables” living in the same society who end up being obese?
It is time to shift our focus away from a poorly defined disease model to one in which we begin looking at our society to find out why we have so many socially vulnerable individuals. The toll of obesity as it is currently defined is many order of magnitudes greater than any natural disaster. We have become communities that can no longer withstand the its obesogenic stressors many of which we have created and/or allowed to accumulate over the last century.
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.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Is Being ‘Manly’ a Threat to a Man’s Health?
When my normally adorable cat Biscuit bit my ankle in a playful stalking exercise gone wrong, I washed it with soap and some rubbing alcohol, slapped on a Band-Aid, and went about my day.
The next morning, when it was swollen, I told myself it was probably just a hematoma and went about my day.
The next day, when the swelling had increased and red lines started creeping up my leg, I called my doctor. Long story short, I ended up hospitalized for intravenous antibiotics.
This is all to say that, yes, I’m sort of an idiot, but also to introduce the idea that maybe I minimized my very obvious lymphangitis because I am a man.
This week, we have empirical evidence that men downplay their medical symptoms — and that manlier men downplay them even more.
I’m going to talk about a study that links manliness (or, scientifically speaking, “male gender expressivity”) to medical diagnoses that are based on hard evidence and medical diagnoses that are based on self-report. You see where this is going but I want to walk you through the methods here because they are fairly interesting.
This study used data from the US National Longitudinal Study of Adolescent to Adult Health. This study enrolled 20,000 adolescents who were in grades 7-12 in the 1994-1995 school year and has been following them ever since — about 30 years so far.
The authors wanted to link early gender roles to long-term outcomes, so they cut that 20,000 number down to the 4230 males in the group who had complete follow-up.
Now comes the first interesting question. How do you quantify the “male gender expressivity” of boys in 7th-12th grade? There was no survey item that asked them how masculine or manly they felt. What the authors did was look at the surveys that were administered and identify the questions on those surveys where boys and girls gave the most disparate answers. I have some examples here. 
Some of these questions make sense when it comes to gender expressivity: “How often do you cry?” for example, has a lot of validity for the social construct that is gender. But some questions where boys and girls gave very different answers — like “How often do you exercise?” — don’t quite fit that mold. Regardless, this structure allowed the researchers to take individual kids’ responses to these questions and combine them into what amounts to a manliness score — how much their answers aligned with the typical male answer.
The score was established in adolescence — which is interesting because I’m sure some of this stuff may change over time — but notable because adolescence is where many gender roles develop.
Now we can fast-forward 30 years and see how these manliness scores link to various outcomes. The authors were interested in fairly common diseases: diabetes, hypertension, and hyperlipidemia.
Let’s start simply. Are males with higher gender expressivity in adolescence more or less likely to have these diseases in the future?
Not really. Those above the average in male gender expressivity had similar rates of hypertension and hyperlipidemia as those below the median. They were actually a bit less likely to have diabetes.
But that’s not what’s really interesting here.
I told you that there was no difference in the rate of hypertension among those with high vs low male gender expressivity. But there was a significant difference in their answer to the question “Do you have hypertension?” The same was seen for hyperlipidemia. In other words, those with higher manliness scores are less likely to admit (or perhaps know) that they have a particular disease.
You can see the relationship across the manliness spectrum here in a series of adjusted models. The x-axis is the male gender expressivity score, and the y-axis is the percentage of people who report having the disease that we know they have based on the actual laboratory tests or vital sign measurements. As manliness increases, the self-report of a given disease decreases.
There are some important consequences of this systematic denial. Specifically, men with the diseases of interest who have higher male gender expressivity are less likely to get treatment. And, as we all know, the lack of treatment of something like hypertension puts people at risk for bad downstream outcomes.
Putting this all together, I’m not that surprised. Society trains boys from a young age to behave in certain ways: to hide emotions, to eschew vulnerability, to not complain when we are hurt. And those lessons can persist into later life. Whether the disease that strikes is hypertension or Pasteurella multocida from a slightly psychotic house cat, men are more likely to ignore it, to their detriment. 
So, gents, be brave. Get your blood tests and check your blood pressure. If there’s something wrong, admit it, and fix it. After all, fixing problems — that’s a manly thing, right?
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
When my normally adorable cat Biscuit bit my ankle in a playful stalking exercise gone wrong, I washed it with soap and some rubbing alcohol, slapped on a Band-Aid, and went about my day.
The next morning, when it was swollen, I told myself it was probably just a hematoma and went about my day.
The next day, when the swelling had increased and red lines started creeping up my leg, I called my doctor. Long story short, I ended up hospitalized for intravenous antibiotics.
This is all to say that, yes, I’m sort of an idiot, but also to introduce the idea that maybe I minimized my very obvious lymphangitis because I am a man.
This week, we have empirical evidence that men downplay their medical symptoms — and that manlier men downplay them even more.
I’m going to talk about a study that links manliness (or, scientifically speaking, “male gender expressivity”) to medical diagnoses that are based on hard evidence and medical diagnoses that are based on self-report. You see where this is going but I want to walk you through the methods here because they are fairly interesting.
This study used data from the US National Longitudinal Study of Adolescent to Adult Health. This study enrolled 20,000 adolescents who were in grades 7-12 in the 1994-1995 school year and has been following them ever since — about 30 years so far.
The authors wanted to link early gender roles to long-term outcomes, so they cut that 20,000 number down to the 4230 males in the group who had complete follow-up.
Now comes the first interesting question. How do you quantify the “male gender expressivity” of boys in 7th-12th grade? There was no survey item that asked them how masculine or manly they felt. What the authors did was look at the surveys that were administered and identify the questions on those surveys where boys and girls gave the most disparate answers. I have some examples here.
Some of these questions make sense when it comes to gender expressivity: “How often do you cry?” for example, has a lot of validity for the social construct that is gender. But some questions where boys and girls gave very different answers — like “How often do you exercise?” — don’t quite fit that mold. Regardless, this structure allowed the researchers to take individual kids’ responses to these questions and combine them into what amounts to a manliness score — how much their answers aligned with the typical male answer.
The score was established in adolescence — which is interesting because I’m sure some of this stuff may change over time — but notable because adolescence is where many gender roles develop.
Now we can fast-forward 30 years and see how these manliness scores link to various outcomes. The authors were interested in fairly common diseases: diabetes, hypertension, and hyperlipidemia.
Let’s start simply. Are males with higher gender expressivity in adolescence more or less likely to have these diseases in the future?
Not really. Those above the average in male gender expressivity had similar rates of hypertension and hyperlipidemia as those below the median. They were actually a bit less likely to have diabetes.
But that’s not what’s really interesting here.
I told you that there was no difference in the rate of hypertension among those with high vs low male gender expressivity. But there was a significant difference in their answer to the question “Do you have hypertension?” The same was seen for hyperlipidemia. In other words, those with higher manliness scores are less likely to admit (or perhaps know) that they have a particular disease.
You can see the relationship across the manliness spectrum here in a series of adjusted models. The x-axis is the male gender expressivity score, and the y-axis is the percentage of people who report having the disease that we know they have based on the actual laboratory tests or vital sign measurements. As manliness increases, the self-report of a given disease decreases.
There are some important consequences of this systematic denial. Specifically, men with the diseases of interest who have higher male gender expressivity are less likely to get treatment. And, as we all know, the lack of treatment of something like hypertension puts people at risk for bad downstream outcomes.
Putting this all together, I’m not that surprised. Society trains boys from a young age to behave in certain ways: to hide emotions, to eschew vulnerability, to not complain when we are hurt. And those lessons can persist into later life. Whether the disease that strikes is hypertension or Pasteurella multocida from a slightly psychotic house cat, men are more likely to ignore it, to their detriment.
So, gents, be brave. Get your blood tests and check your blood pressure. If there’s something wrong, admit it, and fix it. After all, fixing problems — that’s a manly thing, right?
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
When my normally adorable cat Biscuit bit my ankle in a playful stalking exercise gone wrong, I washed it with soap and some rubbing alcohol, slapped on a Band-Aid, and went about my day.
The next morning, when it was swollen, I told myself it was probably just a hematoma and went about my day.
The next day, when the swelling had increased and red lines started creeping up my leg, I called my doctor. Long story short, I ended up hospitalized for intravenous antibiotics.
This is all to say that, yes, I’m sort of an idiot, but also to introduce the idea that maybe I minimized my very obvious lymphangitis because I am a man.
This week, we have empirical evidence that men downplay their medical symptoms — and that manlier men downplay them even more.
I’m going to talk about a study that links manliness (or, scientifically speaking, “male gender expressivity”) to medical diagnoses that are based on hard evidence and medical diagnoses that are based on self-report. You see where this is going but I want to walk you through the methods here because they are fairly interesting.
This study used data from the US National Longitudinal Study of Adolescent to Adult Health. This study enrolled 20,000 adolescents who were in grades 7-12 in the 1994-1995 school year and has been following them ever since — about 30 years so far.
The authors wanted to link early gender roles to long-term outcomes, so they cut that 20,000 number down to the 4230 males in the group who had complete follow-up.
Now comes the first interesting question. How do you quantify the “male gender expressivity” of boys in 7th-12th grade? There was no survey item that asked them how masculine or manly they felt. What the authors did was look at the surveys that were administered and identify the questions on those surveys where boys and girls gave the most disparate answers. I have some examples here.
Some of these questions make sense when it comes to gender expressivity: “How often do you cry?” for example, has a lot of validity for the social construct that is gender. But some questions where boys and girls gave very different answers — like “How often do you exercise?” — don’t quite fit that mold. Regardless, this structure allowed the researchers to take individual kids’ responses to these questions and combine them into what amounts to a manliness score — how much their answers aligned with the typical male answer.
The score was established in adolescence — which is interesting because I’m sure some of this stuff may change over time — but notable because adolescence is where many gender roles develop.
Now we can fast-forward 30 years and see how these manliness scores link to various outcomes. The authors were interested in fairly common diseases: diabetes, hypertension, and hyperlipidemia.
Let’s start simply. Are males with higher gender expressivity in adolescence more or less likely to have these diseases in the future?
Not really. Those above the average in male gender expressivity had similar rates of hypertension and hyperlipidemia as those below the median. They were actually a bit less likely to have diabetes.
But that’s not what’s really interesting here.
I told you that there was no difference in the rate of hypertension among those with high vs low male gender expressivity. But there was a significant difference in their answer to the question “Do you have hypertension?” The same was seen for hyperlipidemia. In other words, those with higher manliness scores are less likely to admit (or perhaps know) that they have a particular disease.
You can see the relationship across the manliness spectrum here in a series of adjusted models. The x-axis is the male gender expressivity score, and the y-axis is the percentage of people who report having the disease that we know they have based on the actual laboratory tests or vital sign measurements. As manliness increases, the self-report of a given disease decreases.
There are some important consequences of this systematic denial. Specifically, men with the diseases of interest who have higher male gender expressivity are less likely to get treatment. And, as we all know, the lack of treatment of something like hypertension puts people at risk for bad downstream outcomes.
Putting this all together, I’m not that surprised. Society trains boys from a young age to behave in certain ways: to hide emotions, to eschew vulnerability, to not complain when we are hurt. And those lessons can persist into later life. Whether the disease that strikes is hypertension or Pasteurella multocida from a slightly psychotic house cat, men are more likely to ignore it, to their detriment.
So, gents, be brave. Get your blood tests and check your blood pressure. If there’s something wrong, admit it, and fix it. After all, fixing problems — that’s a manly thing, right?
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Cardiovascular Disease 2050: No, GLP-1s Won’t Save the Day
This transcript has been edited for clarity .
Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.
Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.
Dhruv S. Kazi, MD, MS: Thank you for having me.
Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.
Kazi: Excited to be here.
Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.
With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?
Kazi: Perfect.
Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?
Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future.
We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?
Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.
Kazi: Absolutely.
Harrington: If we’re going to make a difference, it might take us 25 years.
Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.
Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.
Kazi: Oh, wow.
Harrington: Now it’s 5%. That’s a big difference in a career.
Trends in the Wrong Direction
Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.
By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.
As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.
Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.
Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.
Harrington: Rather substantially.
Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.
Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.
Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.
Harrington: Diabetes is tightly linked to it but not totally explained.
Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.
Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.
Kazi: Yeah.
Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.
Kazi: In the adolescents/young adults age group, most of it is type 2.
Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.
Kazi: Yeah.
Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.
Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
Cigarettes and Vaping
Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.
Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.
Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.
Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.
Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
Healthcare Spending Not Sustainable
Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.
Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.
It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.
Harrington: Healthcare as it is today, is it 21% of our economy?
Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.
Harrington: We’re talking about a quadrupling.
Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.
Harrington: That’s both direct and indirect costs.
Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.
The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.
Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.
What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.
The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?
Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.
The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.
My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.
Harrington: If nothing changes, this is what it’s going to look like.
Kazi: This is where we’re headed.
Harrington: We can change. We’ve got some time to change, but we don’t have forever.
Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.
Harrington: Give me two things from the policy perspective, because it’s mostly policy.
Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.
The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.
GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.
Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.
Kazi: Exactly, yes.
Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.
Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.
Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.
Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?
Harrington: This is where you get to the children as well.
Kazi: Exactly.
Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.
Kazi: Thank you.
Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity .
Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.
Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.
Dhruv S. Kazi, MD, MS: Thank you for having me.
Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.
Kazi: Excited to be here.
Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.
With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?
Kazi: Perfect.
Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?
Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future.
We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?
Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.
Kazi: Absolutely.
Harrington: If we’re going to make a difference, it might take us 25 years.
Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.
Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.
Kazi: Oh, wow.
Harrington: Now it’s 5%. That’s a big difference in a career.
Trends in the Wrong Direction
Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.
By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.
As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.
Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.
Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.
Harrington: Rather substantially.
Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.
Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.
Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.
Harrington: Diabetes is tightly linked to it but not totally explained.
Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.
Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.
Kazi: Yeah.
Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.
Kazi: In the adolescents/young adults age group, most of it is type 2.
Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.
Kazi: Yeah.
Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.
Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
Cigarettes and Vaping
Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.
Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.
Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.
Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.
Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
Healthcare Spending Not Sustainable
Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.
Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.
It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.
Harrington: Healthcare as it is today, is it 21% of our economy?
Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.
Harrington: We’re talking about a quadrupling.
Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.
Harrington: That’s both direct and indirect costs.
Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.
The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.
Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.
What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.
The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?
Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.
The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.
My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.
Harrington: If nothing changes, this is what it’s going to look like.
Kazi: This is where we’re headed.
Harrington: We can change. We’ve got some time to change, but we don’t have forever.
Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.
Harrington: Give me two things from the policy perspective, because it’s mostly policy.
Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.
The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.
GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.
Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.
Kazi: Exactly, yes.
Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.
Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.
Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.
Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?
Harrington: This is where you get to the children as well.
Kazi: Exactly.
Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.
Kazi: Thank you.
Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity .
Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.
Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.
Dhruv S. Kazi, MD, MS: Thank you for having me.
Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.
Kazi: Excited to be here.
Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.
With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?
Kazi: Perfect.
Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?
Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future.
We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?
Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.
Kazi: Absolutely.
Harrington: If we’re going to make a difference, it might take us 25 years.
Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.
Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.
Kazi: Oh, wow.
Harrington: Now it’s 5%. That’s a big difference in a career.
Trends in the Wrong Direction
Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.
By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.
As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.
Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.
Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.
Harrington: Rather substantially.
Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.
Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.
Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.
Harrington: Diabetes is tightly linked to it but not totally explained.
Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.
Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.
Kazi: Yeah.
Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.
Kazi: In the adolescents/young adults age group, most of it is type 2.
Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.
Kazi: Yeah.
Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.
Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
Cigarettes and Vaping
Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.
Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.
Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.
Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.
Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
Healthcare Spending Not Sustainable
Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.
Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.
It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.
Harrington: Healthcare as it is today, is it 21% of our economy?
Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.
Harrington: We’re talking about a quadrupling.
Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.
Harrington: That’s both direct and indirect costs.
Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.
The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.
Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.
What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.
The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?
Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.
The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.
My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.
Harrington: If nothing changes, this is what it’s going to look like.
Kazi: This is where we’re headed.
Harrington: We can change. We’ve got some time to change, but we don’t have forever.
Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.
Harrington: Give me two things from the policy perspective, because it’s mostly policy.
Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.
The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.
GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.
Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.
Kazi: Exactly, yes.
Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.
Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.
Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.
Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?
Harrington: This is where you get to the children as well.
Kazi: Exactly.
Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.
Kazi: Thank you.
Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).
A version of this article appeared on Medscape.com.
Six Tips for Media Interviews
As a physician, you might be contacted by the media to provide your professional opinion and advice. Or you might be looking for media interview opportunities to market your practice or side project. And if you do research, media interviews can be an effective way to spread the word. It’s important to prepare for a media interview so that you achieve the outcome you are looking for.
Keep your message simple. When you are a subject expert, you might think that the basics are obvious or even boring, and that the nuances are more important. However, most of the audience is looking for big-picture information that they can apply to their lives. Consider a few key takeaways, keeping in mind that your interview is likely to be edited to short sound bites or a few quotes. It may help to jot down notes so that you cover the fundamentals clearly. You could even write and rehearse a script beforehand. If there is something complicated or subtle that you want to convey, you can preface it by saying, “This is confusing but very important …” to let the audience know to give extra consideration to what you are about to say.
Avoid extremes and hyperbole. Sometimes, exaggerated statements make their way into medical discussions. Statements such as “it doesn’t matter how many calories you consume — it’s all about the quality” are common oversimplifications. But you might be upset to see your name next to a comment like this because it is not actually correct. Check the phrasing of your key takeaways to avoid being stuck defending or explaining an inaccurate statement when your patients ask you about it later.
Ask the interviewers what they are looking for. Many medical topics have some controversial element, so it is good to know what you’re getting into. Find out the purpose of the article or interview before you decide whether it is right for you. It could be about another doctor in town who is being sued; if you don’t want to be associated with that story, it might be best to decline the interview.
Explain your goals. You might accept or pursue an interview to raise awareness about an underrecognized condition. You might want the public to identify and get help for early symptoms, or you might want to create empathy for people coping with a disease you treat. Consider why you are participating in an interview, and communicate that to the interviewer to ensure that your objective can be part of the final product.
Know whom you’re dealing with. It is good to learn about the publication/media channel before you agree to participate. It may have a political bias, or perhaps the interview is intended to promote a specific product. If you agree with and support their purposes, then you may be happy to lend your opinion. But learning about the “voice” of the publication in advance allows you to make an informed decision about whether you want to be identified with a particular political ideology or product endorsement.
Ask to see your quotes before publication. It’s good to have the opportunity to make corrections in case you are accidentally misquoted or misunderstood. It is best to ask to see quotes before you agree to the interview. Some reporters may agree to (or even prefer) a written question-and-answer format so that they can directly quote your responses without rephrasing your words. You could suggest this, especially if you are too busy for a call or live meeting.
As a physician, your insights and advice can be highly beneficial to others. You can also use media interviews to propel your career forward. Doing your homework can ensure that you will be pleased with the final product and how your words were used.
Dr. Moawad, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
As a physician, you might be contacted by the media to provide your professional opinion and advice. Or you might be looking for media interview opportunities to market your practice or side project. And if you do research, media interviews can be an effective way to spread the word. It’s important to prepare for a media interview so that you achieve the outcome you are looking for.
Keep your message simple. When you are a subject expert, you might think that the basics are obvious or even boring, and that the nuances are more important. However, most of the audience is looking for big-picture information that they can apply to their lives. Consider a few key takeaways, keeping in mind that your interview is likely to be edited to short sound bites or a few quotes. It may help to jot down notes so that you cover the fundamentals clearly. You could even write and rehearse a script beforehand. If there is something complicated or subtle that you want to convey, you can preface it by saying, “This is confusing but very important …” to let the audience know to give extra consideration to what you are about to say.
Avoid extremes and hyperbole. Sometimes, exaggerated statements make their way into medical discussions. Statements such as “it doesn’t matter how many calories you consume — it’s all about the quality” are common oversimplifications. But you might be upset to see your name next to a comment like this because it is not actually correct. Check the phrasing of your key takeaways to avoid being stuck defending or explaining an inaccurate statement when your patients ask you about it later.
Ask the interviewers what they are looking for. Many medical topics have some controversial element, so it is good to know what you’re getting into. Find out the purpose of the article or interview before you decide whether it is right for you. It could be about another doctor in town who is being sued; if you don’t want to be associated with that story, it might be best to decline the interview.
Explain your goals. You might accept or pursue an interview to raise awareness about an underrecognized condition. You might want the public to identify and get help for early symptoms, or you might want to create empathy for people coping with a disease you treat. Consider why you are participating in an interview, and communicate that to the interviewer to ensure that your objective can be part of the final product.
Know whom you’re dealing with. It is good to learn about the publication/media channel before you agree to participate. It may have a political bias, or perhaps the interview is intended to promote a specific product. If you agree with and support their purposes, then you may be happy to lend your opinion. But learning about the “voice” of the publication in advance allows you to make an informed decision about whether you want to be identified with a particular political ideology or product endorsement.
Ask to see your quotes before publication. It’s good to have the opportunity to make corrections in case you are accidentally misquoted or misunderstood. It is best to ask to see quotes before you agree to the interview. Some reporters may agree to (or even prefer) a written question-and-answer format so that they can directly quote your responses without rephrasing your words. You could suggest this, especially if you are too busy for a call or live meeting.
As a physician, your insights and advice can be highly beneficial to others. You can also use media interviews to propel your career forward. Doing your homework can ensure that you will be pleased with the final product and how your words were used.
Dr. Moawad, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
As a physician, you might be contacted by the media to provide your professional opinion and advice. Or you might be looking for media interview opportunities to market your practice or side project. And if you do research, media interviews can be an effective way to spread the word. It’s important to prepare for a media interview so that you achieve the outcome you are looking for.
Keep your message simple. When you are a subject expert, you might think that the basics are obvious or even boring, and that the nuances are more important. However, most of the audience is looking for big-picture information that they can apply to their lives. Consider a few key takeaways, keeping in mind that your interview is likely to be edited to short sound bites or a few quotes. It may help to jot down notes so that you cover the fundamentals clearly. You could even write and rehearse a script beforehand. If there is something complicated or subtle that you want to convey, you can preface it by saying, “This is confusing but very important …” to let the audience know to give extra consideration to what you are about to say.
Avoid extremes and hyperbole. Sometimes, exaggerated statements make their way into medical discussions. Statements such as “it doesn’t matter how many calories you consume — it’s all about the quality” are common oversimplifications. But you might be upset to see your name next to a comment like this because it is not actually correct. Check the phrasing of your key takeaways to avoid being stuck defending or explaining an inaccurate statement when your patients ask you about it later.
Ask the interviewers what they are looking for. Many medical topics have some controversial element, so it is good to know what you’re getting into. Find out the purpose of the article or interview before you decide whether it is right for you. It could be about another doctor in town who is being sued; if you don’t want to be associated with that story, it might be best to decline the interview.
Explain your goals. You might accept or pursue an interview to raise awareness about an underrecognized condition. You might want the public to identify and get help for early symptoms, or you might want to create empathy for people coping with a disease you treat. Consider why you are participating in an interview, and communicate that to the interviewer to ensure that your objective can be part of the final product.
Know whom you’re dealing with. It is good to learn about the publication/media channel before you agree to participate. It may have a political bias, or perhaps the interview is intended to promote a specific product. If you agree with and support their purposes, then you may be happy to lend your opinion. But learning about the “voice” of the publication in advance allows you to make an informed decision about whether you want to be identified with a particular political ideology or product endorsement.
Ask to see your quotes before publication. It’s good to have the opportunity to make corrections in case you are accidentally misquoted or misunderstood. It is best to ask to see quotes before you agree to the interview. Some reporters may agree to (or even prefer) a written question-and-answer format so that they can directly quote your responses without rephrasing your words. You could suggest this, especially if you are too busy for a call or live meeting.
As a physician, your insights and advice can be highly beneficial to others. You can also use media interviews to propel your career forward. Doing your homework can ensure that you will be pleased with the final product and how your words were used.
Dr. Moawad, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
A 51-year-old woman presented for a routine full body skin exam after vacationing in Hawaii.
Primary adrenal insufficiency (Addison’s disease) results from a dysfunction of the adrenal glands, which may be secondary to autoimmune diseases, genetic conditions, infections, and vasculopathies,or may be drug-induced (e.g. checkpoint inhibitors), among others . In contrast, secondary adrenal insufficiency results from pituitary dysfunction of low adrenocorticotropic hormone (ACTH). The most common cause of primary adrenal insufficiency in developed countries is autoimmune adrenalitis, which accounts for upwards of 90% of cases. Typically, 21-hydroxylase autoantibodies are identified and account for destruction of the adrenal cortex through cell-mediated and humoral immune responses.
Palmar creases, subungual surfaces, sites of trauma, and joint spaces (including the knees, spine, elbows, and shoulders) are commonly affected. Hair depletes in the pubic area and axillary vaults. Nevi may also appear darker. In patients with autoimmune adrenalitis, vitiligo may be seen secondary to autoimmune destruction of melanocytes.
Diagnosis may be difficult in the early stages, but historical findings of fatigue and clinical findings of hyperpigmentation in classic areas may prompt appropriate lab screening workup. It is essential to determine whether adrenal insufficiency is primary or secondary. Evaluation of decreased cortisol production, determination of whether production is ACTH-dependent or -independent, and evaluation for the underlying causes of adrenal dysfunction are important. Lab screening includes morning serum cortisol, morning ACTH (cosyntropin) stimulation test, fasting CBC with differential, and CMP to evaluate for normocytic normochromic anemia, hyponatremia, hyperkalemia, hypoglycemia, plasma renin/aldosterone ratio, and 21-hydroxylase autoantibodies.
Management strategies of primary adrenal insufficiency require corticosteroid supplementation and multidisciplinary collaboration with endocrinology. If untreated, primary adrenal insufficiency can be fatal. Adrenal crisis is a critical condition following a precipitating event, such as GI infection, fever, acute stress, and/or untreated adrenal or pituitary disorders. Clinical findings include acute shock with hypotension, nausea, vomiting, abdominal pain, back or leg pain, and a change in mental status. In this scenario, increasing the dose of corticosteroid supplementation is essential for reducing mortality.
Upon examining this patient’s new skin findings of hyperpigmentation and discussing her fatigue, primary adrenal insufficiency was suspected. With further prompting, the patient reported an ICU hospitalization several months prior because of sepsis originating from a peritonsillar abscess. With these clinical and historical findings, preliminary workup was conducted by dermatology, which included morning cortisol level, ACTH, CBC with differential, CMP, plasma renin-aldosterone ratio, and 21-hydroxylase autoantibodies. Work up demonstrated a low morning cortisol level of 1.3 mcg/dL, an elevated ACTH of 2,739 pg/mL, and positive 21-hydroxylase autoantibodies. The patient was urgently referred to endocrinology and started on oral hydrocortisone. Her fatigue immediately improved, and at 1-year follow-up with dermatology, her mucocutaneous hyperpigmentation had subsided dramatically.
Dermatologists can play a major role in the early diagnosis of primary adrenal insufficiency, which is essential for reducing patient morbidity and mortality. Skin findings on full body skin exams can clue in dermatologists for ordering preliminary workup to expedite care for these patients.
The case and photos were submitted by Dr. Akhiyat, Scripps Clinic Medical Group, La Jolla, California. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
J Am Acad Dermatol. 2014 May;70(5):Supplement 1AB118. doi: 10.1016/j.jaad.2014.01.491.
Michels A, Michels N. Am Fam Physician. 2014 Apr 1;89(7):563-568.
Kauzman A et al. J Can Dent Assoc. 2004 Nov;70(10):682-683.
Primary adrenal insufficiency (Addison’s disease) results from a dysfunction of the adrenal glands, which may be secondary to autoimmune diseases, genetic conditions, infections, and vasculopathies,or may be drug-induced (e.g. checkpoint inhibitors), among others . In contrast, secondary adrenal insufficiency results from pituitary dysfunction of low adrenocorticotropic hormone (ACTH). The most common cause of primary adrenal insufficiency in developed countries is autoimmune adrenalitis, which accounts for upwards of 90% of cases. Typically, 21-hydroxylase autoantibodies are identified and account for destruction of the adrenal cortex through cell-mediated and humoral immune responses.
Palmar creases, subungual surfaces, sites of trauma, and joint spaces (including the knees, spine, elbows, and shoulders) are commonly affected. Hair depletes in the pubic area and axillary vaults. Nevi may also appear darker. In patients with autoimmune adrenalitis, vitiligo may be seen secondary to autoimmune destruction of melanocytes.
Diagnosis may be difficult in the early stages, but historical findings of fatigue and clinical findings of hyperpigmentation in classic areas may prompt appropriate lab screening workup. It is essential to determine whether adrenal insufficiency is primary or secondary. Evaluation of decreased cortisol production, determination of whether production is ACTH-dependent or -independent, and evaluation for the underlying causes of adrenal dysfunction are important. Lab screening includes morning serum cortisol, morning ACTH (cosyntropin) stimulation test, fasting CBC with differential, and CMP to evaluate for normocytic normochromic anemia, hyponatremia, hyperkalemia, hypoglycemia, plasma renin/aldosterone ratio, and 21-hydroxylase autoantibodies.
Management strategies of primary adrenal insufficiency require corticosteroid supplementation and multidisciplinary collaboration with endocrinology. If untreated, primary adrenal insufficiency can be fatal. Adrenal crisis is a critical condition following a precipitating event, such as GI infection, fever, acute stress, and/or untreated adrenal or pituitary disorders. Clinical findings include acute shock with hypotension, nausea, vomiting, abdominal pain, back or leg pain, and a change in mental status. In this scenario, increasing the dose of corticosteroid supplementation is essential for reducing mortality.
Upon examining this patient’s new skin findings of hyperpigmentation and discussing her fatigue, primary adrenal insufficiency was suspected. With further prompting, the patient reported an ICU hospitalization several months prior because of sepsis originating from a peritonsillar abscess. With these clinical and historical findings, preliminary workup was conducted by dermatology, which included morning cortisol level, ACTH, CBC with differential, CMP, plasma renin-aldosterone ratio, and 21-hydroxylase autoantibodies. Work up demonstrated a low morning cortisol level of 1.3 mcg/dL, an elevated ACTH of 2,739 pg/mL, and positive 21-hydroxylase autoantibodies. The patient was urgently referred to endocrinology and started on oral hydrocortisone. Her fatigue immediately improved, and at 1-year follow-up with dermatology, her mucocutaneous hyperpigmentation had subsided dramatically.
Dermatologists can play a major role in the early diagnosis of primary adrenal insufficiency, which is essential for reducing patient morbidity and mortality. Skin findings on full body skin exams can clue in dermatologists for ordering preliminary workup to expedite care for these patients.
The case and photos were submitted by Dr. Akhiyat, Scripps Clinic Medical Group, La Jolla, California. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
J Am Acad Dermatol. 2014 May;70(5):Supplement 1AB118. doi: 10.1016/j.jaad.2014.01.491.
Michels A, Michels N. Am Fam Physician. 2014 Apr 1;89(7):563-568.
Kauzman A et al. J Can Dent Assoc. 2004 Nov;70(10):682-683.
Primary adrenal insufficiency (Addison’s disease) results from a dysfunction of the adrenal glands, which may be secondary to autoimmune diseases, genetic conditions, infections, and vasculopathies,or may be drug-induced (e.g. checkpoint inhibitors), among others . In contrast, secondary adrenal insufficiency results from pituitary dysfunction of low adrenocorticotropic hormone (ACTH). The most common cause of primary adrenal insufficiency in developed countries is autoimmune adrenalitis, which accounts for upwards of 90% of cases. Typically, 21-hydroxylase autoantibodies are identified and account for destruction of the adrenal cortex through cell-mediated and humoral immune responses.
Palmar creases, subungual surfaces, sites of trauma, and joint spaces (including the knees, spine, elbows, and shoulders) are commonly affected. Hair depletes in the pubic area and axillary vaults. Nevi may also appear darker. In patients with autoimmune adrenalitis, vitiligo may be seen secondary to autoimmune destruction of melanocytes.
Diagnosis may be difficult in the early stages, but historical findings of fatigue and clinical findings of hyperpigmentation in classic areas may prompt appropriate lab screening workup. It is essential to determine whether adrenal insufficiency is primary or secondary. Evaluation of decreased cortisol production, determination of whether production is ACTH-dependent or -independent, and evaluation for the underlying causes of adrenal dysfunction are important. Lab screening includes morning serum cortisol, morning ACTH (cosyntropin) stimulation test, fasting CBC with differential, and CMP to evaluate for normocytic normochromic anemia, hyponatremia, hyperkalemia, hypoglycemia, plasma renin/aldosterone ratio, and 21-hydroxylase autoantibodies.
Management strategies of primary adrenal insufficiency require corticosteroid supplementation and multidisciplinary collaboration with endocrinology. If untreated, primary adrenal insufficiency can be fatal. Adrenal crisis is a critical condition following a precipitating event, such as GI infection, fever, acute stress, and/or untreated adrenal or pituitary disorders. Clinical findings include acute shock with hypotension, nausea, vomiting, abdominal pain, back or leg pain, and a change in mental status. In this scenario, increasing the dose of corticosteroid supplementation is essential for reducing mortality.
Upon examining this patient’s new skin findings of hyperpigmentation and discussing her fatigue, primary adrenal insufficiency was suspected. With further prompting, the patient reported an ICU hospitalization several months prior because of sepsis originating from a peritonsillar abscess. With these clinical and historical findings, preliminary workup was conducted by dermatology, which included morning cortisol level, ACTH, CBC with differential, CMP, plasma renin-aldosterone ratio, and 21-hydroxylase autoantibodies. Work up demonstrated a low morning cortisol level of 1.3 mcg/dL, an elevated ACTH of 2,739 pg/mL, and positive 21-hydroxylase autoantibodies. The patient was urgently referred to endocrinology and started on oral hydrocortisone. Her fatigue immediately improved, and at 1-year follow-up with dermatology, her mucocutaneous hyperpigmentation had subsided dramatically.
Dermatologists can play a major role in the early diagnosis of primary adrenal insufficiency, which is essential for reducing patient morbidity and mortality. Skin findings on full body skin exams can clue in dermatologists for ordering preliminary workup to expedite care for these patients.
The case and photos were submitted by Dr. Akhiyat, Scripps Clinic Medical Group, La Jolla, California. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
J Am Acad Dermatol. 2014 May;70(5):Supplement 1AB118. doi: 10.1016/j.jaad.2014.01.491.
Michels A, Michels N. Am Fam Physician. 2014 Apr 1;89(7):563-568.
Kauzman A et al. J Can Dent Assoc. 2004 Nov;70(10):682-683.
How Old Are You? Stand on One Leg and I’ll Tell You
This transcript has been edited for clarity.
So I was lying in bed the other night, trying to read my phone, and started complaining to my wife about how my vision keeps getting worse, and then how stiff I feel when I wake up in the morning, and how a recent injury is taking too long to heal, and she said, “Well, yeah. You’re 44. That’s when things start to head downhill.”
And I was like, “Forty-four? That seems very specific. I thought 50 was what people complain about.” And she said, “No, it’s a thing — 44 years old and 60 years old. There’s a drop-off there.”
And you know what? She was right.
A study, “Nonlinear dynamics of multi-omics profiles during human aging,” published in Nature Aging in August 2024, analyzed a ton of proteins and metabolites in people of various ages and found, when you put it all together, that I should know better than to doubt my brilliant spouse.
But deep down, I believe the cliché that age is just a number. I don’t particularly care about being 44, or turning 50 or 60. I care about how my body and brain are aging. If I can be a happy, healthy, 80-year-old in full command of my faculties, I would consider that a major win no matter what the calendar says.
So I’m always interested in ways to quantify how my body is aging, independent of how many birthdays I have passed. And, according to a new study, there’s actually a really easy way to do this: Just stand on one leg.
The surprising results come from “Age-related changes in gait, balance, and strength parameters: A cross-sectional study,” appearing in PLOS One, which analyzed 40 individuals — half under age 65 and half over age 65 — across a variety of domains of strength, balance, and gait. The conceit of the study? We all know that things like strength and balance worsen over time, but what worsens fastest? What might be the best metric to tell us how our bodies are aging?
To that end, you have a variety of correlations between various metrics and calendar age.
As age increases, grip strength goes down. Men (inexplicably in pink) have higher grip strength overall, and women (confusingly in blue) lower. Somewhat less strong correlations were seen for knee strength.
What about balance?
To assess this, the researchers had the participants stand on a pressure plate. In one scenario, they did this with eyes open, and the next with eyes closed. They then measured how much the pressure varied around the center of the individual on the plate — basically, how much the person swayed while they were standing there.
Sway increased as age increased. Sway increased a bit more with eyes closed than with eyes open.
But the strongest correlation between any of these metrics and age was a simple one: How long can you stand on one leg?
Particularly for the nondominant leg, what you see here is a pretty dramatic drop-off in balance time around age 65, with younger people able to do 10 seconds with ease and some older people barely being able to make it to 2. 
Of course, I had to try this for myself. And as I was standing around on one leg, it became clear to me exactly why this might be a good metric. It really integrates balance and strength in a way that the other tests don’t: balance, clearly, since you have to stay vertical over a relatively small base; but strength as well, because, well, one leg is holding up all the rest of you. You do feel it after a while.
So this metric passes the smell test to me, at least as a potential proxy for age-related physical decline.
But I should be careful to note that this was a cross-sectional study; the researchers looked at various people who were all different ages, not the same people over time to watch how these things change as they aged.
Also, the use of the correlation coefficient in graphs like this implies a certain linear relationship between age and standing-on-one-foot time. The raw data — the points on this graph — don’t appear that linear to me. As I mentioned above, it seems like there might be a bit of a sharp drop-off somewhere in the mid-60s. That means that we may not be able to use this as a sensitive test for aging that slowly changes as your body gets older. It might be that you’re able to essentially stand on one leg as long as you want until, one day, you can’t. That gives us less warning and less to act on.
And finally, we don’t know that changing this metric will change your health for the better. I’m sure a good physiatrist or physical therapist could design some exercises to increase any of our standing-on-one leg times. And no doubt, with practice, you could get your numbers way up. But that doesn’t necessarily mean you’re healthier. It’s like “teaching to the test”; you might score better on the standardized exam but you didn’t really learn the material.
So I am not adding one-leg standing to my daily exercise routine. But I won’t lie and tell you that, from time to time, and certainly on my 60th birthday, you may find me standing like a flamingo with a stopwatch in my hand.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Connecticut. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
So I was lying in bed the other night, trying to read my phone, and started complaining to my wife about how my vision keeps getting worse, and then how stiff I feel when I wake up in the morning, and how a recent injury is taking too long to heal, and she said, “Well, yeah. You’re 44. That’s when things start to head downhill.”
And I was like, “Forty-four? That seems very specific. I thought 50 was what people complain about.” And she said, “No, it’s a thing — 44 years old and 60 years old. There’s a drop-off there.”
And you know what? She was right.
A study, “Nonlinear dynamics of multi-omics profiles during human aging,” published in Nature Aging in August 2024, analyzed a ton of proteins and metabolites in people of various ages and found, when you put it all together, that I should know better than to doubt my brilliant spouse.
But deep down, I believe the cliché that age is just a number. I don’t particularly care about being 44, or turning 50 or 60. I care about how my body and brain are aging. If I can be a happy, healthy, 80-year-old in full command of my faculties, I would consider that a major win no matter what the calendar says.
So I’m always interested in ways to quantify how my body is aging, independent of how many birthdays I have passed. And, according to a new study, there’s actually a really easy way to do this: Just stand on one leg.
The surprising results come from “Age-related changes in gait, balance, and strength parameters: A cross-sectional study,” appearing in PLOS One, which analyzed 40 individuals — half under age 65 and half over age 65 — across a variety of domains of strength, balance, and gait. The conceit of the study? We all know that things like strength and balance worsen over time, but what worsens fastest? What might be the best metric to tell us how our bodies are aging?
To that end, you have a variety of correlations between various metrics and calendar age.
As age increases, grip strength goes down. Men (inexplicably in pink) have higher grip strength overall, and women (confusingly in blue) lower. Somewhat less strong correlations were seen for knee strength.
What about balance?
To assess this, the researchers had the participants stand on a pressure plate. In one scenario, they did this with eyes open, and the next with eyes closed. They then measured how much the pressure varied around the center of the individual on the plate — basically, how much the person swayed while they were standing there.
Sway increased as age increased. Sway increased a bit more with eyes closed than with eyes open.
But the strongest correlation between any of these metrics and age was a simple one: How long can you stand on one leg?
Particularly for the nondominant leg, what you see here is a pretty dramatic drop-off in balance time around age 65, with younger people able to do 10 seconds with ease and some older people barely being able to make it to 2.
Of course, I had to try this for myself. And as I was standing around on one leg, it became clear to me exactly why this might be a good metric. It really integrates balance and strength in a way that the other tests don’t: balance, clearly, since you have to stay vertical over a relatively small base; but strength as well, because, well, one leg is holding up all the rest of you. You do feel it after a while.
So this metric passes the smell test to me, at least as a potential proxy for age-related physical decline.
But I should be careful to note that this was a cross-sectional study; the researchers looked at various people who were all different ages, not the same people over time to watch how these things change as they aged.
Also, the use of the correlation coefficient in graphs like this implies a certain linear relationship between age and standing-on-one-foot time. The raw data — the points on this graph — don’t appear that linear to me. As I mentioned above, it seems like there might be a bit of a sharp drop-off somewhere in the mid-60s. That means that we may not be able to use this as a sensitive test for aging that slowly changes as your body gets older. It might be that you’re able to essentially stand on one leg as long as you want until, one day, you can’t. That gives us less warning and less to act on.
And finally, we don’t know that changing this metric will change your health for the better. I’m sure a good physiatrist or physical therapist could design some exercises to increase any of our standing-on-one leg times. And no doubt, with practice, you could get your numbers way up. But that doesn’t necessarily mean you’re healthier. It’s like “teaching to the test”; you might score better on the standardized exam but you didn’t really learn the material.
So I am not adding one-leg standing to my daily exercise routine. But I won’t lie and tell you that, from time to time, and certainly on my 60th birthday, you may find me standing like a flamingo with a stopwatch in my hand.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Connecticut. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
So I was lying in bed the other night, trying to read my phone, and started complaining to my wife about how my vision keeps getting worse, and then how stiff I feel when I wake up in the morning, and how a recent injury is taking too long to heal, and she said, “Well, yeah. You’re 44. That’s when things start to head downhill.”
And I was like, “Forty-four? That seems very specific. I thought 50 was what people complain about.” And she said, “No, it’s a thing — 44 years old and 60 years old. There’s a drop-off there.”
And you know what? She was right.
A study, “Nonlinear dynamics of multi-omics profiles during human aging,” published in Nature Aging in August 2024, analyzed a ton of proteins and metabolites in people of various ages and found, when you put it all together, that I should know better than to doubt my brilliant spouse.
But deep down, I believe the cliché that age is just a number. I don’t particularly care about being 44, or turning 50 or 60. I care about how my body and brain are aging. If I can be a happy, healthy, 80-year-old in full command of my faculties, I would consider that a major win no matter what the calendar says.
So I’m always interested in ways to quantify how my body is aging, independent of how many birthdays I have passed. And, according to a new study, there’s actually a really easy way to do this: Just stand on one leg.
The surprising results come from “Age-related changes in gait, balance, and strength parameters: A cross-sectional study,” appearing in PLOS One, which analyzed 40 individuals — half under age 65 and half over age 65 — across a variety of domains of strength, balance, and gait. The conceit of the study? We all know that things like strength and balance worsen over time, but what worsens fastest? What might be the best metric to tell us how our bodies are aging?
To that end, you have a variety of correlations between various metrics and calendar age.
As age increases, grip strength goes down. Men (inexplicably in pink) have higher grip strength overall, and women (confusingly in blue) lower. Somewhat less strong correlations were seen for knee strength.
What about balance?
To assess this, the researchers had the participants stand on a pressure plate. In one scenario, they did this with eyes open, and the next with eyes closed. They then measured how much the pressure varied around the center of the individual on the plate — basically, how much the person swayed while they were standing there.
Sway increased as age increased. Sway increased a bit more with eyes closed than with eyes open.
But the strongest correlation between any of these metrics and age was a simple one: How long can you stand on one leg?
Particularly for the nondominant leg, what you see here is a pretty dramatic drop-off in balance time around age 65, with younger people able to do 10 seconds with ease and some older people barely being able to make it to 2.
Of course, I had to try this for myself. And as I was standing around on one leg, it became clear to me exactly why this might be a good metric. It really integrates balance and strength in a way that the other tests don’t: balance, clearly, since you have to stay vertical over a relatively small base; but strength as well, because, well, one leg is holding up all the rest of you. You do feel it after a while.
So this metric passes the smell test to me, at least as a potential proxy for age-related physical decline.
But I should be careful to note that this was a cross-sectional study; the researchers looked at various people who were all different ages, not the same people over time to watch how these things change as they aged.
Also, the use of the correlation coefficient in graphs like this implies a certain linear relationship between age and standing-on-one-foot time. The raw data — the points on this graph — don’t appear that linear to me. As I mentioned above, it seems like there might be a bit of a sharp drop-off somewhere in the mid-60s. That means that we may not be able to use this as a sensitive test for aging that slowly changes as your body gets older. It might be that you’re able to essentially stand on one leg as long as you want until, one day, you can’t. That gives us less warning and less to act on.
And finally, we don’t know that changing this metric will change your health for the better. I’m sure a good physiatrist or physical therapist could design some exercises to increase any of our standing-on-one leg times. And no doubt, with practice, you could get your numbers way up. But that doesn’t necessarily mean you’re healthier. It’s like “teaching to the test”; you might score better on the standardized exam but you didn’t really learn the material.
So I am not adding one-leg standing to my daily exercise routine. But I won’t lie and tell you that, from time to time, and certainly on my 60th birthday, you may find me standing like a flamingo with a stopwatch in my hand.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Connecticut. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
H pylori: ACG Guideline Advises New Approaches to Treatment
Helicobacter pylori is one of the most common human bacterial chronic infections globally. Its prevalence has actually decreased in North America in recent years, although its current range of approximately 30%-40% remains substantial given the potential clinical implications of infection.
Standards have changed considerably regarding the testing, treatment, and follow-up of H pylori. This is made clear by the just-published clinical practice guideline from the American College of Gastroenterology (ACG), which provides several new recommendations based on recent scientific evidence that should change your clinical approach to managing this common infection.
This discussion aims to synthesize and highlight key concepts from the ACG’s comprehensive publication.
Who Should Be Tested and Treated?
The cardinal diseases caused by H pylori have traditionally included peptic ulcer disease, marginal zone B-cell lymphoma, gastric adenocarcinoma, and dyspepsia.
Additional associations have been made with idiopathic thrombocytopenic purpura and otherwise unexplained iron deficiency.
New evidence suggests that patients taking long-term nonsteroidal anti-inflammatory drugs, including low-dose aspirin, are relatively more susceptible to infection.
The ACG’s guideline also recommends testing persons at an increased risk for gastric adenocarcinoma (eg, those with autoimmune gastritis, current or history of premalignant conditions, or first-degree relative with gastric cancer), as well as household members of patients with a positive nonserologic test for H pylori.
The authors note that those with an indication for testing should be offered treatment if determined to have an infection. These patients should also undergo a posttreatment test-of-cure, which should occur at least 4 weeks afterwards using a urea breath test, fecal antigen test, or gastric biopsy.
Caveats to Treatment
Patients with H pylori infections are advised to undergo treatment for a duration of 14 days. Some of the commercial prepackaged H pylori treatment options (eg, Pylera, which contains bismuth subcitrate/metronidazole/tetracycline) are dispensed in regimens lasting only 10 days and currently are viewed as inadequate.
In the United States, the patterns of antibiotic resistance for the previously used standard drugs in the treatment of H pylori have increased considerably. They range from 32% for clarithromycin, 38% for levofloxacin, and 42% for metronidazole, in contrast to 3% for amoxicillin, 1% for tetracycline, and 0% for rifabutin.
Clarithromycin- and levofloxacin-containing treatments should be avoided in treatment-naive patients unless specifically directed following the results of susceptibility tests with either a phenotypic method (culture-based) or a molecular method (polymerase chain reaction or next-generation sequencing). Notably, the mutations responsible for both clarithromycin and levofloxacin resistance may be detectable by stool-based testing.
Maintenance of intragastric acid suppression is key to H pylori eradication, as elevated intragastric pH promotes active replication of H pylori and makes it more susceptible to bactericidal antibiotics.
Therefore, the use of histamine-2 receptors is not recommended, as they are inadequate for achieving acid suppression. Instead, a dual-based therapy of either the potassium-competitive acid blocker (PCAB) vonoprazan (20 mg) or a high-dose proton pump inhibitor (PPI) and amoxicillin, administered twice daily, is effective, although this finding is based on limited evidence.
Treatment-Naive Patients
In treatment-naive patients without penicillin allergy and for whom antibiotic susceptibility testing has not been obtained, the guideline offers its strongest recommendation for bismuth quadruple therapy. This therapy typically consists of a PPI, bismuth subcitrate or subsalicylate, tetracycline, and metronidazole.
Among those with a penicillin allergy, bismuth quadruple therapy is also the primary treatment choice. The authors suggest that patients with a suspected allergy are referred to an allergist for possible penicillin desensitization, given that less than 1% of the population is thought to present with a “true” allergy.
The guideline also presented conditional recommendations, based on low- to moderate-quality evidence, for using a rifabutin-based triple regimen of omeprazole, amoxicillin, and rifabutin (Talicia); a PCAB-based dual regimen of vonoprazan and amoxicillin (Voquezna Dual Pak); and a PCAB-based triple regimen of vonoprazan, clarithromycin, and amoxicillin (Voquezna Triple Pak). In patients with unknown clarithromycin susceptibility, the PCAB-based triple therapy is preferred over PPI-clarithromycin triple therapy.
Although probiotics have been suggested to possibly lead to increased effectiveness or tolerability for H pylori eradication, this was based on studies with significant heterogeneity in their designs. At present, no high-quality data support probiotic therapy.
Clinicians may substitute doxycycline for tetracycline due to availability or cost, and also may prescribe metronidazole at a lower dose than recommended (1.5-2 g/d) to limit side effects. Both modifications have been associated with lower rates of H pylori eradication and are not recommended.
Treatment-Experienced Patients
Quadruple bismuth therapy is the optimal approach among treatment-experienced patients with persistent H pylori infection who have not previously received this therapy. However, this recommendation was rated as conditional, given that it was based on a low quality of evidence.
The guideline offered other recommendations for treatment-experienced patients with persistent infection who had received bismuth quadruple therapy — also conditionally based on a low quality of evidence.
In such patients, it is recommended to consider the use of a rifabutin-based triple therapy (ie, a PPI standard to double dose, amoxicillin, and rifabutin) and a levofloxacin-based triple therapy (ie, a PPI standard dose, levofloxacin, and amoxicillin or metronidazole).
Although significant evidence gaps prevented the authors from providing formal recommendations, they included a PCAB-based triple therapy of vonoprazan, clarithromycin, and amoxicillin (Voquezna Triple Pak) and a high-dose dual therapy of either vonoprazan (20 mg) or PPI (double dose) and amoxicillin among their suggested salvage regimens for these patients.
A New Standard
We must recognize, however, that there are still substantial evidence gaps, particularly around the use of a PCAB-based regimen and its relative advantages over a standard or high-dose PPI-based regimen. This may be of particular importance based on the variable prevalence of cytochrome P450 2C19 (CYP2C19) polymorphisms in the specific patient populations, as PCABs are not metabolized by CYP2C19.
Reviewing the entirety of the ACG’s clinical guideline is encouraged for additional details about the management of H pylori beyond what is highlighted herein.
Dr. Johnson, Professor of Medicine, Chief of Gastroenterology, Eastern Virginia Medical School, Norfolk, Virginia, disclosed ties with ISOTHRIVE and Johnson & Johnson.
A version of this article appeared on Medscape.com.
Helicobacter pylori is one of the most common human bacterial chronic infections globally. Its prevalence has actually decreased in North America in recent years, although its current range of approximately 30%-40% remains substantial given the potential clinical implications of infection.
Standards have changed considerably regarding the testing, treatment, and follow-up of H pylori. This is made clear by the just-published clinical practice guideline from the American College of Gastroenterology (ACG), which provides several new recommendations based on recent scientific evidence that should change your clinical approach to managing this common infection.
This discussion aims to synthesize and highlight key concepts from the ACG’s comprehensive publication.
Who Should Be Tested and Treated?
The cardinal diseases caused by H pylori have traditionally included peptic ulcer disease, marginal zone B-cell lymphoma, gastric adenocarcinoma, and dyspepsia.
Additional associations have been made with idiopathic thrombocytopenic purpura and otherwise unexplained iron deficiency.
New evidence suggests that patients taking long-term nonsteroidal anti-inflammatory drugs, including low-dose aspirin, are relatively more susceptible to infection.
The ACG’s guideline also recommends testing persons at an increased risk for gastric adenocarcinoma (eg, those with autoimmune gastritis, current or history of premalignant conditions, or first-degree relative with gastric cancer), as well as household members of patients with a positive nonserologic test for H pylori.
The authors note that those with an indication for testing should be offered treatment if determined to have an infection. These patients should also undergo a posttreatment test-of-cure, which should occur at least 4 weeks afterwards using a urea breath test, fecal antigen test, or gastric biopsy.
Caveats to Treatment
Patients with H pylori infections are advised to undergo treatment for a duration of 14 days. Some of the commercial prepackaged H pylori treatment options (eg, Pylera, which contains bismuth subcitrate/metronidazole/tetracycline) are dispensed in regimens lasting only 10 days and currently are viewed as inadequate.
In the United States, the patterns of antibiotic resistance for the previously used standard drugs in the treatment of H pylori have increased considerably. They range from 32% for clarithromycin, 38% for levofloxacin, and 42% for metronidazole, in contrast to 3% for amoxicillin, 1% for tetracycline, and 0% for rifabutin.
Clarithromycin- and levofloxacin-containing treatments should be avoided in treatment-naive patients unless specifically directed following the results of susceptibility tests with either a phenotypic method (culture-based) or a molecular method (polymerase chain reaction or next-generation sequencing). Notably, the mutations responsible for both clarithromycin and levofloxacin resistance may be detectable by stool-based testing.
Maintenance of intragastric acid suppression is key to H pylori eradication, as elevated intragastric pH promotes active replication of H pylori and makes it more susceptible to bactericidal antibiotics.
Therefore, the use of histamine-2 receptors is not recommended, as they are inadequate for achieving acid suppression. Instead, a dual-based therapy of either the potassium-competitive acid blocker (PCAB) vonoprazan (20 mg) or a high-dose proton pump inhibitor (PPI) and amoxicillin, administered twice daily, is effective, although this finding is based on limited evidence.
Treatment-Naive Patients
In treatment-naive patients without penicillin allergy and for whom antibiotic susceptibility testing has not been obtained, the guideline offers its strongest recommendation for bismuth quadruple therapy. This therapy typically consists of a PPI, bismuth subcitrate or subsalicylate, tetracycline, and metronidazole.
Among those with a penicillin allergy, bismuth quadruple therapy is also the primary treatment choice. The authors suggest that patients with a suspected allergy are referred to an allergist for possible penicillin desensitization, given that less than 1% of the population is thought to present with a “true” allergy.
The guideline also presented conditional recommendations, based on low- to moderate-quality evidence, for using a rifabutin-based triple regimen of omeprazole, amoxicillin, and rifabutin (Talicia); a PCAB-based dual regimen of vonoprazan and amoxicillin (Voquezna Dual Pak); and a PCAB-based triple regimen of vonoprazan, clarithromycin, and amoxicillin (Voquezna Triple Pak). In patients with unknown clarithromycin susceptibility, the PCAB-based triple therapy is preferred over PPI-clarithromycin triple therapy.
Although probiotics have been suggested to possibly lead to increased effectiveness or tolerability for H pylori eradication, this was based on studies with significant heterogeneity in their designs. At present, no high-quality data support probiotic therapy.
Clinicians may substitute doxycycline for tetracycline due to availability or cost, and also may prescribe metronidazole at a lower dose than recommended (1.5-2 g/d) to limit side effects. Both modifications have been associated with lower rates of H pylori eradication and are not recommended.
Treatment-Experienced Patients
Quadruple bismuth therapy is the optimal approach among treatment-experienced patients with persistent H pylori infection who have not previously received this therapy. However, this recommendation was rated as conditional, given that it was based on a low quality of evidence.
The guideline offered other recommendations for treatment-experienced patients with persistent infection who had received bismuth quadruple therapy — also conditionally based on a low quality of evidence.
In such patients, it is recommended to consider the use of a rifabutin-based triple therapy (ie, a PPI standard to double dose, amoxicillin, and rifabutin) and a levofloxacin-based triple therapy (ie, a PPI standard dose, levofloxacin, and amoxicillin or metronidazole).
Although significant evidence gaps prevented the authors from providing formal recommendations, they included a PCAB-based triple therapy of vonoprazan, clarithromycin, and amoxicillin (Voquezna Triple Pak) and a high-dose dual therapy of either vonoprazan (20 mg) or PPI (double dose) and amoxicillin among their suggested salvage regimens for these patients.
A New Standard
We must recognize, however, that there are still substantial evidence gaps, particularly around the use of a PCAB-based regimen and its relative advantages over a standard or high-dose PPI-based regimen. This may be of particular importance based on the variable prevalence of cytochrome P450 2C19 (CYP2C19) polymorphisms in the specific patient populations, as PCABs are not metabolized by CYP2C19.
Reviewing the entirety of the ACG’s clinical guideline is encouraged for additional details about the management of H pylori beyond what is highlighted herein.
Dr. Johnson, Professor of Medicine, Chief of Gastroenterology, Eastern Virginia Medical School, Norfolk, Virginia, disclosed ties with ISOTHRIVE and Johnson & Johnson.
A version of this article appeared on Medscape.com.
Helicobacter pylori is one of the most common human bacterial chronic infections globally. Its prevalence has actually decreased in North America in recent years, although its current range of approximately 30%-40% remains substantial given the potential clinical implications of infection.
Standards have changed considerably regarding the testing, treatment, and follow-up of H pylori. This is made clear by the just-published clinical practice guideline from the American College of Gastroenterology (ACG), which provides several new recommendations based on recent scientific evidence that should change your clinical approach to managing this common infection.
This discussion aims to synthesize and highlight key concepts from the ACG’s comprehensive publication.
Who Should Be Tested and Treated?
The cardinal diseases caused by H pylori have traditionally included peptic ulcer disease, marginal zone B-cell lymphoma, gastric adenocarcinoma, and dyspepsia.
Additional associations have been made with idiopathic thrombocytopenic purpura and otherwise unexplained iron deficiency.
New evidence suggests that patients taking long-term nonsteroidal anti-inflammatory drugs, including low-dose aspirin, are relatively more susceptible to infection.
The ACG’s guideline also recommends testing persons at an increased risk for gastric adenocarcinoma (eg, those with autoimmune gastritis, current or history of premalignant conditions, or first-degree relative with gastric cancer), as well as household members of patients with a positive nonserologic test for H pylori.
The authors note that those with an indication for testing should be offered treatment if determined to have an infection. These patients should also undergo a posttreatment test-of-cure, which should occur at least 4 weeks afterwards using a urea breath test, fecal antigen test, or gastric biopsy.
Caveats to Treatment
Patients with H pylori infections are advised to undergo treatment for a duration of 14 days. Some of the commercial prepackaged H pylori treatment options (eg, Pylera, which contains bismuth subcitrate/metronidazole/tetracycline) are dispensed in regimens lasting only 10 days and currently are viewed as inadequate.
In the United States, the patterns of antibiotic resistance for the previously used standard drugs in the treatment of H pylori have increased considerably. They range from 32% for clarithromycin, 38% for levofloxacin, and 42% for metronidazole, in contrast to 3% for amoxicillin, 1% for tetracycline, and 0% for rifabutin.
Clarithromycin- and levofloxacin-containing treatments should be avoided in treatment-naive patients unless specifically directed following the results of susceptibility tests with either a phenotypic method (culture-based) or a molecular method (polymerase chain reaction or next-generation sequencing). Notably, the mutations responsible for both clarithromycin and levofloxacin resistance may be detectable by stool-based testing.
Maintenance of intragastric acid suppression is key to H pylori eradication, as elevated intragastric pH promotes active replication of H pylori and makes it more susceptible to bactericidal antibiotics.
Therefore, the use of histamine-2 receptors is not recommended, as they are inadequate for achieving acid suppression. Instead, a dual-based therapy of either the potassium-competitive acid blocker (PCAB) vonoprazan (20 mg) or a high-dose proton pump inhibitor (PPI) and amoxicillin, administered twice daily, is effective, although this finding is based on limited evidence.
Treatment-Naive Patients
In treatment-naive patients without penicillin allergy and for whom antibiotic susceptibility testing has not been obtained, the guideline offers its strongest recommendation for bismuth quadruple therapy. This therapy typically consists of a PPI, bismuth subcitrate or subsalicylate, tetracycline, and metronidazole.
Among those with a penicillin allergy, bismuth quadruple therapy is also the primary treatment choice. The authors suggest that patients with a suspected allergy are referred to an allergist for possible penicillin desensitization, given that less than 1% of the population is thought to present with a “true” allergy.
The guideline also presented conditional recommendations, based on low- to moderate-quality evidence, for using a rifabutin-based triple regimen of omeprazole, amoxicillin, and rifabutin (Talicia); a PCAB-based dual regimen of vonoprazan and amoxicillin (Voquezna Dual Pak); and a PCAB-based triple regimen of vonoprazan, clarithromycin, and amoxicillin (Voquezna Triple Pak). In patients with unknown clarithromycin susceptibility, the PCAB-based triple therapy is preferred over PPI-clarithromycin triple therapy.
Although probiotics have been suggested to possibly lead to increased effectiveness or tolerability for H pylori eradication, this was based on studies with significant heterogeneity in their designs. At present, no high-quality data support probiotic therapy.
Clinicians may substitute doxycycline for tetracycline due to availability or cost, and also may prescribe metronidazole at a lower dose than recommended (1.5-2 g/d) to limit side effects. Both modifications have been associated with lower rates of H pylori eradication and are not recommended.
Treatment-Experienced Patients
Quadruple bismuth therapy is the optimal approach among treatment-experienced patients with persistent H pylori infection who have not previously received this therapy. However, this recommendation was rated as conditional, given that it was based on a low quality of evidence.
The guideline offered other recommendations for treatment-experienced patients with persistent infection who had received bismuth quadruple therapy — also conditionally based on a low quality of evidence.
In such patients, it is recommended to consider the use of a rifabutin-based triple therapy (ie, a PPI standard to double dose, amoxicillin, and rifabutin) and a levofloxacin-based triple therapy (ie, a PPI standard dose, levofloxacin, and amoxicillin or metronidazole).
Although significant evidence gaps prevented the authors from providing formal recommendations, they included a PCAB-based triple therapy of vonoprazan, clarithromycin, and amoxicillin (Voquezna Triple Pak) and a high-dose dual therapy of either vonoprazan (20 mg) or PPI (double dose) and amoxicillin among their suggested salvage regimens for these patients.
A New Standard
We must recognize, however, that there are still substantial evidence gaps, particularly around the use of a PCAB-based regimen and its relative advantages over a standard or high-dose PPI-based regimen. This may be of particular importance based on the variable prevalence of cytochrome P450 2C19 (CYP2C19) polymorphisms in the specific patient populations, as PCABs are not metabolized by CYP2C19.
Reviewing the entirety of the ACG’s clinical guideline is encouraged for additional details about the management of H pylori beyond what is highlighted herein.
Dr. Johnson, Professor of Medicine, Chief of Gastroenterology, Eastern Virginia Medical School, Norfolk, Virginia, disclosed ties with ISOTHRIVE and Johnson & Johnson.
A version of this article appeared on Medscape.com.
Help Your Patients Reap the Benefits of Plant-Based Diets
Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets.
Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet.
Inflammation and Obesity
Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.
Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1.
If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
Plant-Based Diet for Type 2 Diabetes
According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group.
Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss.
It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups.
Plant-Based Diet for Chronic Kidney Disease (CKD)
Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.
However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought.
Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
Realistic Options for Patients on Medical Diets
There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t.
I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities.
Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.
Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation?
This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ health.
Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets.
Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet.
Inflammation and Obesity
Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.
Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1.
If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
Plant-Based Diet for Type 2 Diabetes
According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group.
Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss.
It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups.
Plant-Based Diet for Chronic Kidney Disease (CKD)
Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.
However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought.
Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
Realistic Options for Patients on Medical Diets
There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t.
I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities.
Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.
Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation?
This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ health.
Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets.
Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet.
Inflammation and Obesity
Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.
Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1.
If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
Plant-Based Diet for Type 2 Diabetes
According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group.
Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss.
It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups.
Plant-Based Diet for Chronic Kidney Disease (CKD)
Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.
However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought.
Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
Realistic Options for Patients on Medical Diets
There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t.
I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities.
Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.
Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation?
This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ health.
Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
The Game We Play Every Day
Words do have power. Names have power. Words are events, they do things, change things. They transform both speaker and hearer ... They feed understanding or emotion back and forth and amplify it. — Ursula K. Le Guin
Every medical student should have a class in linguistics. I’m just unsure what it might replace. Maybe physiology? (When was the last time you used Fick’s or Fourier’s Laws anyway?). Even if we don’t supplant any core curriculum, it’s worth noting that we spend more time in our daily work calculating how to communicate things than calculating cardiac outputs. That we can convey so much so consistently and without specific training is a marvel. Making the diagnosis or a plan is often the easy part.
Linguistics is a broad field. At its essence, it studies how we communicate. It’s fascinating how we use tone, word choice, gestures, syntax, and grammar to explain, reassure, instruct or implore patients. Medical appointments are sometimes high stakes and occur within a huge variety of circumstances. In a single day of clinic, I had a patient with dementia, and one pursuing a PhD in P-Chem. I had English speakers, second language English speakers, and a Vietnamese patient who knew no English. In just one day, I explained things to toddlers and adults, a Black woman from Oklahoma and a Jewish woman from New York. For a brief few minutes, each of them was my partner in a game of medical charades. For each one, I had to figure out how to get them to know what I’m thinking.
I learned of this game of charades concept from a podcast featuring Morten Christiansen, professor of psychology at Cornell University, and professor in Cognitive Science of Language, at Aarhus University, Denmark. The idea is that language can be thought of as a game where speakers constantly improvise based on the topic, each one’s expertise, and the shared understanding. I found this intriguing. In his explanation, grammar and definitions are less important than the mutual understanding of what is being communicated. It helps explain the wide variations of speech even among those speaking the same language. It also flips the idea that brains are designed for language, a concept proposed by linguistic greats such as Noam Chomsky and Steven Pinker. Rather, what we call language is just the best solution our brains could create to convey information.
I thought about how each of us instinctively varies the complexity of sentences and tone of voice based on the ability of each patient to understand. Gestures, storytelling and analogies are linguistic tools we use without thinking about them. We’ve a unique communications conundrum in that we often need patients to understand a complex idea, but only have minutes to get them there. We don’t want them to panic. We also don’t want them to be so dispassionate as to not act. To speed things up, we often use a technique known as chunking, short phrases that capture an idea in one bite. For example, “soak and smear” to get atopic patients to moisturize or “scrape and burn” to describe a curettage and electrodesiccation of a basal cell carcinoma or “a stick and a burn” before injecting them (I never liked that one). These are pithy, efficient. But they don’t always work.
One afternoon I had a 93-year-old woman with glossodynia. She had dementia and her 96-year-old husband was helping. When I explained how she’d “swish and spit” her magic mouthwash, he looked perplexed. Is she swishing a wand or something? I shook my head, “No” and gestured with my hands palms down, waving back and forth. It is just a mouthwash. She should rinse, then spit it out. I lost that round.
Then a 64-year-old woman whom I had to advise that the pink bump on her arm was a cutaneous neuroendocrine tumor. Do I call it a Merkel cell carcinoma? Do I say, “You know, like the one Jimmy Buffett had?” (Nope, not a good use of storytelling). She wanted to know how she got it. Sun exposure, we think. Or, perhaps a virus. Just how does one explain a virus called MCPyV that is ubiquitous but somehow caused cancer just for you? How do you convey, “This is serious, but you might not die like Jimmy Buffett?” I had to use all my language skills to get this right.
Then there is the Henderson-Hasselbalch problem of linguistics: communicating through a translator. When doing so, I’m cognizant of choosing short, simple sentences. Subject, verb, object. First this, then that. This mitigates what’s lost in translation and reduces waiting for translations (especially when your patient is storytelling in paragraphs). But try doing this with an emotionally wrought condition like alopecia. Finding the fewest words to convey that your FSH and estrogen levels are irrelevant to your telogen effluvium to a Vietnamese speaker is tricky. “Yes, I see your primary care physician ordered these tests. No, the numbers do not matter.” Did that translate as they are normal? Or that they don’t matter because she is 54? Or that they don’t matter to me because I didn’t order them?
When you find yourself exhausted at the day’s end, perhaps you’ll better appreciate how it was not only the graduate level medicine you did today; you’ve practically got a PhD in linguistics as well. You just didn’t realize it.
Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].
Words do have power. Names have power. Words are events, they do things, change things. They transform both speaker and hearer ... They feed understanding or emotion back and forth and amplify it. — Ursula K. Le Guin
Every medical student should have a class in linguistics. I’m just unsure what it might replace. Maybe physiology? (When was the last time you used Fick’s or Fourier’s Laws anyway?). Even if we don’t supplant any core curriculum, it’s worth noting that we spend more time in our daily work calculating how to communicate things than calculating cardiac outputs. That we can convey so much so consistently and without specific training is a marvel. Making the diagnosis or a plan is often the easy part.
Linguistics is a broad field. At its essence, it studies how we communicate. It’s fascinating how we use tone, word choice, gestures, syntax, and grammar to explain, reassure, instruct or implore patients. Medical appointments are sometimes high stakes and occur within a huge variety of circumstances. In a single day of clinic, I had a patient with dementia, and one pursuing a PhD in P-Chem. I had English speakers, second language English speakers, and a Vietnamese patient who knew no English. In just one day, I explained things to toddlers and adults, a Black woman from Oklahoma and a Jewish woman from New York. For a brief few minutes, each of them was my partner in a game of medical charades. For each one, I had to figure out how to get them to know what I’m thinking.
I learned of this game of charades concept from a podcast featuring Morten Christiansen, professor of psychology at Cornell University, and professor in Cognitive Science of Language, at Aarhus University, Denmark. The idea is that language can be thought of as a game where speakers constantly improvise based on the topic, each one’s expertise, and the shared understanding. I found this intriguing. In his explanation, grammar and definitions are less important than the mutual understanding of what is being communicated. It helps explain the wide variations of speech even among those speaking the same language. It also flips the idea that brains are designed for language, a concept proposed by linguistic greats such as Noam Chomsky and Steven Pinker. Rather, what we call language is just the best solution our brains could create to convey information.
I thought about how each of us instinctively varies the complexity of sentences and tone of voice based on the ability of each patient to understand. Gestures, storytelling and analogies are linguistic tools we use without thinking about them. We’ve a unique communications conundrum in that we often need patients to understand a complex idea, but only have minutes to get them there. We don’t want them to panic. We also don’t want them to be so dispassionate as to not act. To speed things up, we often use a technique known as chunking, short phrases that capture an idea in one bite. For example, “soak and smear” to get atopic patients to moisturize or “scrape and burn” to describe a curettage and electrodesiccation of a basal cell carcinoma or “a stick and a burn” before injecting them (I never liked that one). These are pithy, efficient. But they don’t always work.
One afternoon I had a 93-year-old woman with glossodynia. She had dementia and her 96-year-old husband was helping. When I explained how she’d “swish and spit” her magic mouthwash, he looked perplexed. Is she swishing a wand or something? I shook my head, “No” and gestured with my hands palms down, waving back and forth. It is just a mouthwash. She should rinse, then spit it out. I lost that round.
Then a 64-year-old woman whom I had to advise that the pink bump on her arm was a cutaneous neuroendocrine tumor. Do I call it a Merkel cell carcinoma? Do I say, “You know, like the one Jimmy Buffett had?” (Nope, not a good use of storytelling). She wanted to know how she got it. Sun exposure, we think. Or, perhaps a virus. Just how does one explain a virus called MCPyV that is ubiquitous but somehow caused cancer just for you? How do you convey, “This is serious, but you might not die like Jimmy Buffett?” I had to use all my language skills to get this right.
Then there is the Henderson-Hasselbalch problem of linguistics: communicating through a translator. When doing so, I’m cognizant of choosing short, simple sentences. Subject, verb, object. First this, then that. This mitigates what’s lost in translation and reduces waiting for translations (especially when your patient is storytelling in paragraphs). But try doing this with an emotionally wrought condition like alopecia. Finding the fewest words to convey that your FSH and estrogen levels are irrelevant to your telogen effluvium to a Vietnamese speaker is tricky. “Yes, I see your primary care physician ordered these tests. No, the numbers do not matter.” Did that translate as they are normal? Or that they don’t matter because she is 54? Or that they don’t matter to me because I didn’t order them?
When you find yourself exhausted at the day’s end, perhaps you’ll better appreciate how it was not only the graduate level medicine you did today; you’ve practically got a PhD in linguistics as well. You just didn’t realize it.
Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].
Words do have power. Names have power. Words are events, they do things, change things. They transform both speaker and hearer ... They feed understanding or emotion back and forth and amplify it. — Ursula K. Le Guin
Every medical student should have a class in linguistics. I’m just unsure what it might replace. Maybe physiology? (When was the last time you used Fick’s or Fourier’s Laws anyway?). Even if we don’t supplant any core curriculum, it’s worth noting that we spend more time in our daily work calculating how to communicate things than calculating cardiac outputs. That we can convey so much so consistently and without specific training is a marvel. Making the diagnosis or a plan is often the easy part.
Linguistics is a broad field. At its essence, it studies how we communicate. It’s fascinating how we use tone, word choice, gestures, syntax, and grammar to explain, reassure, instruct or implore patients. Medical appointments are sometimes high stakes and occur within a huge variety of circumstances. In a single day of clinic, I had a patient with dementia, and one pursuing a PhD in P-Chem. I had English speakers, second language English speakers, and a Vietnamese patient who knew no English. In just one day, I explained things to toddlers and adults, a Black woman from Oklahoma and a Jewish woman from New York. For a brief few minutes, each of them was my partner in a game of medical charades. For each one, I had to figure out how to get them to know what I’m thinking.
I learned of this game of charades concept from a podcast featuring Morten Christiansen, professor of psychology at Cornell University, and professor in Cognitive Science of Language, at Aarhus University, Denmark. The idea is that language can be thought of as a game where speakers constantly improvise based on the topic, each one’s expertise, and the shared understanding. I found this intriguing. In his explanation, grammar and definitions are less important than the mutual understanding of what is being communicated. It helps explain the wide variations of speech even among those speaking the same language. It also flips the idea that brains are designed for language, a concept proposed by linguistic greats such as Noam Chomsky and Steven Pinker. Rather, what we call language is just the best solution our brains could create to convey information.
I thought about how each of us instinctively varies the complexity of sentences and tone of voice based on the ability of each patient to understand. Gestures, storytelling and analogies are linguistic tools we use without thinking about them. We’ve a unique communications conundrum in that we often need patients to understand a complex idea, but only have minutes to get them there. We don’t want them to panic. We also don’t want them to be so dispassionate as to not act. To speed things up, we often use a technique known as chunking, short phrases that capture an idea in one bite. For example, “soak and smear” to get atopic patients to moisturize or “scrape and burn” to describe a curettage and electrodesiccation of a basal cell carcinoma or “a stick and a burn” before injecting them (I never liked that one). These are pithy, efficient. But they don’t always work.
One afternoon I had a 93-year-old woman with glossodynia. She had dementia and her 96-year-old husband was helping. When I explained how she’d “swish and spit” her magic mouthwash, he looked perplexed. Is she swishing a wand or something? I shook my head, “No” and gestured with my hands palms down, waving back and forth. It is just a mouthwash. She should rinse, then spit it out. I lost that round.
Then a 64-year-old woman whom I had to advise that the pink bump on her arm was a cutaneous neuroendocrine tumor. Do I call it a Merkel cell carcinoma? Do I say, “You know, like the one Jimmy Buffett had?” (Nope, not a good use of storytelling). She wanted to know how she got it. Sun exposure, we think. Or, perhaps a virus. Just how does one explain a virus called MCPyV that is ubiquitous but somehow caused cancer just for you? How do you convey, “This is serious, but you might not die like Jimmy Buffett?” I had to use all my language skills to get this right.
Then there is the Henderson-Hasselbalch problem of linguistics: communicating through a translator. When doing so, I’m cognizant of choosing short, simple sentences. Subject, verb, object. First this, then that. This mitigates what’s lost in translation and reduces waiting for translations (especially when your patient is storytelling in paragraphs). But try doing this with an emotionally wrought condition like alopecia. Finding the fewest words to convey that your FSH and estrogen levels are irrelevant to your telogen effluvium to a Vietnamese speaker is tricky. “Yes, I see your primary care physician ordered these tests. No, the numbers do not matter.” Did that translate as they are normal? Or that they don’t matter because she is 54? Or that they don’t matter to me because I didn’t order them?
When you find yourself exhausted at the day’s end, perhaps you’ll better appreciate how it was not only the graduate level medicine you did today; you’ve practically got a PhD in linguistics as well. You just didn’t realize it.
Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].
A Doctor Gets the Save When a Little League Umpire Collapses
Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a Medscape Medical News series telling these stories.
I sincerely believe that what goes around comes around. Good things come to good people. And sometimes that saves lives.
My 10-year-old son was in the semifinals of the Little League district championship. And we were losing. My son is an excellent pitcher, and he had started the game. But that night, he was struggling. He just couldn’t find where to throw the ball. Needless to say, he was frustrated.
He was changed to shortstop in the second inning, and the home plate umpire walked over to him. This umpire is well known in the area for his kindness and commitment, how he encourages the kids and helps make baseball fun even when it’s stressful.
We didn’t know him well, but he was really supportive of my kid in that moment, talking to him about how baseball is a team sport and we’re here to have fun. Just being really positive.
As the game continued, I saw the umpire suddenly walk to the side of the field. I hadn’t seen it, but he had been hit by a wild pitch on the side of his neck. He was wearing protective gear, but the ball managed to bounce up the side and caught bare neck. I knew something wasn’t right.
I went down to talk to him, and my medical assistant (MA), who was also at the game, came with me. I could tell the umpire was injured, but he didn’t want to leave the game. I suggested going to the hospital, but he wouldn’t consider it. So I sat there with my arms crossed, watching him.
His symptoms got worse. I could see he was in pain, and it was getting harder for him to speak.
Again, I strongly urged him to go to the hospital, but again, he said no.
In the sixth inning, things got bad enough that the umpire finally agreed to leave the game. As I was figuring out how to get him to the hospital, he disappeared on me. He had walked up to the second floor of the snack shack. My MA and I got him back downstairs and sat him on a bench behind home plate.
We were in the process of calling 911 ... when he arrested.
Luckily, when he lost vital signs, my MA and I were standing right next to him. We were able to activate ACLS protocol and start CPR within seconds.
Many times in these critical situations — especially if people are scared or have never seen an emergency like this — there’s the potential for chaos. Well, that was the polar opposite of what happened.
As soon as I started to run the code, there was this sense of order. People were keeping their composure and following directions. My MA and I would say, “this is what we need,” and the task would immediately be assigned to someone. It was quiet. There was no yelling. Everyone trusted me, even though some of them had never met me before. It was so surprising. I remember thinking, we’re running an arrest, but it’s so calm.
We were an organized team, and it really worked like clockwork, which was remarkable given where we were. It’s one thing to be in the hospital for an event like that. But to be on a baseball field where you have nothing is a completely different scenario.
Meanwhile, the game went on.
I had requested that all the kids be placed in the dugout when they weren’t on the field. So they saw the umpire walk off, but none of them saw him arrest. Some parents were really helpful with making sure the kids were okay.
The president of Oxford Little League ran across the street to a fire station to get an AED. But the fire department personnel were out on a call. He had to break down the door.
By the time he got back, the umpire’s vital signs were returning. And then EMS arrived.
They loaded him in the ambulance, and I called ahead to the trauma team, so they knew exactly what was happening.
I was pretty worried. My hypothesis was that there was probably compression on the vasculature, which had caused him to lose his vital signs. I thought he probably had an impending airway loss. I wasn’t sure if he was going to make it through the night.
What I didn’t know was that while I was giving CPR, my son stole home, and we won the game. As the ambulance was leaving, the celebration was going on in the outfield.
The umpire was in the hospital for several days. Early on, I got permission from his family to visit him. The first time I saw him, I felt this incredible gratitude and peace.
My dad was an ER doctor, and growing up, it seemed like every time we went on a family vacation, there was an emergency. We would be near a car accident or something, and my father would fly in and save the day. I remember being on the Autobahn somewhere in Europe, and there was a devastating accident between a car and a motorcycle. My father stabilized the guy, had him airlifted out, and apparently, he did fine. I grew up watching things like this and thinking, wow, that’s incredible.
Fast forward to 2 years ago, my father was diagnosed with a lung cancer he never should have had. He never smoked. As a cancer surgeon, I know we did everything in our power to save him. But it didn’t happen. He passed away.
I realize this is superstitious, but seeing the umpire alive, I had this feeling that somehow my dad was there. It was bittersweet but also a joyful moment — like I could breathe again.
I met the umpire’s family that first time, and it was like meeting family that you didn’t know you had but now you have forever. Even though the event was traumatic — I’m still trying not to be on high alert every time I go to a game — it felt like a gift to be part of this journey with them.
Little League’s mission is to teach kids about teamwork, leadership, and making good choices so communities are stronger. Our umpire is a guy who does that every day. He’s not a Little League umpire because he makes any money. He shows up at every single game to support these kids and engage them, to model respect, gratitude, and kindness.
I think our obligation as people is to live with intentionality. We all need to make sure we leave the world a better place, even when we are called upon to do uncomfortable things. Our umpire showed our kids what that looks like, and in that moment when he could have died, we were able to do the same for him.
Jennifer LaFemina, MD, is a surgical oncologist at UMass Memorial Medical Center in Massachusetts.
Are you a medical professional with a dramatic story outside the clinic? Medscape Medical News would love to consider your story for Is There a Doctor in the House? Please email your contact information and a short summary to [email protected].
A version of this article appeared on Medscape.com.
Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a Medscape Medical News series telling these stories.
I sincerely believe that what goes around comes around. Good things come to good people. And sometimes that saves lives.
My 10-year-old son was in the semifinals of the Little League district championship. And we were losing. My son is an excellent pitcher, and he had started the game. But that night, he was struggling. He just couldn’t find where to throw the ball. Needless to say, he was frustrated.
He was changed to shortstop in the second inning, and the home plate umpire walked over to him. This umpire is well known in the area for his kindness and commitment, how he encourages the kids and helps make baseball fun even when it’s stressful.
We didn’t know him well, but he was really supportive of my kid in that moment, talking to him about how baseball is a team sport and we’re here to have fun. Just being really positive.
As the game continued, I saw the umpire suddenly walk to the side of the field. I hadn’t seen it, but he had been hit by a wild pitch on the side of his neck. He was wearing protective gear, but the ball managed to bounce up the side and caught bare neck. I knew something wasn’t right.
I went down to talk to him, and my medical assistant (MA), who was also at the game, came with me. I could tell the umpire was injured, but he didn’t want to leave the game. I suggested going to the hospital, but he wouldn’t consider it. So I sat there with my arms crossed, watching him.
His symptoms got worse. I could see he was in pain, and it was getting harder for him to speak.
Again, I strongly urged him to go to the hospital, but again, he said no.
In the sixth inning, things got bad enough that the umpire finally agreed to leave the game. As I was figuring out how to get him to the hospital, he disappeared on me. He had walked up to the second floor of the snack shack. My MA and I got him back downstairs and sat him on a bench behind home plate.
We were in the process of calling 911 ... when he arrested.
Luckily, when he lost vital signs, my MA and I were standing right next to him. We were able to activate ACLS protocol and start CPR within seconds.
Many times in these critical situations — especially if people are scared or have never seen an emergency like this — there’s the potential for chaos. Well, that was the polar opposite of what happened.
As soon as I started to run the code, there was this sense of order. People were keeping their composure and following directions. My MA and I would say, “this is what we need,” and the task would immediately be assigned to someone. It was quiet. There was no yelling. Everyone trusted me, even though some of them had never met me before. It was so surprising. I remember thinking, we’re running an arrest, but it’s so calm.
We were an organized team, and it really worked like clockwork, which was remarkable given where we were. It’s one thing to be in the hospital for an event like that. But to be on a baseball field where you have nothing is a completely different scenario.
Meanwhile, the game went on.
I had requested that all the kids be placed in the dugout when they weren’t on the field. So they saw the umpire walk off, but none of them saw him arrest. Some parents were really helpful with making sure the kids were okay.
The president of Oxford Little League ran across the street to a fire station to get an AED. But the fire department personnel were out on a call. He had to break down the door.
By the time he got back, the umpire’s vital signs were returning. And then EMS arrived.
They loaded him in the ambulance, and I called ahead to the trauma team, so they knew exactly what was happening.
I was pretty worried. My hypothesis was that there was probably compression on the vasculature, which had caused him to lose his vital signs. I thought he probably had an impending airway loss. I wasn’t sure if he was going to make it through the night.
What I didn’t know was that while I was giving CPR, my son stole home, and we won the game. As the ambulance was leaving, the celebration was going on in the outfield.
The umpire was in the hospital for several days. Early on, I got permission from his family to visit him. The first time I saw him, I felt this incredible gratitude and peace.
My dad was an ER doctor, and growing up, it seemed like every time we went on a family vacation, there was an emergency. We would be near a car accident or something, and my father would fly in and save the day. I remember being on the Autobahn somewhere in Europe, and there was a devastating accident between a car and a motorcycle. My father stabilized the guy, had him airlifted out, and apparently, he did fine. I grew up watching things like this and thinking, wow, that’s incredible.
Fast forward to 2 years ago, my father was diagnosed with a lung cancer he never should have had. He never smoked. As a cancer surgeon, I know we did everything in our power to save him. But it didn’t happen. He passed away.
I realize this is superstitious, but seeing the umpire alive, I had this feeling that somehow my dad was there. It was bittersweet but also a joyful moment — like I could breathe again.
I met the umpire’s family that first time, and it was like meeting family that you didn’t know you had but now you have forever. Even though the event was traumatic — I’m still trying not to be on high alert every time I go to a game — it felt like a gift to be part of this journey with them.
Little League’s mission is to teach kids about teamwork, leadership, and making good choices so communities are stronger. Our umpire is a guy who does that every day. He’s not a Little League umpire because he makes any money. He shows up at every single game to support these kids and engage them, to model respect, gratitude, and kindness.
I think our obligation as people is to live with intentionality. We all need to make sure we leave the world a better place, even when we are called upon to do uncomfortable things. Our umpire showed our kids what that looks like, and in that moment when he could have died, we were able to do the same for him.
Jennifer LaFemina, MD, is a surgical oncologist at UMass Memorial Medical Center in Massachusetts.
Are you a medical professional with a dramatic story outside the clinic? Medscape Medical News would love to consider your story for Is There a Doctor in the House? Please email your contact information and a short summary to [email protected].
A version of this article appeared on Medscape.com.
Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a Medscape Medical News series telling these stories.
I sincerely believe that what goes around comes around. Good things come to good people. And sometimes that saves lives.
My 10-year-old son was in the semifinals of the Little League district championship. And we were losing. My son is an excellent pitcher, and he had started the game. But that night, he was struggling. He just couldn’t find where to throw the ball. Needless to say, he was frustrated.
He was changed to shortstop in the second inning, and the home plate umpire walked over to him. This umpire is well known in the area for his kindness and commitment, how he encourages the kids and helps make baseball fun even when it’s stressful.
We didn’t know him well, but he was really supportive of my kid in that moment, talking to him about how baseball is a team sport and we’re here to have fun. Just being really positive.
As the game continued, I saw the umpire suddenly walk to the side of the field. I hadn’t seen it, but he had been hit by a wild pitch on the side of his neck. He was wearing protective gear, but the ball managed to bounce up the side and caught bare neck. I knew something wasn’t right.
I went down to talk to him, and my medical assistant (MA), who was also at the game, came with me. I could tell the umpire was injured, but he didn’t want to leave the game. I suggested going to the hospital, but he wouldn’t consider it. So I sat there with my arms crossed, watching him.
His symptoms got worse. I could see he was in pain, and it was getting harder for him to speak.
Again, I strongly urged him to go to the hospital, but again, he said no.
In the sixth inning, things got bad enough that the umpire finally agreed to leave the game. As I was figuring out how to get him to the hospital, he disappeared on me. He had walked up to the second floor of the snack shack. My MA and I got him back downstairs and sat him on a bench behind home plate.
We were in the process of calling 911 ... when he arrested.
Luckily, when he lost vital signs, my MA and I were standing right next to him. We were able to activate ACLS protocol and start CPR within seconds.
Many times in these critical situations — especially if people are scared or have never seen an emergency like this — there’s the potential for chaos. Well, that was the polar opposite of what happened.
As soon as I started to run the code, there was this sense of order. People were keeping their composure and following directions. My MA and I would say, “this is what we need,” and the task would immediately be assigned to someone. It was quiet. There was no yelling. Everyone trusted me, even though some of them had never met me before. It was so surprising. I remember thinking, we’re running an arrest, but it’s so calm.
We were an organized team, and it really worked like clockwork, which was remarkable given where we were. It’s one thing to be in the hospital for an event like that. But to be on a baseball field where you have nothing is a completely different scenario.
Meanwhile, the game went on.
I had requested that all the kids be placed in the dugout when they weren’t on the field. So they saw the umpire walk off, but none of them saw him arrest. Some parents were really helpful with making sure the kids were okay.
The president of Oxford Little League ran across the street to a fire station to get an AED. But the fire department personnel were out on a call. He had to break down the door.
By the time he got back, the umpire’s vital signs were returning. And then EMS arrived.
They loaded him in the ambulance, and I called ahead to the trauma team, so they knew exactly what was happening.
I was pretty worried. My hypothesis was that there was probably compression on the vasculature, which had caused him to lose his vital signs. I thought he probably had an impending airway loss. I wasn’t sure if he was going to make it through the night.
What I didn’t know was that while I was giving CPR, my son stole home, and we won the game. As the ambulance was leaving, the celebration was going on in the outfield.
The umpire was in the hospital for several days. Early on, I got permission from his family to visit him. The first time I saw him, I felt this incredible gratitude and peace.
My dad was an ER doctor, and growing up, it seemed like every time we went on a family vacation, there was an emergency. We would be near a car accident or something, and my father would fly in and save the day. I remember being on the Autobahn somewhere in Europe, and there was a devastating accident between a car and a motorcycle. My father stabilized the guy, had him airlifted out, and apparently, he did fine. I grew up watching things like this and thinking, wow, that’s incredible.
Fast forward to 2 years ago, my father was diagnosed with a lung cancer he never should have had. He never smoked. As a cancer surgeon, I know we did everything in our power to save him. But it didn’t happen. He passed away.
I realize this is superstitious, but seeing the umpire alive, I had this feeling that somehow my dad was there. It was bittersweet but also a joyful moment — like I could breathe again.
I met the umpire’s family that first time, and it was like meeting family that you didn’t know you had but now you have forever. Even though the event was traumatic — I’m still trying not to be on high alert every time I go to a game — it felt like a gift to be part of this journey with them.
Little League’s mission is to teach kids about teamwork, leadership, and making good choices so communities are stronger. Our umpire is a guy who does that every day. He’s not a Little League umpire because he makes any money. He shows up at every single game to support these kids and engage them, to model respect, gratitude, and kindness.
I think our obligation as people is to live with intentionality. We all need to make sure we leave the world a better place, even when we are called upon to do uncomfortable things. Our umpire showed our kids what that looks like, and in that moment when he could have died, we were able to do the same for him.
Jennifer LaFemina, MD, is a surgical oncologist at UMass Memorial Medical Center in Massachusetts.
Are you a medical professional with a dramatic story outside the clinic? Medscape Medical News would love to consider your story for Is There a Doctor in the House? Please email your contact information and a short summary to [email protected].
A version of this article appeared on Medscape.com.