User login
Barbie has an anxiety disorder
And it’s a great time to be a therapist
The Barbie movie is generating a lot of feelings, ranging from praise to vitriol. However one feels about the movie, let’s all pause and reflect for a moment on the fact that the number-one grossing film of 2023 is about our childhood doll trying to treat her anxiety disorder.
“Life imitates art more than art imitates life.” So said Oscar Wilde in 1889.
When my adult daughter, a childhood Barbie enthusiast, asked me to see the film, we put on pink and went. Twice. Little did I know that it would stir up so many thoughts and feelings. The one I want to share is how blessed I feel at this moment in time to be a mental health care provider! No longer is mental health something to be whispered about at the water cooler; instead, even Barbie is suffering. And with all the controversy in the press about the movie, no one seems at all surprised by this storyline.
I was raised by two child psychiatrists and have been practicing as an adult psychiatrist since 1991. The start of the pandemic was the most difficult time of my career, as almost every patient was struggling simultaneously, as was I. Three long years later, we are gradually emerging from our shared trauma. How ironic, now with the opportunity to go back to work, I have elected to maintain the majority of my practice online from home. It seems that most patients and providers prefer this mode of treatment, with a full 90 percent of practitioners saying they are using a hybrid model.
As mental health professionals, we know that anywhere from 3% to 49% of those experiencing trauma will develop posttraumatic stress disorder (PTSD), and we have been trained to treat them.
But what happens when an entire global population is exposed simultaneously to trauma? Historians and social scientists refer to such events by many different names, such as: Singularity, Black Swan Event, and Tipping Point. These events are incredibly rare, and afterwards everything is different. These global traumas always lead to massive change.
I think we are at that tipping point. This is the singularity. This is our Black Swan Event. Within a 3-year span, we have experienced the following:
- A global traumatic event (COVID-19).
- A sudden and seemingly permanent shift from office to remote video meetings mostly from home.
- Upending of traditional fundamentals of the stock market as the game literally stopped in January 2021.
- Rapid and widespread availability of Artificial Intelligence.
- The first generation to be fully raised on the Internet and social media (Gen Z) is now entering the workforce.
- Ongoing war in Ukraine.
That’s already an overwhelming list, and I could go on, but let’s get back to Barbie’s anxiety disorder.
The awareness about and acceptance of mental health issues has never been higher. The access to treatment never greater. There are now more online therapy options than ever. Treatment options have dramatically expanded in recent years, from Transcranial Magnetic Stimulation (TMS) to ketamine centers and psychedelics, as well as more mainstream options such as dialectical behavior therapy (DBT), cognitive behavioral therapy (CBT), selective serotonin reuptake inhibitors (SSRIs), and so many more.
What is particularly unique about this moment is the direct access to care. Self-help books abound with many making it to the New York Times bestseller list. YouTube is loaded with fantastic content on overcoming many mental health issues, although one should be careful with selecting reliable sources. Apps like HeadSpace and Calm are being downloaded by millions of people around the globe. Investors provided a record-breaking $1.5 billion to mental health startups in 2020 alone.
For most practitioners, our phones have been ringing off the hook since 2020. Applications to psychology, psychiatric residency, social work, and counseling degree programs are on the rise, with workforce shortages expected to continue for decades. Psychological expertise has been embraced by businesses especially for DEI (diversity, equity, and inclusion). Mental health experts are the most asked-for experts through media request services. Elite athletes are talking openly about bringing us on their teams.
In this unique moment, when everything seems set to transform into something else, it is time for mental health professionals to exert some agency and influence over where mental health will go from here. I think the next frontier for mental health specialists is to figure out how to speak collectively and help guide society.
Neil Howe, in his sweeping book “The Fourth Turning is Here,” says we have another 10 years in this “Millennial Crisis” phase. He calls this our “winter,” and it remains to be seen how we will emerge from our current challenges. I think we can make a difference.
If the Barbie movie is indeed a canary in the coal mine, I see positive trends ahead as we move past some of the societal and structural issues facing us, and work together to create a more open and egalitarian society. We must find creative solutions that will solve truly massive problems threatening our well-being and perhaps even our existence.
I am so grateful to be able to continue to practice and share my thoughts with you here from my home office, and I hope you can take a break and see this movie, which is not only entertaining but also thought- and emotion-provoking.
Dr. Ritvo has almost 30 years’ experience in psychiatry and is currently practicing telemedicine. She is the author of “Bekindr – The Transformative Power of Kindness” (Hellertown, Pa.: Momosa Publishing, 2018). She has no conflicts of interest.
And it’s a great time to be a therapist
And it’s a great time to be a therapist
The Barbie movie is generating a lot of feelings, ranging from praise to vitriol. However one feels about the movie, let’s all pause and reflect for a moment on the fact that the number-one grossing film of 2023 is about our childhood doll trying to treat her anxiety disorder.
“Life imitates art more than art imitates life.” So said Oscar Wilde in 1889.
When my adult daughter, a childhood Barbie enthusiast, asked me to see the film, we put on pink and went. Twice. Little did I know that it would stir up so many thoughts and feelings. The one I want to share is how blessed I feel at this moment in time to be a mental health care provider! No longer is mental health something to be whispered about at the water cooler; instead, even Barbie is suffering. And with all the controversy in the press about the movie, no one seems at all surprised by this storyline.
I was raised by two child psychiatrists and have been practicing as an adult psychiatrist since 1991. The start of the pandemic was the most difficult time of my career, as almost every patient was struggling simultaneously, as was I. Three long years later, we are gradually emerging from our shared trauma. How ironic, now with the opportunity to go back to work, I have elected to maintain the majority of my practice online from home. It seems that most patients and providers prefer this mode of treatment, with a full 90 percent of practitioners saying they are using a hybrid model.
As mental health professionals, we know that anywhere from 3% to 49% of those experiencing trauma will develop posttraumatic stress disorder (PTSD), and we have been trained to treat them.
But what happens when an entire global population is exposed simultaneously to trauma? Historians and social scientists refer to such events by many different names, such as: Singularity, Black Swan Event, and Tipping Point. These events are incredibly rare, and afterwards everything is different. These global traumas always lead to massive change.
I think we are at that tipping point. This is the singularity. This is our Black Swan Event. Within a 3-year span, we have experienced the following:
- A global traumatic event (COVID-19).
- A sudden and seemingly permanent shift from office to remote video meetings mostly from home.
- Upending of traditional fundamentals of the stock market as the game literally stopped in January 2021.
- Rapid and widespread availability of Artificial Intelligence.
- The first generation to be fully raised on the Internet and social media (Gen Z) is now entering the workforce.
- Ongoing war in Ukraine.
That’s already an overwhelming list, and I could go on, but let’s get back to Barbie’s anxiety disorder.
The awareness about and acceptance of mental health issues has never been higher. The access to treatment never greater. There are now more online therapy options than ever. Treatment options have dramatically expanded in recent years, from Transcranial Magnetic Stimulation (TMS) to ketamine centers and psychedelics, as well as more mainstream options such as dialectical behavior therapy (DBT), cognitive behavioral therapy (CBT), selective serotonin reuptake inhibitors (SSRIs), and so many more.
What is particularly unique about this moment is the direct access to care. Self-help books abound with many making it to the New York Times bestseller list. YouTube is loaded with fantastic content on overcoming many mental health issues, although one should be careful with selecting reliable sources. Apps like HeadSpace and Calm are being downloaded by millions of people around the globe. Investors provided a record-breaking $1.5 billion to mental health startups in 2020 alone.
For most practitioners, our phones have been ringing off the hook since 2020. Applications to psychology, psychiatric residency, social work, and counseling degree programs are on the rise, with workforce shortages expected to continue for decades. Psychological expertise has been embraced by businesses especially for DEI (diversity, equity, and inclusion). Mental health experts are the most asked-for experts through media request services. Elite athletes are talking openly about bringing us on their teams.
In this unique moment, when everything seems set to transform into something else, it is time for mental health professionals to exert some agency and influence over where mental health will go from here. I think the next frontier for mental health specialists is to figure out how to speak collectively and help guide society.
Neil Howe, in his sweeping book “The Fourth Turning is Here,” says we have another 10 years in this “Millennial Crisis” phase. He calls this our “winter,” and it remains to be seen how we will emerge from our current challenges. I think we can make a difference.
If the Barbie movie is indeed a canary in the coal mine, I see positive trends ahead as we move past some of the societal and structural issues facing us, and work together to create a more open and egalitarian society. We must find creative solutions that will solve truly massive problems threatening our well-being and perhaps even our existence.
I am so grateful to be able to continue to practice and share my thoughts with you here from my home office, and I hope you can take a break and see this movie, which is not only entertaining but also thought- and emotion-provoking.
Dr. Ritvo has almost 30 years’ experience in psychiatry and is currently practicing telemedicine. She is the author of “Bekindr – The Transformative Power of Kindness” (Hellertown, Pa.: Momosa Publishing, 2018). She has no conflicts of interest.
The Barbie movie is generating a lot of feelings, ranging from praise to vitriol. However one feels about the movie, let’s all pause and reflect for a moment on the fact that the number-one grossing film of 2023 is about our childhood doll trying to treat her anxiety disorder.
“Life imitates art more than art imitates life.” So said Oscar Wilde in 1889.
When my adult daughter, a childhood Barbie enthusiast, asked me to see the film, we put on pink and went. Twice. Little did I know that it would stir up so many thoughts and feelings. The one I want to share is how blessed I feel at this moment in time to be a mental health care provider! No longer is mental health something to be whispered about at the water cooler; instead, even Barbie is suffering. And with all the controversy in the press about the movie, no one seems at all surprised by this storyline.
I was raised by two child psychiatrists and have been practicing as an adult psychiatrist since 1991. The start of the pandemic was the most difficult time of my career, as almost every patient was struggling simultaneously, as was I. Three long years later, we are gradually emerging from our shared trauma. How ironic, now with the opportunity to go back to work, I have elected to maintain the majority of my practice online from home. It seems that most patients and providers prefer this mode of treatment, with a full 90 percent of practitioners saying they are using a hybrid model.
As mental health professionals, we know that anywhere from 3% to 49% of those experiencing trauma will develop posttraumatic stress disorder (PTSD), and we have been trained to treat them.
But what happens when an entire global population is exposed simultaneously to trauma? Historians and social scientists refer to such events by many different names, such as: Singularity, Black Swan Event, and Tipping Point. These events are incredibly rare, and afterwards everything is different. These global traumas always lead to massive change.
I think we are at that tipping point. This is the singularity. This is our Black Swan Event. Within a 3-year span, we have experienced the following:
- A global traumatic event (COVID-19).
- A sudden and seemingly permanent shift from office to remote video meetings mostly from home.
- Upending of traditional fundamentals of the stock market as the game literally stopped in January 2021.
- Rapid and widespread availability of Artificial Intelligence.
- The first generation to be fully raised on the Internet and social media (Gen Z) is now entering the workforce.
- Ongoing war in Ukraine.
That’s already an overwhelming list, and I could go on, but let’s get back to Barbie’s anxiety disorder.
The awareness about and acceptance of mental health issues has never been higher. The access to treatment never greater. There are now more online therapy options than ever. Treatment options have dramatically expanded in recent years, from Transcranial Magnetic Stimulation (TMS) to ketamine centers and psychedelics, as well as more mainstream options such as dialectical behavior therapy (DBT), cognitive behavioral therapy (CBT), selective serotonin reuptake inhibitors (SSRIs), and so many more.
What is particularly unique about this moment is the direct access to care. Self-help books abound with many making it to the New York Times bestseller list. YouTube is loaded with fantastic content on overcoming many mental health issues, although one should be careful with selecting reliable sources. Apps like HeadSpace and Calm are being downloaded by millions of people around the globe. Investors provided a record-breaking $1.5 billion to mental health startups in 2020 alone.
For most practitioners, our phones have been ringing off the hook since 2020. Applications to psychology, psychiatric residency, social work, and counseling degree programs are on the rise, with workforce shortages expected to continue for decades. Psychological expertise has been embraced by businesses especially for DEI (diversity, equity, and inclusion). Mental health experts are the most asked-for experts through media request services. Elite athletes are talking openly about bringing us on their teams.
In this unique moment, when everything seems set to transform into something else, it is time for mental health professionals to exert some agency and influence over where mental health will go from here. I think the next frontier for mental health specialists is to figure out how to speak collectively and help guide society.
Neil Howe, in his sweeping book “The Fourth Turning is Here,” says we have another 10 years in this “Millennial Crisis” phase. He calls this our “winter,” and it remains to be seen how we will emerge from our current challenges. I think we can make a difference.
If the Barbie movie is indeed a canary in the coal mine, I see positive trends ahead as we move past some of the societal and structural issues facing us, and work together to create a more open and egalitarian society. We must find creative solutions that will solve truly massive problems threatening our well-being and perhaps even our existence.
I am so grateful to be able to continue to practice and share my thoughts with you here from my home office, and I hope you can take a break and see this movie, which is not only entertaining but also thought- and emotion-provoking.
Dr. Ritvo has almost 30 years’ experience in psychiatry and is currently practicing telemedicine. She is the author of “Bekindr – The Transformative Power of Kindness” (Hellertown, Pa.: Momosa Publishing, 2018). She has no conflicts of interest.
The new normal in body temperature
This transcript has been edited for clarity.
Every branch of science has its constants. Physics has the speed of light, the gravitational constant, the Planck constant. Chemistry gives us Avogadro’s number, Faraday’s constant, the charge of an electron. Medicine isn’t quite as reliable as physics when it comes to these things, but insofar as there are any constants in medicine, might I suggest normal body temperature: 37° Celsius, 98.6° Fahrenheit.
Sure, serum sodium may be less variable and lactate concentration more clinically relevant, but even my 7-year-old knows that normal body temperature is 98.6°.
Except, as it turns out, 98.6° isn’t normal at all.
How did we arrive at 37.0° C for normal body temperature? We got it from this guy – German physician Carl Reinhold August Wunderlich, who, in addition to looking eerily like Luciano Pavarotti, was the first to realize that fever was not itself a disease but a symptom of one.
In 1851, Dr. Wunderlich released his measurements of more than 1 million body temperatures taken from 25,000 Germans – a painstaking process at the time, which employed a foot-long thermometer and took 20 minutes to obtain a measurement.
The average temperature measured, of course, was 37° C.
We’re more than 150 years post-Wunderlich right now, and the average person in the United States might be quite a bit different from the average German in 1850. Moreover, we can do a lot better than just measuring a ton of people and taking the average, because we have statistics. The problem with measuring a bunch of people and taking the average temperature as normal is that you can’t be sure that the people you are measuring are normal. There are obvious causes of elevated temperature that you could exclude. Let’s not take people with a respiratory infection or who are taking Tylenol, for example. But as highlighted in this paper in JAMA Internal Medicine, we can do a lot better than that.
The study leverages the fact that body temperature is typically measured during all medical office visits and recorded in the ever-present electronic medical record.
Researchers from Stanford identified 724,199 patient encounters with outpatient temperature data. They excluded extreme temperatures – less than 34° C or greater than 40° C – excluded patients under 20 or above 80 years, and excluded those with extremes of height, weight, or body mass index.
You end up with a distribution like this. Note that the peak is clearly lower than 37° C.
But we’re still not at “normal.” Some people would be seeing their doctor for conditions that affect body temperature, such as infection. You could use diagnosis codes to flag these individuals and drop them, but that feels a bit arbitrary.
I really love how the researchers used data to fix this problem. They used a technique called LIMIT (Laboratory Information Mining for Individualized Thresholds). It works like this:
Take all the temperature measurements and then identify the outliers – the very tails of the distribution.
Look at all the diagnosis codes in those distributions. Determine which diagnosis codes are overrepresented in those distributions. Now you have a data-driven way to say that yes, these diagnoses are associated with weird temperatures. Next, eliminate everyone with those diagnoses from the dataset. What you are left with is a normal population, or at least a population that doesn’t have a condition that seems to meaningfully affect temperature.
So, who was dropped? Well, a lot of people, actually. It turned out that diabetes was way overrepresented in the outlier group. Although 9.2% of the population had diabetes, 26% of people with very low temperatures did, so everyone with diabetes is removed from the dataset. While 5% of the population had a cough at their encounter, 7% of the people with very high temperature and 7% of the people with very low temperature had a cough, so everyone with cough gets thrown out.
The algorithm excluded people on antibiotics or who had sinusitis, urinary tract infections, pneumonia, and, yes, a diagnosis of “fever.” The list makes sense, which is always nice when you have a purely algorithmic classification system.
What do we have left? What is the real normal temperature? Ready?
It’s 36.64° C, or about 98.0° F.
Of course, normal temperature varied depending on the time of day it was measured – higher in the afternoon.
The normal temperature in women tended to be higher than in men. The normal temperature declined with age as well.
In fact, the researchers built a nice online calculator where you can enter your own, or your patient’s, parameters and calculate a normal body temperature for them. Here’s mine. My normal temperature at around 2 p.m. should be 36.7° C.
So, we’re all more cold-blooded than we thought. Is this just because of better methods? Maybe. But studies have actually shown that body temperature may be decreasing over time in humans, possibly because of the lower levels of inflammation we face in modern life (thanks to improvements in hygiene and antibiotics).
Of course, I’m sure some of you are asking yourselves whether any of this really matters. Is 37° C close enough?
Sure, this may be sort of puttering around the edges of physical diagnosis, but I think the methodology is really interesting and can obviously be applied to other broadly collected data points. But these data show us that thin, older individuals really do run cooler, and that we may need to pay more attention to a low-grade fever in that population than we otherwise would.
In any case, it’s time for a little re-education. If someone asks you what normal body temperature is, just say 36.6° C, 98.0° F. For his work in this area, I suggest we call it Wunderlich’s constant.
Dr. Wilson is associate professor of medicine and public health at Yale University, New Haven, Conn., and director of Yale’s Clinical and Translational Research Accelerator. He has no disclosures.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Every branch of science has its constants. Physics has the speed of light, the gravitational constant, the Planck constant. Chemistry gives us Avogadro’s number, Faraday’s constant, the charge of an electron. Medicine isn’t quite as reliable as physics when it comes to these things, but insofar as there are any constants in medicine, might I suggest normal body temperature: 37° Celsius, 98.6° Fahrenheit.
Sure, serum sodium may be less variable and lactate concentration more clinically relevant, but even my 7-year-old knows that normal body temperature is 98.6°.
Except, as it turns out, 98.6° isn’t normal at all.
How did we arrive at 37.0° C for normal body temperature? We got it from this guy – German physician Carl Reinhold August Wunderlich, who, in addition to looking eerily like Luciano Pavarotti, was the first to realize that fever was not itself a disease but a symptom of one.
In 1851, Dr. Wunderlich released his measurements of more than 1 million body temperatures taken from 25,000 Germans – a painstaking process at the time, which employed a foot-long thermometer and took 20 minutes to obtain a measurement.
The average temperature measured, of course, was 37° C.
We’re more than 150 years post-Wunderlich right now, and the average person in the United States might be quite a bit different from the average German in 1850. Moreover, we can do a lot better than just measuring a ton of people and taking the average, because we have statistics. The problem with measuring a bunch of people and taking the average temperature as normal is that you can’t be sure that the people you are measuring are normal. There are obvious causes of elevated temperature that you could exclude. Let’s not take people with a respiratory infection or who are taking Tylenol, for example. But as highlighted in this paper in JAMA Internal Medicine, we can do a lot better than that.
The study leverages the fact that body temperature is typically measured during all medical office visits and recorded in the ever-present electronic medical record.
Researchers from Stanford identified 724,199 patient encounters with outpatient temperature data. They excluded extreme temperatures – less than 34° C or greater than 40° C – excluded patients under 20 or above 80 years, and excluded those with extremes of height, weight, or body mass index.
You end up with a distribution like this. Note that the peak is clearly lower than 37° C.
But we’re still not at “normal.” Some people would be seeing their doctor for conditions that affect body temperature, such as infection. You could use diagnosis codes to flag these individuals and drop them, but that feels a bit arbitrary.
I really love how the researchers used data to fix this problem. They used a technique called LIMIT (Laboratory Information Mining for Individualized Thresholds). It works like this:
Take all the temperature measurements and then identify the outliers – the very tails of the distribution.
Look at all the diagnosis codes in those distributions. Determine which diagnosis codes are overrepresented in those distributions. Now you have a data-driven way to say that yes, these diagnoses are associated with weird temperatures. Next, eliminate everyone with those diagnoses from the dataset. What you are left with is a normal population, or at least a population that doesn’t have a condition that seems to meaningfully affect temperature.
So, who was dropped? Well, a lot of people, actually. It turned out that diabetes was way overrepresented in the outlier group. Although 9.2% of the population had diabetes, 26% of people with very low temperatures did, so everyone with diabetes is removed from the dataset. While 5% of the population had a cough at their encounter, 7% of the people with very high temperature and 7% of the people with very low temperature had a cough, so everyone with cough gets thrown out.
The algorithm excluded people on antibiotics or who had sinusitis, urinary tract infections, pneumonia, and, yes, a diagnosis of “fever.” The list makes sense, which is always nice when you have a purely algorithmic classification system.
What do we have left? What is the real normal temperature? Ready?
It’s 36.64° C, or about 98.0° F.
Of course, normal temperature varied depending on the time of day it was measured – higher in the afternoon.
The normal temperature in women tended to be higher than in men. The normal temperature declined with age as well.
In fact, the researchers built a nice online calculator where you can enter your own, or your patient’s, parameters and calculate a normal body temperature for them. Here’s mine. My normal temperature at around 2 p.m. should be 36.7° C.
So, we’re all more cold-blooded than we thought. Is this just because of better methods? Maybe. But studies have actually shown that body temperature may be decreasing over time in humans, possibly because of the lower levels of inflammation we face in modern life (thanks to improvements in hygiene and antibiotics).
Of course, I’m sure some of you are asking yourselves whether any of this really matters. Is 37° C close enough?
Sure, this may be sort of puttering around the edges of physical diagnosis, but I think the methodology is really interesting and can obviously be applied to other broadly collected data points. But these data show us that thin, older individuals really do run cooler, and that we may need to pay more attention to a low-grade fever in that population than we otherwise would.
In any case, it’s time for a little re-education. If someone asks you what normal body temperature is, just say 36.6° C, 98.0° F. For his work in this area, I suggest we call it Wunderlich’s constant.
Dr. Wilson is associate professor of medicine and public health at Yale University, New Haven, Conn., and director of Yale’s Clinical and Translational Research Accelerator. He has no disclosures.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Every branch of science has its constants. Physics has the speed of light, the gravitational constant, the Planck constant. Chemistry gives us Avogadro’s number, Faraday’s constant, the charge of an electron. Medicine isn’t quite as reliable as physics when it comes to these things, but insofar as there are any constants in medicine, might I suggest normal body temperature: 37° Celsius, 98.6° Fahrenheit.
Sure, serum sodium may be less variable and lactate concentration more clinically relevant, but even my 7-year-old knows that normal body temperature is 98.6°.
Except, as it turns out, 98.6° isn’t normal at all.
How did we arrive at 37.0° C for normal body temperature? We got it from this guy – German physician Carl Reinhold August Wunderlich, who, in addition to looking eerily like Luciano Pavarotti, was the first to realize that fever was not itself a disease but a symptom of one.
In 1851, Dr. Wunderlich released his measurements of more than 1 million body temperatures taken from 25,000 Germans – a painstaking process at the time, which employed a foot-long thermometer and took 20 minutes to obtain a measurement.
The average temperature measured, of course, was 37° C.
We’re more than 150 years post-Wunderlich right now, and the average person in the United States might be quite a bit different from the average German in 1850. Moreover, we can do a lot better than just measuring a ton of people and taking the average, because we have statistics. The problem with measuring a bunch of people and taking the average temperature as normal is that you can’t be sure that the people you are measuring are normal. There are obvious causes of elevated temperature that you could exclude. Let’s not take people with a respiratory infection or who are taking Tylenol, for example. But as highlighted in this paper in JAMA Internal Medicine, we can do a lot better than that.
The study leverages the fact that body temperature is typically measured during all medical office visits and recorded in the ever-present electronic medical record.
Researchers from Stanford identified 724,199 patient encounters with outpatient temperature data. They excluded extreme temperatures – less than 34° C or greater than 40° C – excluded patients under 20 or above 80 years, and excluded those with extremes of height, weight, or body mass index.
You end up with a distribution like this. Note that the peak is clearly lower than 37° C.
But we’re still not at “normal.” Some people would be seeing their doctor for conditions that affect body temperature, such as infection. You could use diagnosis codes to flag these individuals and drop them, but that feels a bit arbitrary.
I really love how the researchers used data to fix this problem. They used a technique called LIMIT (Laboratory Information Mining for Individualized Thresholds). It works like this:
Take all the temperature measurements and then identify the outliers – the very tails of the distribution.
Look at all the diagnosis codes in those distributions. Determine which diagnosis codes are overrepresented in those distributions. Now you have a data-driven way to say that yes, these diagnoses are associated with weird temperatures. Next, eliminate everyone with those diagnoses from the dataset. What you are left with is a normal population, or at least a population that doesn’t have a condition that seems to meaningfully affect temperature.
So, who was dropped? Well, a lot of people, actually. It turned out that diabetes was way overrepresented in the outlier group. Although 9.2% of the population had diabetes, 26% of people with very low temperatures did, so everyone with diabetes is removed from the dataset. While 5% of the population had a cough at their encounter, 7% of the people with very high temperature and 7% of the people with very low temperature had a cough, so everyone with cough gets thrown out.
The algorithm excluded people on antibiotics or who had sinusitis, urinary tract infections, pneumonia, and, yes, a diagnosis of “fever.” The list makes sense, which is always nice when you have a purely algorithmic classification system.
What do we have left? What is the real normal temperature? Ready?
It’s 36.64° C, or about 98.0° F.
Of course, normal temperature varied depending on the time of day it was measured – higher in the afternoon.
The normal temperature in women tended to be higher than in men. The normal temperature declined with age as well.
In fact, the researchers built a nice online calculator where you can enter your own, or your patient’s, parameters and calculate a normal body temperature for them. Here’s mine. My normal temperature at around 2 p.m. should be 36.7° C.
So, we’re all more cold-blooded than we thought. Is this just because of better methods? Maybe. But studies have actually shown that body temperature may be decreasing over time in humans, possibly because of the lower levels of inflammation we face in modern life (thanks to improvements in hygiene and antibiotics).
Of course, I’m sure some of you are asking yourselves whether any of this really matters. Is 37° C close enough?
Sure, this may be sort of puttering around the edges of physical diagnosis, but I think the methodology is really interesting and can obviously be applied to other broadly collected data points. But these data show us that thin, older individuals really do run cooler, and that we may need to pay more attention to a low-grade fever in that population than we otherwise would.
In any case, it’s time for a little re-education. If someone asks you what normal body temperature is, just say 36.6° C, 98.0° F. For his work in this area, I suggest we call it Wunderlich’s constant.
Dr. Wilson is associate professor of medicine and public health at Yale University, New Haven, Conn., and director of Yale’s Clinical and Translational Research Accelerator. He has no disclosures.
A version of this article appeared on Medscape.com.
The cult of the suicide risk assessment
Suicide is not a trivial matter – it upends families, robs partners of a loved one, prevents children from having a parent, and can destroy a parent’s most cherished being. It is not surprising that societies have repeatedly made it a goal to study and reduce suicide within their populations.
The suicide rate in the United States is trending upward, from about 10 per 100,000 in 2000 to about 15 per 100,000 in more recent reports. The increasing suicide rates have been accompanied by increasing distress among many strata of society. From a public health level, analysts are not just witnessing increasing suicide rates, but a shocking rise in all “deaths of despair,”1 among which suicide can be considered the ultimate example.
On an individual level, many know someone who has died of suicide or suffered from a serious suicide attempt. From the public health level to the individual level, advocacy has called for various interventions in the field of psychiatry to remedy this tragic problem.
Psychiatrists have been firsthand witnesses to this increasing demand for suicide interventions. When in residency, the norm was to perform a suicide risk assessment at the time of admission to the hospital and again at the time of discharge. As the years passed, the new normal within psychiatric hospitals has shifted to asking about suicidality on a daily basis.
In what seems to us like an escalating arms race, the emerging standard of care at many facilities is now not only for daily suicide risk assessments by each psychiatrist, but also to require nurses to ask about suicidality during every 8-hour shift – in addition to documented inquiries about suicidality by other allied staff on the psychiatric unit. As a result, it is not uncommon for a patient hospitalized at an academic center to receive more than half a dozen suicide risk assessments in a day (first by the medical student, at least once – often more than once – by the resident, again by the attending psychiatrist, then the social worker and three nurses in 24 hours).
One of the concerns about such an approach is the lack of logic inherent to many risk assessment tools and symptom scales. Many of us are familiar with the Patient Health Questionnaire (PHQ-9) to assess depression.2 The PHQ-9 asks to consider “over the last 2 weeks, how often have you ...” in relation to nine symptoms associated with depression. It has always defied reason to perform a PHQ-9 every day and expect the answers to change from “nearly every day” to “not at all,” considering only 1 day has passed since the last time the patient has answered the questions. Yet daily, or near daily, PHQ-9 scores are a frequently used tool of tracking symptom improvement in response to treatments, such as electroconvulsive therapy, performed multiple times a week.
One can argue that the patient’s perspective on how symptomatic he or she has been over the past 2 weeks may change rapidly with alleviation of a depressed mood. However, the PHQ-9 is both reported to be, and often regarded as, an objective score. If one wishes to utilize it as such, the defense of its use should not be that it is a subjective report with just as much utility as “Rate your depression on a scale of 0-27.”
Similarly, many suicide scales were intended to assess thoughts of suicide in the past month3 or have been re-tooled to address this particular concern by asking “since the last contact.”4 It is baffling to see a chart with many dozens of suicide risk assessments with at times widely differing answers, yet all measuring thoughts of suicide in the past month. Is one to expect the answer to “How many times have you had these thoughts [of suicide ideation]? (1) Less than once a week (2) Once a week ...” to change between 8 a.m. and noon? Furthermore, for the purpose of assessing acute risk of suicidality in the immediate future, to only consider symptoms since the last contact – or past 2 weeks, past month, etc. – is of unclear significance.
Provider liability
Another concern is the liability placed on providers. A common problem encountered in the inpatient setting is insurance companies refusing to reimburse a hospital stay for depressed patients denying suicidality.
Any provider in the position of caring for such a patient must ask: What is the likelihood of someone providing a false negative – a false denial of suicidality? Is the likelihood of a suicidal person denying suicidality different if asked 5 or 10 or more times in a day? There are innumerable instances where a patient at a very high risk of self-harm has denied suicidality, been discharged from the hospital, and suffered terrible consequences. Ethically, the psychiatrist aware of this risk is no more at ease discharging these patients, whether it is one suicide risk scale or a dozen that suggests a patient is at low risk.
Alternatively, it may feel untenable from a medicolegal perspective for a psychiatrist to discharge a patient denying suicidality when the chart includes over a dozen previously documented elevated suicide risk assessments in the past 72 hours. By placing the job of suicide risk assessment in the hands of providers of varying levels of training and responsibility, a situation is created in which the seasoned psychiatrist who would otherwise be comfortable discharging a patient feels unable to do so because every other note-writer in the record – from the triage nurse to the medical assistant to the sitter in the emergency department – has recorded the patient as high risk for suicide. When put in such a position, the thought often occurs that systems of care, rather than individual providers, are protected most by ever escalating requirements for suicide risk documentation. To make a clinical decision contrary to the body of suicide risk documentation puts the provider at risk of being scapegoated by the system of care, which can point to its illogical and ineffective, though profusely documented, suicide prevention protocols.
Limitations of risk assessments
Considering the ongoing rise in the use of suicide risk assessments, one would expect that the evidence for their efficacy was robust and well established. Yet a thorough review of suicide risk assessments funded by the MacArthur Foundation, which examined decades of research, came to disheartening conclusions: “predictive ability has not improved over the past 50 years”; “no risk factor category or subcategory is substantially stronger than any other”; and “predicting solely according to base rates may be comparable to prediction with current risk factors.”5
Those findings were consistent with the conclusions of many other studies, which have summarized the utility of suicide risk assessments as follows: “occurrence of suicide is too low to identify those individuals who are likely to die by suicide”;6 “suicide prediction models produce accurate overall classification models, but their accuracy of predicting a future event is near zero”;7 “risk stratification is too inaccurate to be clinically useful and might even be harmful”;8 “suicide risk prediction [lacks] any items or information that to a useful degree permit the identification of persons who will complete suicide”;9 “existing suicide prediction tools have little current clinical value”;10 “our current preoccupation with risk assessment has ... created a mythology with no evidence to support it.”11 And that’s to cite just a few.
Sadly, we have known about the limitations of suicide risk assessments for many decades. In 1983 a large VA prospective study, which aimed to identify veterans who will die by suicide, examined 4,800 patients with a wide range of instruments and measures.12 This study concluded that “discriminant analysis was clearly inadequate in correctly classifying the subjects. For an event as rare as suicide, our predictive tools and guides are simply not equal to the task.” The authors described the feelings of many in stating “courts and public opinion expect physicians to be able to pick out the particular persons who will later commit suicide. Although we may reconstruct causal chains and motives, we do not possess the tools to predict suicides.”
Yet, even several decades prior, in 1954, Dr. Albert Rosen performed an elegant statistical analysis and predicted that, considering the low base rate of suicide, suicide risk assessments are “of no practical value, for it would be impossible to treat the prodigious number of false positives.”13 It seems that we continue to be unable to accept Dr. Rosen’s premonition despite decades of confirmatory evidence.
“Quantity over quality”
Regardless of those sobering reports,
One can reasonably argue that the periodic performance of a suicide risk assessment may have clinical utility in reminding us of modifiable risk factors such as intoxication, social isolation, and access to lethal means. One can also reasonably argue that these risk assessments may provide useful education to patients and their families on epidemiological risk factors such as gender, age, and marital status. But our pursuit of serial suicide risk assessments throughout the day is encouraging providers to focus on a particular risk factor that changes from moment to moment and has particularly low validity, that being self-reported suicidality.
Reported suicidality is one of the few risk factors that can change from shift to shift. But 80% of people who die by suicide had not previously expressed suicidality, and 98.3% of people who have endorsed suicidality do not die by suicide.14 While the former statistic may improve with increased assessment, the later will likely worsen.
Suicide is not a trivial matter. We admire those that study it and advocate for better interventions. We have compassion for those who have suffered the loss of a loved one to suicide. Our patients have died as a result of the human limitations surrounding suicide prevention. Recognizing the weight of suicide and making an effort to avoid minimizing its immense consequences drive our desire to be honest with ourselves, our patients and their families, and society. That includes the unfortunate truth regarding the current state of the evidence and our ability to enact change.
It is our concern that the rising fascination with repeated suicide risk assessment is misguided in its current form and serves the purpose of appeasing administrators more than reflecting a scientific understanding of the literature. More sadly, we are concerned that this “quantity-over-quality” approach is yet another barrier to practicing what may be one of the few interventions with any hope of meaningfully impacting a patient’s risk of suicide in the clinical setting – spending time connecting with our patients.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Compton is a member of the psychiatry faculty at University of California, San Diego. His background includes medical education, mental health advocacy, work with underserved populations, and brain cancer research. Dr. Badre and Dr. Compton have no conflicts of interest.
References
1. Joint Economic Committee. (2019). Long Term Trends in Deaths of Despair. SCP Report 4-19.
2. Kroenke K and Spitzer RL. The PHQ-9: A new depression diagnostic and severity measure. Psychiatr Ann. 2013;32(9):509-15. doi: 10.3928/0048-5713-20020901-06.
3. Columbia-Suicide Severity Rating Scale (C-SSRS) Full Lifetime/Recent.
4. Columbia-Suicide Severity Rating Scale (C-SSRS) Full Since Last Contact.
5. Franklin JC et al. Risk factors for suicidal thoughts and behaviors: A meta-analysis of 50 years of research. Psychol Bull. 2017 Feb;143(2):187-232. doi: 10.1037/bul0000084.
6. Beautrais AL. Further suicidal behavior among medically serious suicide attempters. Suicide Life Threat Behav. 2004 Spring;34(1):1-11. doi: 10.1521/suli.34.1.1.27772.
7. Belsher BE. Prediction models for suicide attempts and deaths: A systematic review and simulation. JAMA Psychiatry. 2019 Jun 1;76(6):642-651. doi: 10.1001/jamapsychiatry.2019.0174.
8. Carter G et al. Royal Australian and New Zealand College of Psychiatrists clinical practice guideline for the management of deliberate self-harm. Aust N Z J Psychiatry. 2016 Oct;50(10):939-1000. doi: 10.1177/0004867416661039.
9. Fosse R et al. Predictors of suicide in the patient population admitted to a locked-door psychiatric acute ward. PLoS One. 2017 Mar 16;12(3):e0173958. doi: 10.1371/journal.pone.0173958.
10. Kessler RC et al. Suicide prediction models: A critical review of recent research with recommendations for the way forward. Mol Psychiatry. 2020 Jan;25(1):168-79. doi: 10.1038/s41380-019-0531-0.
11. Mulder R. Problems with suicide risk assessment. Aust N Z J Psychiatry. 2011 Aug;45(8):605-7. doi: 10.3109/00048674.2011.594786.
12. Pokorny AD. Prediction of suicide in psychiatric patients: Report of a prospective study. Arch Gen Psychiatry. 1983 Mar;40(3):249-57. doi: 10.1001/archpsyc.1983.01790030019002.
13. Rosen A. Detection of suicidal patients: An example of some limitations in the prediction of infrequent events. J Consult Psychol. 1954 Dec;18(6):397-403. doi: 10.1037/h0058579.
14. McHugh CM et al. (2019). Association between suicidal ideation and suicide: Meta-analyses of odds ratios, sensitivity, specificity and positive predictive value. BJPsych Open. 2019 Mar;5(2):e18. doi: 10.1192/bjo.2018.88.
Suicide is not a trivial matter – it upends families, robs partners of a loved one, prevents children from having a parent, and can destroy a parent’s most cherished being. It is not surprising that societies have repeatedly made it a goal to study and reduce suicide within their populations.
The suicide rate in the United States is trending upward, from about 10 per 100,000 in 2000 to about 15 per 100,000 in more recent reports. The increasing suicide rates have been accompanied by increasing distress among many strata of society. From a public health level, analysts are not just witnessing increasing suicide rates, but a shocking rise in all “deaths of despair,”1 among which suicide can be considered the ultimate example.
On an individual level, many know someone who has died of suicide or suffered from a serious suicide attempt. From the public health level to the individual level, advocacy has called for various interventions in the field of psychiatry to remedy this tragic problem.
Psychiatrists have been firsthand witnesses to this increasing demand for suicide interventions. When in residency, the norm was to perform a suicide risk assessment at the time of admission to the hospital and again at the time of discharge. As the years passed, the new normal within psychiatric hospitals has shifted to asking about suicidality on a daily basis.
In what seems to us like an escalating arms race, the emerging standard of care at many facilities is now not only for daily suicide risk assessments by each psychiatrist, but also to require nurses to ask about suicidality during every 8-hour shift – in addition to documented inquiries about suicidality by other allied staff on the psychiatric unit. As a result, it is not uncommon for a patient hospitalized at an academic center to receive more than half a dozen suicide risk assessments in a day (first by the medical student, at least once – often more than once – by the resident, again by the attending psychiatrist, then the social worker and three nurses in 24 hours).
One of the concerns about such an approach is the lack of logic inherent to many risk assessment tools and symptom scales. Many of us are familiar with the Patient Health Questionnaire (PHQ-9) to assess depression.2 The PHQ-9 asks to consider “over the last 2 weeks, how often have you ...” in relation to nine symptoms associated with depression. It has always defied reason to perform a PHQ-9 every day and expect the answers to change from “nearly every day” to “not at all,” considering only 1 day has passed since the last time the patient has answered the questions. Yet daily, or near daily, PHQ-9 scores are a frequently used tool of tracking symptom improvement in response to treatments, such as electroconvulsive therapy, performed multiple times a week.
One can argue that the patient’s perspective on how symptomatic he or she has been over the past 2 weeks may change rapidly with alleviation of a depressed mood. However, the PHQ-9 is both reported to be, and often regarded as, an objective score. If one wishes to utilize it as such, the defense of its use should not be that it is a subjective report with just as much utility as “Rate your depression on a scale of 0-27.”
Similarly, many suicide scales were intended to assess thoughts of suicide in the past month3 or have been re-tooled to address this particular concern by asking “since the last contact.”4 It is baffling to see a chart with many dozens of suicide risk assessments with at times widely differing answers, yet all measuring thoughts of suicide in the past month. Is one to expect the answer to “How many times have you had these thoughts [of suicide ideation]? (1) Less than once a week (2) Once a week ...” to change between 8 a.m. and noon? Furthermore, for the purpose of assessing acute risk of suicidality in the immediate future, to only consider symptoms since the last contact – or past 2 weeks, past month, etc. – is of unclear significance.
Provider liability
Another concern is the liability placed on providers. A common problem encountered in the inpatient setting is insurance companies refusing to reimburse a hospital stay for depressed patients denying suicidality.
Any provider in the position of caring for such a patient must ask: What is the likelihood of someone providing a false negative – a false denial of suicidality? Is the likelihood of a suicidal person denying suicidality different if asked 5 or 10 or more times in a day? There are innumerable instances where a patient at a very high risk of self-harm has denied suicidality, been discharged from the hospital, and suffered terrible consequences. Ethically, the psychiatrist aware of this risk is no more at ease discharging these patients, whether it is one suicide risk scale or a dozen that suggests a patient is at low risk.
Alternatively, it may feel untenable from a medicolegal perspective for a psychiatrist to discharge a patient denying suicidality when the chart includes over a dozen previously documented elevated suicide risk assessments in the past 72 hours. By placing the job of suicide risk assessment in the hands of providers of varying levels of training and responsibility, a situation is created in which the seasoned psychiatrist who would otherwise be comfortable discharging a patient feels unable to do so because every other note-writer in the record – from the triage nurse to the medical assistant to the sitter in the emergency department – has recorded the patient as high risk for suicide. When put in such a position, the thought often occurs that systems of care, rather than individual providers, are protected most by ever escalating requirements for suicide risk documentation. To make a clinical decision contrary to the body of suicide risk documentation puts the provider at risk of being scapegoated by the system of care, which can point to its illogical and ineffective, though profusely documented, suicide prevention protocols.
Limitations of risk assessments
Considering the ongoing rise in the use of suicide risk assessments, one would expect that the evidence for their efficacy was robust and well established. Yet a thorough review of suicide risk assessments funded by the MacArthur Foundation, which examined decades of research, came to disheartening conclusions: “predictive ability has not improved over the past 50 years”; “no risk factor category or subcategory is substantially stronger than any other”; and “predicting solely according to base rates may be comparable to prediction with current risk factors.”5
Those findings were consistent with the conclusions of many other studies, which have summarized the utility of suicide risk assessments as follows: “occurrence of suicide is too low to identify those individuals who are likely to die by suicide”;6 “suicide prediction models produce accurate overall classification models, but their accuracy of predicting a future event is near zero”;7 “risk stratification is too inaccurate to be clinically useful and might even be harmful”;8 “suicide risk prediction [lacks] any items or information that to a useful degree permit the identification of persons who will complete suicide”;9 “existing suicide prediction tools have little current clinical value”;10 “our current preoccupation with risk assessment has ... created a mythology with no evidence to support it.”11 And that’s to cite just a few.
Sadly, we have known about the limitations of suicide risk assessments for many decades. In 1983 a large VA prospective study, which aimed to identify veterans who will die by suicide, examined 4,800 patients with a wide range of instruments and measures.12 This study concluded that “discriminant analysis was clearly inadequate in correctly classifying the subjects. For an event as rare as suicide, our predictive tools and guides are simply not equal to the task.” The authors described the feelings of many in stating “courts and public opinion expect physicians to be able to pick out the particular persons who will later commit suicide. Although we may reconstruct causal chains and motives, we do not possess the tools to predict suicides.”
Yet, even several decades prior, in 1954, Dr. Albert Rosen performed an elegant statistical analysis and predicted that, considering the low base rate of suicide, suicide risk assessments are “of no practical value, for it would be impossible to treat the prodigious number of false positives.”13 It seems that we continue to be unable to accept Dr. Rosen’s premonition despite decades of confirmatory evidence.
“Quantity over quality”
Regardless of those sobering reports,
One can reasonably argue that the periodic performance of a suicide risk assessment may have clinical utility in reminding us of modifiable risk factors such as intoxication, social isolation, and access to lethal means. One can also reasonably argue that these risk assessments may provide useful education to patients and their families on epidemiological risk factors such as gender, age, and marital status. But our pursuit of serial suicide risk assessments throughout the day is encouraging providers to focus on a particular risk factor that changes from moment to moment and has particularly low validity, that being self-reported suicidality.
Reported suicidality is one of the few risk factors that can change from shift to shift. But 80% of people who die by suicide had not previously expressed suicidality, and 98.3% of people who have endorsed suicidality do not die by suicide.14 While the former statistic may improve with increased assessment, the later will likely worsen.
Suicide is not a trivial matter. We admire those that study it and advocate for better interventions. We have compassion for those who have suffered the loss of a loved one to suicide. Our patients have died as a result of the human limitations surrounding suicide prevention. Recognizing the weight of suicide and making an effort to avoid minimizing its immense consequences drive our desire to be honest with ourselves, our patients and their families, and society. That includes the unfortunate truth regarding the current state of the evidence and our ability to enact change.
It is our concern that the rising fascination with repeated suicide risk assessment is misguided in its current form and serves the purpose of appeasing administrators more than reflecting a scientific understanding of the literature. More sadly, we are concerned that this “quantity-over-quality” approach is yet another barrier to practicing what may be one of the few interventions with any hope of meaningfully impacting a patient’s risk of suicide in the clinical setting – spending time connecting with our patients.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Compton is a member of the psychiatry faculty at University of California, San Diego. His background includes medical education, mental health advocacy, work with underserved populations, and brain cancer research. Dr. Badre and Dr. Compton have no conflicts of interest.
References
1. Joint Economic Committee. (2019). Long Term Trends in Deaths of Despair. SCP Report 4-19.
2. Kroenke K and Spitzer RL. The PHQ-9: A new depression diagnostic and severity measure. Psychiatr Ann. 2013;32(9):509-15. doi: 10.3928/0048-5713-20020901-06.
3. Columbia-Suicide Severity Rating Scale (C-SSRS) Full Lifetime/Recent.
4. Columbia-Suicide Severity Rating Scale (C-SSRS) Full Since Last Contact.
5. Franklin JC et al. Risk factors for suicidal thoughts and behaviors: A meta-analysis of 50 years of research. Psychol Bull. 2017 Feb;143(2):187-232. doi: 10.1037/bul0000084.
6. Beautrais AL. Further suicidal behavior among medically serious suicide attempters. Suicide Life Threat Behav. 2004 Spring;34(1):1-11. doi: 10.1521/suli.34.1.1.27772.
7. Belsher BE. Prediction models for suicide attempts and deaths: A systematic review and simulation. JAMA Psychiatry. 2019 Jun 1;76(6):642-651. doi: 10.1001/jamapsychiatry.2019.0174.
8. Carter G et al. Royal Australian and New Zealand College of Psychiatrists clinical practice guideline for the management of deliberate self-harm. Aust N Z J Psychiatry. 2016 Oct;50(10):939-1000. doi: 10.1177/0004867416661039.
9. Fosse R et al. Predictors of suicide in the patient population admitted to a locked-door psychiatric acute ward. PLoS One. 2017 Mar 16;12(3):e0173958. doi: 10.1371/journal.pone.0173958.
10. Kessler RC et al. Suicide prediction models: A critical review of recent research with recommendations for the way forward. Mol Psychiatry. 2020 Jan;25(1):168-79. doi: 10.1038/s41380-019-0531-0.
11. Mulder R. Problems with suicide risk assessment. Aust N Z J Psychiatry. 2011 Aug;45(8):605-7. doi: 10.3109/00048674.2011.594786.
12. Pokorny AD. Prediction of suicide in psychiatric patients: Report of a prospective study. Arch Gen Psychiatry. 1983 Mar;40(3):249-57. doi: 10.1001/archpsyc.1983.01790030019002.
13. Rosen A. Detection of suicidal patients: An example of some limitations in the prediction of infrequent events. J Consult Psychol. 1954 Dec;18(6):397-403. doi: 10.1037/h0058579.
14. McHugh CM et al. (2019). Association between suicidal ideation and suicide: Meta-analyses of odds ratios, sensitivity, specificity and positive predictive value. BJPsych Open. 2019 Mar;5(2):e18. doi: 10.1192/bjo.2018.88.
Suicide is not a trivial matter – it upends families, robs partners of a loved one, prevents children from having a parent, and can destroy a parent’s most cherished being. It is not surprising that societies have repeatedly made it a goal to study and reduce suicide within their populations.
The suicide rate in the United States is trending upward, from about 10 per 100,000 in 2000 to about 15 per 100,000 in more recent reports. The increasing suicide rates have been accompanied by increasing distress among many strata of society. From a public health level, analysts are not just witnessing increasing suicide rates, but a shocking rise in all “deaths of despair,”1 among which suicide can be considered the ultimate example.
On an individual level, many know someone who has died of suicide or suffered from a serious suicide attempt. From the public health level to the individual level, advocacy has called for various interventions in the field of psychiatry to remedy this tragic problem.
Psychiatrists have been firsthand witnesses to this increasing demand for suicide interventions. When in residency, the norm was to perform a suicide risk assessment at the time of admission to the hospital and again at the time of discharge. As the years passed, the new normal within psychiatric hospitals has shifted to asking about suicidality on a daily basis.
In what seems to us like an escalating arms race, the emerging standard of care at many facilities is now not only for daily suicide risk assessments by each psychiatrist, but also to require nurses to ask about suicidality during every 8-hour shift – in addition to documented inquiries about suicidality by other allied staff on the psychiatric unit. As a result, it is not uncommon for a patient hospitalized at an academic center to receive more than half a dozen suicide risk assessments in a day (first by the medical student, at least once – often more than once – by the resident, again by the attending psychiatrist, then the social worker and three nurses in 24 hours).
One of the concerns about such an approach is the lack of logic inherent to many risk assessment tools and symptom scales. Many of us are familiar with the Patient Health Questionnaire (PHQ-9) to assess depression.2 The PHQ-9 asks to consider “over the last 2 weeks, how often have you ...” in relation to nine symptoms associated with depression. It has always defied reason to perform a PHQ-9 every day and expect the answers to change from “nearly every day” to “not at all,” considering only 1 day has passed since the last time the patient has answered the questions. Yet daily, or near daily, PHQ-9 scores are a frequently used tool of tracking symptom improvement in response to treatments, such as electroconvulsive therapy, performed multiple times a week.
One can argue that the patient’s perspective on how symptomatic he or she has been over the past 2 weeks may change rapidly with alleviation of a depressed mood. However, the PHQ-9 is both reported to be, and often regarded as, an objective score. If one wishes to utilize it as such, the defense of its use should not be that it is a subjective report with just as much utility as “Rate your depression on a scale of 0-27.”
Similarly, many suicide scales were intended to assess thoughts of suicide in the past month3 or have been re-tooled to address this particular concern by asking “since the last contact.”4 It is baffling to see a chart with many dozens of suicide risk assessments with at times widely differing answers, yet all measuring thoughts of suicide in the past month. Is one to expect the answer to “How many times have you had these thoughts [of suicide ideation]? (1) Less than once a week (2) Once a week ...” to change between 8 a.m. and noon? Furthermore, for the purpose of assessing acute risk of suicidality in the immediate future, to only consider symptoms since the last contact – or past 2 weeks, past month, etc. – is of unclear significance.
Provider liability
Another concern is the liability placed on providers. A common problem encountered in the inpatient setting is insurance companies refusing to reimburse a hospital stay for depressed patients denying suicidality.
Any provider in the position of caring for such a patient must ask: What is the likelihood of someone providing a false negative – a false denial of suicidality? Is the likelihood of a suicidal person denying suicidality different if asked 5 or 10 or more times in a day? There are innumerable instances where a patient at a very high risk of self-harm has denied suicidality, been discharged from the hospital, and suffered terrible consequences. Ethically, the psychiatrist aware of this risk is no more at ease discharging these patients, whether it is one suicide risk scale or a dozen that suggests a patient is at low risk.
Alternatively, it may feel untenable from a medicolegal perspective for a psychiatrist to discharge a patient denying suicidality when the chart includes over a dozen previously documented elevated suicide risk assessments in the past 72 hours. By placing the job of suicide risk assessment in the hands of providers of varying levels of training and responsibility, a situation is created in which the seasoned psychiatrist who would otherwise be comfortable discharging a patient feels unable to do so because every other note-writer in the record – from the triage nurse to the medical assistant to the sitter in the emergency department – has recorded the patient as high risk for suicide. When put in such a position, the thought often occurs that systems of care, rather than individual providers, are protected most by ever escalating requirements for suicide risk documentation. To make a clinical decision contrary to the body of suicide risk documentation puts the provider at risk of being scapegoated by the system of care, which can point to its illogical and ineffective, though profusely documented, suicide prevention protocols.
Limitations of risk assessments
Considering the ongoing rise in the use of suicide risk assessments, one would expect that the evidence for their efficacy was robust and well established. Yet a thorough review of suicide risk assessments funded by the MacArthur Foundation, which examined decades of research, came to disheartening conclusions: “predictive ability has not improved over the past 50 years”; “no risk factor category or subcategory is substantially stronger than any other”; and “predicting solely according to base rates may be comparable to prediction with current risk factors.”5
Those findings were consistent with the conclusions of many other studies, which have summarized the utility of suicide risk assessments as follows: “occurrence of suicide is too low to identify those individuals who are likely to die by suicide”;6 “suicide prediction models produce accurate overall classification models, but their accuracy of predicting a future event is near zero”;7 “risk stratification is too inaccurate to be clinically useful and might even be harmful”;8 “suicide risk prediction [lacks] any items or information that to a useful degree permit the identification of persons who will complete suicide”;9 “existing suicide prediction tools have little current clinical value”;10 “our current preoccupation with risk assessment has ... created a mythology with no evidence to support it.”11 And that’s to cite just a few.
Sadly, we have known about the limitations of suicide risk assessments for many decades. In 1983 a large VA prospective study, which aimed to identify veterans who will die by suicide, examined 4,800 patients with a wide range of instruments and measures.12 This study concluded that “discriminant analysis was clearly inadequate in correctly classifying the subjects. For an event as rare as suicide, our predictive tools and guides are simply not equal to the task.” The authors described the feelings of many in stating “courts and public opinion expect physicians to be able to pick out the particular persons who will later commit suicide. Although we may reconstruct causal chains and motives, we do not possess the tools to predict suicides.”
Yet, even several decades prior, in 1954, Dr. Albert Rosen performed an elegant statistical analysis and predicted that, considering the low base rate of suicide, suicide risk assessments are “of no practical value, for it would be impossible to treat the prodigious number of false positives.”13 It seems that we continue to be unable to accept Dr. Rosen’s premonition despite decades of confirmatory evidence.
“Quantity over quality”
Regardless of those sobering reports,
One can reasonably argue that the periodic performance of a suicide risk assessment may have clinical utility in reminding us of modifiable risk factors such as intoxication, social isolation, and access to lethal means. One can also reasonably argue that these risk assessments may provide useful education to patients and their families on epidemiological risk factors such as gender, age, and marital status. But our pursuit of serial suicide risk assessments throughout the day is encouraging providers to focus on a particular risk factor that changes from moment to moment and has particularly low validity, that being self-reported suicidality.
Reported suicidality is one of the few risk factors that can change from shift to shift. But 80% of people who die by suicide had not previously expressed suicidality, and 98.3% of people who have endorsed suicidality do not die by suicide.14 While the former statistic may improve with increased assessment, the later will likely worsen.
Suicide is not a trivial matter. We admire those that study it and advocate for better interventions. We have compassion for those who have suffered the loss of a loved one to suicide. Our patients have died as a result of the human limitations surrounding suicide prevention. Recognizing the weight of suicide and making an effort to avoid minimizing its immense consequences drive our desire to be honest with ourselves, our patients and their families, and society. That includes the unfortunate truth regarding the current state of the evidence and our ability to enact change.
It is our concern that the rising fascination with repeated suicide risk assessment is misguided in its current form and serves the purpose of appeasing administrators more than reflecting a scientific understanding of the literature. More sadly, we are concerned that this “quantity-over-quality” approach is yet another barrier to practicing what may be one of the few interventions with any hope of meaningfully impacting a patient’s risk of suicide in the clinical setting – spending time connecting with our patients.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Compton is a member of the psychiatry faculty at University of California, San Diego. His background includes medical education, mental health advocacy, work with underserved populations, and brain cancer research. Dr. Badre and Dr. Compton have no conflicts of interest.
References
1. Joint Economic Committee. (2019). Long Term Trends in Deaths of Despair. SCP Report 4-19.
2. Kroenke K and Spitzer RL. The PHQ-9: A new depression diagnostic and severity measure. Psychiatr Ann. 2013;32(9):509-15. doi: 10.3928/0048-5713-20020901-06.
3. Columbia-Suicide Severity Rating Scale (C-SSRS) Full Lifetime/Recent.
4. Columbia-Suicide Severity Rating Scale (C-SSRS) Full Since Last Contact.
5. Franklin JC et al. Risk factors for suicidal thoughts and behaviors: A meta-analysis of 50 years of research. Psychol Bull. 2017 Feb;143(2):187-232. doi: 10.1037/bul0000084.
6. Beautrais AL. Further suicidal behavior among medically serious suicide attempters. Suicide Life Threat Behav. 2004 Spring;34(1):1-11. doi: 10.1521/suli.34.1.1.27772.
7. Belsher BE. Prediction models for suicide attempts and deaths: A systematic review and simulation. JAMA Psychiatry. 2019 Jun 1;76(6):642-651. doi: 10.1001/jamapsychiatry.2019.0174.
8. Carter G et al. Royal Australian and New Zealand College of Psychiatrists clinical practice guideline for the management of deliberate self-harm. Aust N Z J Psychiatry. 2016 Oct;50(10):939-1000. doi: 10.1177/0004867416661039.
9. Fosse R et al. Predictors of suicide in the patient population admitted to a locked-door psychiatric acute ward. PLoS One. 2017 Mar 16;12(3):e0173958. doi: 10.1371/journal.pone.0173958.
10. Kessler RC et al. Suicide prediction models: A critical review of recent research with recommendations for the way forward. Mol Psychiatry. 2020 Jan;25(1):168-79. doi: 10.1038/s41380-019-0531-0.
11. Mulder R. Problems with suicide risk assessment. Aust N Z J Psychiatry. 2011 Aug;45(8):605-7. doi: 10.3109/00048674.2011.594786.
12. Pokorny AD. Prediction of suicide in psychiatric patients: Report of a prospective study. Arch Gen Psychiatry. 1983 Mar;40(3):249-57. doi: 10.1001/archpsyc.1983.01790030019002.
13. Rosen A. Detection of suicidal patients: An example of some limitations in the prediction of infrequent events. J Consult Psychol. 1954 Dec;18(6):397-403. doi: 10.1037/h0058579.
14. McHugh CM et al. (2019). Association between suicidal ideation and suicide: Meta-analyses of odds ratios, sensitivity, specificity and positive predictive value. BJPsych Open. 2019 Mar;5(2):e18. doi: 10.1192/bjo.2018.88.
Almonds and almond oil
Almonds and almond oil are known to exhibit anti-inflammatory, antihepatotoxicity, and immunity-boosting activity.1 The seed from the deciduous almond tree (Oleum amygdalae), which is native to Iran and parts of the Levant, almonds contain copious amounts of phenols and polyphenols, fatty acids, and vitamin E, all of which are known to exert antioxidant activity.2-5 These seeds have been found to have a substantial impact on serum lipids.4 Emollient and sclerosant characteristics have also been linked to almond oil, which has been found to ameliorate complexion and skin tone.5 Significantly, in vitro and in vivo studies have shown that UVB-induced photoaging can be attenuated through the use of almond oil and almond skin extract.2 Further, in traditional Chinese Medicine, Ayurveda, and ancient Greco-Persian medicine, almond oil was used to treat cutaneous conditions, including eczema and psoriasis.1.
Antiphotoaging activity
In 2019, Foolad and Vaughn conducted a prospective, investigator-blind, randomized controlled trial to determine the effects of almond consumption on facial sebum production and wrinkles. Participants (28 postmenopausal women with Fitzpatrick skin types I and II completed the study) consumed 20% of their daily energy intake in almonds or a calorie-matched snack over 16 weeks through the UC Davis Dermatology Clinic. Photographic analysis revealed that the almond group experienced significantly diminished wrinkle severity, compared with the control group. The investigators concluded that daily almond consumption has the potential to decrease wrinkle severity in postmenopausal women and that almonds may confer natural antiaging effects.4
In a similar investigation 2 years later, Rybak et al. reported on a prospective, randomized controlled study to ascertain the effects of almond consumption on photoaging in postmenopausal women with Fitzpatrick skin types I or II who obtained 20% of their daily energy consumption via almonds or a calorie-matched snack for 24 weeks. Results demonstrated significant effects conferred by almond consumption, with average wrinkle severity substantially diminished in the almond group at weeks 16 (by 15%) and 24 (by 16%), compared with baseline. In addition, facial pigment intensity was reduced by 20% in the almond group by week 16 and this was maintained through the end of the study. Further, sebum excretion was higher in the control group. The investigators concluded that the daily consumption of almonds may have the potential to enhance protection against photoaging, particularly in terms of facial wrinkles and pigment intensity, in postmenopausal women.3
Later in 2021, Li et al. conducted a study in 39 healthy Asian women (18-45 years old) with Fitzpatrick skin types II to IV to investigate the effects of almond consumption on UVB resistance. The researchers randomized participants to eat either 1.5 oz of almonds or 1.8 oz of pretzels daily for 12 weeks. Results showed that the minimal erythema dose was higher in the almond group as compared with the control group. No differences were observed in hydration, melanin, roughness, or sebum on facial skin. The authors concluded that daily oral almond intake may improve photoprotection by raising the minimal erythema dose.2
In a 2022 review on the cutaneous benefits of sweet almond, evening primrose, and jojoba oils, Blaak and Staib noted that all three have been used for hundreds if not thousands of years in traditional medicine to treat various conditions, including skin disorders. Further, they concluded that the longstanding uses of these oils has been borne out by contemporary data, which reveal cutaneous benefits for adult and young skin, particularly in bolstering stratum corneum integrity, recovery, and lipid ratio.6
Later that year, Sanju et al., reporting on the development and assessment of a broad-spectrum polyherbal sunscreen delivered through solid lipid nanoparticles, noted that almond oil was among the natural ingredients used because of its photoprotective characteristics. Overall, the sunscreen formulation, Safranal, was found to impart robust protection against UV radiation.7
Wound healing
In 2020, Borzou et al. conducted a single-blind randomized clinical trial to ascertain the impact of topical almond oil in preventing pressure injuries. Data collection occurred over 8 months in a hospital setting, with 108 patients randomly assigned to receive almond oil, placebo (liquid paraffin), or the control (standard of care). The researchers found that topically applied almond oil was linked to a lower incidence of pressure injuries, and they arose later in the study as compared with those injuries in the groups receiving paraffin or standard of care. Pressure injury incidence was 5.6% in the almond oil group, 13.9% in the placebo group, and 25.1% in the control group.8
That same year, Caglar et al. completed a randomized controlled trial in 90 preterm infants to assess the effects of sunflower seed oil and almond oil on the stratum corneum. Infants were randomly selected for treatment with either oil or control. A nurse researcher applied oils to the whole body except for the head and face four times daily for 5 days. Investigators determined that stratum corneum hydration was better in the oil groups as compared with control, with no difference found between sunflower seed and almond oils.9
Eczema, hand dermatitis, and striae
In 2018, Simon et al. performed a randomized, double-blind study to determine the short- and long-term effects of two emollients on pruritus and skin restoration in xerotic eczema. The emollients contained lactic acid and refined almond oil, with one also including polidocanol. Both emollients were effective in reducing the severity of itching, with skin moisture and lipid content found to have risen after the initial administration and yielding steady improvement over 2 weeks.10
Earlier that year, Zeichner et al. found that the use of an OTC sweet almond oil, rich in fatty acids and a standard-bearing treatment for eczema and psoriasis for centuries, was effective in treating hand dermatitis. Specifically, the moisturizer, which contained 7% sweet almond oil and 2% colloidal oatmeal, was identified as safe and effective in resolving moderate to severe hand dermatitis.11
Some studies have also shown almond oil to be effective against striae gravidarum. Hajhashemi et al. conducted a double-blind clinical trial in 160 nulliparous women to compare the effects of aloe vera gel and sweet almond oil on striae gravidarum in 2018. Volunteers were randomly assigned to one of three case groups (Aloe vera, sweet almond oil, or base cream) who received topical treatment on the abdomen, or the fourth group, which received no treatment. Results showed that both treatment creams were effective in decreasing erythema and the pruritus associated with striae as well as in preventing their expansion.12 Previously, Tashan and Kafkasli showed in a nonrandomized study that massage with bitter almond oil may diminish the visibility of present striae gravidarum and prevent the emergence of new striae.13
Conclusion
Almonds and almond oil have been used as food and in traditional medical practices dating back several centuries. In the last decade, intriguing results have emerged regarding the effects of almond consumption or topical almond oil administration on skin health. While much more research is necessary, the recent data seem to support the traditional uses of this tree seed for dermatologic purposes.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology” (New York: McGraw Hill), was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as an e-commerce solution. Write to her at [email protected].
References
1. Ahmad Z. Complement Ther Clin Pract. 2010 Feb;16(1):10-2.
2. Li JN et al. J Cosmet Dermatol. 2021 Sep;20(9):2975-80.
3. Rybak I et al. Nutrients. 2021 Feb 27;13(3):785.
4. Foolad N et al. Phytother Res. 2019 Dec;33(12):3212-7.
5. Lin TK et al. Int J Mol Sci. 2017 Dec 27;19(1):70.
6. Blaak J, Staib P. Int J Cosmet Sci. 2022 Feb;44(1):1-9.
7. Sanju N et al. J Cosmet Dermatol. 2022 Oct;21(10):4433-46.
8. Borzou SR et al. J Wound Ostomy Continence Nurs. 2020 Jul/Aug;47(4):336-42.
9. Caglar S et al. Adv Skin Wound Care. 2020 Aug;33(8):1-6.
10. Simon D et al. Dermatol Ther. 2018 Nov;31(6):e12692.
11. Zeichner JA at al. J Drugs Dermatol. 2018 Jan 1;17(1):78-82.
12. Hajhashemi M et al. J Matern Fetal Neonatal Med. 2018 Jul;31(13):1703-8.
13. Timur Tashan S and Kafkasli A. J Clin Nurs. 2012 Jun;21(11-12):1570-6.
Almonds and almond oil are known to exhibit anti-inflammatory, antihepatotoxicity, and immunity-boosting activity.1 The seed from the deciduous almond tree (Oleum amygdalae), which is native to Iran and parts of the Levant, almonds contain copious amounts of phenols and polyphenols, fatty acids, and vitamin E, all of which are known to exert antioxidant activity.2-5 These seeds have been found to have a substantial impact on serum lipids.4 Emollient and sclerosant characteristics have also been linked to almond oil, which has been found to ameliorate complexion and skin tone.5 Significantly, in vitro and in vivo studies have shown that UVB-induced photoaging can be attenuated through the use of almond oil and almond skin extract.2 Further, in traditional Chinese Medicine, Ayurveda, and ancient Greco-Persian medicine, almond oil was used to treat cutaneous conditions, including eczema and psoriasis.1.
Antiphotoaging activity
In 2019, Foolad and Vaughn conducted a prospective, investigator-blind, randomized controlled trial to determine the effects of almond consumption on facial sebum production and wrinkles. Participants (28 postmenopausal women with Fitzpatrick skin types I and II completed the study) consumed 20% of their daily energy intake in almonds or a calorie-matched snack over 16 weeks through the UC Davis Dermatology Clinic. Photographic analysis revealed that the almond group experienced significantly diminished wrinkle severity, compared with the control group. The investigators concluded that daily almond consumption has the potential to decrease wrinkle severity in postmenopausal women and that almonds may confer natural antiaging effects.4
In a similar investigation 2 years later, Rybak et al. reported on a prospective, randomized controlled study to ascertain the effects of almond consumption on photoaging in postmenopausal women with Fitzpatrick skin types I or II who obtained 20% of their daily energy consumption via almonds or a calorie-matched snack for 24 weeks. Results demonstrated significant effects conferred by almond consumption, with average wrinkle severity substantially diminished in the almond group at weeks 16 (by 15%) and 24 (by 16%), compared with baseline. In addition, facial pigment intensity was reduced by 20% in the almond group by week 16 and this was maintained through the end of the study. Further, sebum excretion was higher in the control group. The investigators concluded that the daily consumption of almonds may have the potential to enhance protection against photoaging, particularly in terms of facial wrinkles and pigment intensity, in postmenopausal women.3
Later in 2021, Li et al. conducted a study in 39 healthy Asian women (18-45 years old) with Fitzpatrick skin types II to IV to investigate the effects of almond consumption on UVB resistance. The researchers randomized participants to eat either 1.5 oz of almonds or 1.8 oz of pretzels daily for 12 weeks. Results showed that the minimal erythema dose was higher in the almond group as compared with the control group. No differences were observed in hydration, melanin, roughness, or sebum on facial skin. The authors concluded that daily oral almond intake may improve photoprotection by raising the minimal erythema dose.2
In a 2022 review on the cutaneous benefits of sweet almond, evening primrose, and jojoba oils, Blaak and Staib noted that all three have been used for hundreds if not thousands of years in traditional medicine to treat various conditions, including skin disorders. Further, they concluded that the longstanding uses of these oils has been borne out by contemporary data, which reveal cutaneous benefits for adult and young skin, particularly in bolstering stratum corneum integrity, recovery, and lipid ratio.6
Later that year, Sanju et al., reporting on the development and assessment of a broad-spectrum polyherbal sunscreen delivered through solid lipid nanoparticles, noted that almond oil was among the natural ingredients used because of its photoprotective characteristics. Overall, the sunscreen formulation, Safranal, was found to impart robust protection against UV radiation.7
Wound healing
In 2020, Borzou et al. conducted a single-blind randomized clinical trial to ascertain the impact of topical almond oil in preventing pressure injuries. Data collection occurred over 8 months in a hospital setting, with 108 patients randomly assigned to receive almond oil, placebo (liquid paraffin), or the control (standard of care). The researchers found that topically applied almond oil was linked to a lower incidence of pressure injuries, and they arose later in the study as compared with those injuries in the groups receiving paraffin or standard of care. Pressure injury incidence was 5.6% in the almond oil group, 13.9% in the placebo group, and 25.1% in the control group.8
That same year, Caglar et al. completed a randomized controlled trial in 90 preterm infants to assess the effects of sunflower seed oil and almond oil on the stratum corneum. Infants were randomly selected for treatment with either oil or control. A nurse researcher applied oils to the whole body except for the head and face four times daily for 5 days. Investigators determined that stratum corneum hydration was better in the oil groups as compared with control, with no difference found between sunflower seed and almond oils.9
Eczema, hand dermatitis, and striae
In 2018, Simon et al. performed a randomized, double-blind study to determine the short- and long-term effects of two emollients on pruritus and skin restoration in xerotic eczema. The emollients contained lactic acid and refined almond oil, with one also including polidocanol. Both emollients were effective in reducing the severity of itching, with skin moisture and lipid content found to have risen after the initial administration and yielding steady improvement over 2 weeks.10
Earlier that year, Zeichner et al. found that the use of an OTC sweet almond oil, rich in fatty acids and a standard-bearing treatment for eczema and psoriasis for centuries, was effective in treating hand dermatitis. Specifically, the moisturizer, which contained 7% sweet almond oil and 2% colloidal oatmeal, was identified as safe and effective in resolving moderate to severe hand dermatitis.11
Some studies have also shown almond oil to be effective against striae gravidarum. Hajhashemi et al. conducted a double-blind clinical trial in 160 nulliparous women to compare the effects of aloe vera gel and sweet almond oil on striae gravidarum in 2018. Volunteers were randomly assigned to one of three case groups (Aloe vera, sweet almond oil, or base cream) who received topical treatment on the abdomen, or the fourth group, which received no treatment. Results showed that both treatment creams were effective in decreasing erythema and the pruritus associated with striae as well as in preventing their expansion.12 Previously, Tashan and Kafkasli showed in a nonrandomized study that massage with bitter almond oil may diminish the visibility of present striae gravidarum and prevent the emergence of new striae.13
Conclusion
Almonds and almond oil have been used as food and in traditional medical practices dating back several centuries. In the last decade, intriguing results have emerged regarding the effects of almond consumption or topical almond oil administration on skin health. While much more research is necessary, the recent data seem to support the traditional uses of this tree seed for dermatologic purposes.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology” (New York: McGraw Hill), was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as an e-commerce solution. Write to her at [email protected].
References
1. Ahmad Z. Complement Ther Clin Pract. 2010 Feb;16(1):10-2.
2. Li JN et al. J Cosmet Dermatol. 2021 Sep;20(9):2975-80.
3. Rybak I et al. Nutrients. 2021 Feb 27;13(3):785.
4. Foolad N et al. Phytother Res. 2019 Dec;33(12):3212-7.
5. Lin TK et al. Int J Mol Sci. 2017 Dec 27;19(1):70.
6. Blaak J, Staib P. Int J Cosmet Sci. 2022 Feb;44(1):1-9.
7. Sanju N et al. J Cosmet Dermatol. 2022 Oct;21(10):4433-46.
8. Borzou SR et al. J Wound Ostomy Continence Nurs. 2020 Jul/Aug;47(4):336-42.
9. Caglar S et al. Adv Skin Wound Care. 2020 Aug;33(8):1-6.
10. Simon D et al. Dermatol Ther. 2018 Nov;31(6):e12692.
11. Zeichner JA at al. J Drugs Dermatol. 2018 Jan 1;17(1):78-82.
12. Hajhashemi M et al. J Matern Fetal Neonatal Med. 2018 Jul;31(13):1703-8.
13. Timur Tashan S and Kafkasli A. J Clin Nurs. 2012 Jun;21(11-12):1570-6.
Almonds and almond oil are known to exhibit anti-inflammatory, antihepatotoxicity, and immunity-boosting activity.1 The seed from the deciduous almond tree (Oleum amygdalae), which is native to Iran and parts of the Levant, almonds contain copious amounts of phenols and polyphenols, fatty acids, and vitamin E, all of which are known to exert antioxidant activity.2-5 These seeds have been found to have a substantial impact on serum lipids.4 Emollient and sclerosant characteristics have also been linked to almond oil, which has been found to ameliorate complexion and skin tone.5 Significantly, in vitro and in vivo studies have shown that UVB-induced photoaging can be attenuated through the use of almond oil and almond skin extract.2 Further, in traditional Chinese Medicine, Ayurveda, and ancient Greco-Persian medicine, almond oil was used to treat cutaneous conditions, including eczema and psoriasis.1.
Antiphotoaging activity
In 2019, Foolad and Vaughn conducted a prospective, investigator-blind, randomized controlled trial to determine the effects of almond consumption on facial sebum production and wrinkles. Participants (28 postmenopausal women with Fitzpatrick skin types I and II completed the study) consumed 20% of their daily energy intake in almonds or a calorie-matched snack over 16 weeks through the UC Davis Dermatology Clinic. Photographic analysis revealed that the almond group experienced significantly diminished wrinkle severity, compared with the control group. The investigators concluded that daily almond consumption has the potential to decrease wrinkle severity in postmenopausal women and that almonds may confer natural antiaging effects.4
In a similar investigation 2 years later, Rybak et al. reported on a prospective, randomized controlled study to ascertain the effects of almond consumption on photoaging in postmenopausal women with Fitzpatrick skin types I or II who obtained 20% of their daily energy consumption via almonds or a calorie-matched snack for 24 weeks. Results demonstrated significant effects conferred by almond consumption, with average wrinkle severity substantially diminished in the almond group at weeks 16 (by 15%) and 24 (by 16%), compared with baseline. In addition, facial pigment intensity was reduced by 20% in the almond group by week 16 and this was maintained through the end of the study. Further, sebum excretion was higher in the control group. The investigators concluded that the daily consumption of almonds may have the potential to enhance protection against photoaging, particularly in terms of facial wrinkles and pigment intensity, in postmenopausal women.3
Later in 2021, Li et al. conducted a study in 39 healthy Asian women (18-45 years old) with Fitzpatrick skin types II to IV to investigate the effects of almond consumption on UVB resistance. The researchers randomized participants to eat either 1.5 oz of almonds or 1.8 oz of pretzels daily for 12 weeks. Results showed that the minimal erythema dose was higher in the almond group as compared with the control group. No differences were observed in hydration, melanin, roughness, or sebum on facial skin. The authors concluded that daily oral almond intake may improve photoprotection by raising the minimal erythema dose.2
In a 2022 review on the cutaneous benefits of sweet almond, evening primrose, and jojoba oils, Blaak and Staib noted that all three have been used for hundreds if not thousands of years in traditional medicine to treat various conditions, including skin disorders. Further, they concluded that the longstanding uses of these oils has been borne out by contemporary data, which reveal cutaneous benefits for adult and young skin, particularly in bolstering stratum corneum integrity, recovery, and lipid ratio.6
Later that year, Sanju et al., reporting on the development and assessment of a broad-spectrum polyherbal sunscreen delivered through solid lipid nanoparticles, noted that almond oil was among the natural ingredients used because of its photoprotective characteristics. Overall, the sunscreen formulation, Safranal, was found to impart robust protection against UV radiation.7
Wound healing
In 2020, Borzou et al. conducted a single-blind randomized clinical trial to ascertain the impact of topical almond oil in preventing pressure injuries. Data collection occurred over 8 months in a hospital setting, with 108 patients randomly assigned to receive almond oil, placebo (liquid paraffin), or the control (standard of care). The researchers found that topically applied almond oil was linked to a lower incidence of pressure injuries, and they arose later in the study as compared with those injuries in the groups receiving paraffin or standard of care. Pressure injury incidence was 5.6% in the almond oil group, 13.9% in the placebo group, and 25.1% in the control group.8
That same year, Caglar et al. completed a randomized controlled trial in 90 preterm infants to assess the effects of sunflower seed oil and almond oil on the stratum corneum. Infants were randomly selected for treatment with either oil or control. A nurse researcher applied oils to the whole body except for the head and face four times daily for 5 days. Investigators determined that stratum corneum hydration was better in the oil groups as compared with control, with no difference found between sunflower seed and almond oils.9
Eczema, hand dermatitis, and striae
In 2018, Simon et al. performed a randomized, double-blind study to determine the short- and long-term effects of two emollients on pruritus and skin restoration in xerotic eczema. The emollients contained lactic acid and refined almond oil, with one also including polidocanol. Both emollients were effective in reducing the severity of itching, with skin moisture and lipid content found to have risen after the initial administration and yielding steady improvement over 2 weeks.10
Earlier that year, Zeichner et al. found that the use of an OTC sweet almond oil, rich in fatty acids and a standard-bearing treatment for eczema and psoriasis for centuries, was effective in treating hand dermatitis. Specifically, the moisturizer, which contained 7% sweet almond oil and 2% colloidal oatmeal, was identified as safe and effective in resolving moderate to severe hand dermatitis.11
Some studies have also shown almond oil to be effective against striae gravidarum. Hajhashemi et al. conducted a double-blind clinical trial in 160 nulliparous women to compare the effects of aloe vera gel and sweet almond oil on striae gravidarum in 2018. Volunteers were randomly assigned to one of three case groups (Aloe vera, sweet almond oil, or base cream) who received topical treatment on the abdomen, or the fourth group, which received no treatment. Results showed that both treatment creams were effective in decreasing erythema and the pruritus associated with striae as well as in preventing their expansion.12 Previously, Tashan and Kafkasli showed in a nonrandomized study that massage with bitter almond oil may diminish the visibility of present striae gravidarum and prevent the emergence of new striae.13
Conclusion
Almonds and almond oil have been used as food and in traditional medical practices dating back several centuries. In the last decade, intriguing results have emerged regarding the effects of almond consumption or topical almond oil administration on skin health. While much more research is necessary, the recent data seem to support the traditional uses of this tree seed for dermatologic purposes.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology” (New York: McGraw Hill), was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as an e-commerce solution. Write to her at [email protected].
References
1. Ahmad Z. Complement Ther Clin Pract. 2010 Feb;16(1):10-2.
2. Li JN et al. J Cosmet Dermatol. 2021 Sep;20(9):2975-80.
3. Rybak I et al. Nutrients. 2021 Feb 27;13(3):785.
4. Foolad N et al. Phytother Res. 2019 Dec;33(12):3212-7.
5. Lin TK et al. Int J Mol Sci. 2017 Dec 27;19(1):70.
6. Blaak J, Staib P. Int J Cosmet Sci. 2022 Feb;44(1):1-9.
7. Sanju N et al. J Cosmet Dermatol. 2022 Oct;21(10):4433-46.
8. Borzou SR et al. J Wound Ostomy Continence Nurs. 2020 Jul/Aug;47(4):336-42.
9. Caglar S et al. Adv Skin Wound Care. 2020 Aug;33(8):1-6.
10. Simon D et al. Dermatol Ther. 2018 Nov;31(6):e12692.
11. Zeichner JA at al. J Drugs Dermatol. 2018 Jan 1;17(1):78-82.
12. Hajhashemi M et al. J Matern Fetal Neonatal Med. 2018 Jul;31(13):1703-8.
13. Timur Tashan S and Kafkasli A. J Clin Nurs. 2012 Jun;21(11-12):1570-6.
Can a decrease in dopamine lead to binge eating?
In medical school, we were repeatedly advised that there is both a science and an art to the practice of medicine. In these days of doc-in-a-box online consultations for obesity, it’s tempting to think that there’s a one-size-fits-all purely scientific approach for these new weight loss medications. Yet, for every nine patients who lose weight seemingly effortlessly on this class of medication, there is always one whose body stubbornly refuses to submit.
Adam is a 58-year-old man who came to me recently because he was having difficulty losing weight. Over the past 20 years, he’d been steadily gaining weight and now, technically has morbid obesity (a term which should arguably be obsolete). His weight gain is complicated by high blood pressure, high cholesterol, and obstructive sleep apnea. His sleep apnea has caused such profound exhaustion that he no longer has the energy to work out. He also has significant ADHD, which has been left untreated because of his ability to white-knuckle it through his many daily meetings and calls. A married father of three, he is a successful portfolio manager at a high-yield bond fund.
Adam tends to eat minimally during the day, thereby baffling his colleagues with the stark contrast between his minimal caloric intake and his large belly. However, when he returns from work late at night (kids safely tucked into bed), the floodgates open. He reports polishing off pints of ice cream, scarfing down bags of cookies, inhaling trays of brownies. No carbohydrate is off limits to him once he steps off the Metro North train and crosses the threshold from work to home.
Does Adam simply lack the desire or common-sense willpower to make the necessary changes in his lifestyle or is there something more complicated at play?
I would argue that Adam’s ADHD triggered a binge-eating disorder (BED) that festered unchecked over the past 20 years. Patients with BED typically eat massive quantities of food over short periods of time – often when they’re not even hungry. Adam admitted that he would generally continue to eat well after feeling stuffed to the brim.
The answer probably lies with dopamine, a neurotransmitter produced in the reward centers of the brain that regulates how people experience pleasure and control impulses. We believe that people with ADHD have low levels of dopamine (it’s actually a bit more complicated, but this is the general idea). These low levels of dopamine lead people to self-medicate with sugars, salt, and fats to increase dopamine levels.
Lisdexamfetamine (Vyvanse) is a Food and Drug Administration–approved treatment option for both ADHD and binge eating. It raises the levels of dopamine (as well as norepinephrine) in the brain’s reward center. Often, the strong urge to binge subsides rapidly once ADHD is properly treated.
Rather than starting Adam on a semaglutide or similar agent, I opted to start him on lisdexamfetamine. When I spoke to him 1 week later, he confided that the world suddenly shifted into focus, and he was able to plan his meals throughout the day and resist the urge to binge late at night.
I may eventually add a semaglutide-like medication if his weight loss plateaus, but for now, I will focus on raising his dopamine levels to tackle the underlying cause of his weight gain.
Dr. Messer is a clinical assistant professor at the Icahn School of Medicine at Mount Sinai, New York. She disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
In medical school, we were repeatedly advised that there is both a science and an art to the practice of medicine. In these days of doc-in-a-box online consultations for obesity, it’s tempting to think that there’s a one-size-fits-all purely scientific approach for these new weight loss medications. Yet, for every nine patients who lose weight seemingly effortlessly on this class of medication, there is always one whose body stubbornly refuses to submit.
Adam is a 58-year-old man who came to me recently because he was having difficulty losing weight. Over the past 20 years, he’d been steadily gaining weight and now, technically has morbid obesity (a term which should arguably be obsolete). His weight gain is complicated by high blood pressure, high cholesterol, and obstructive sleep apnea. His sleep apnea has caused such profound exhaustion that he no longer has the energy to work out. He also has significant ADHD, which has been left untreated because of his ability to white-knuckle it through his many daily meetings and calls. A married father of three, he is a successful portfolio manager at a high-yield bond fund.
Adam tends to eat minimally during the day, thereby baffling his colleagues with the stark contrast between his minimal caloric intake and his large belly. However, when he returns from work late at night (kids safely tucked into bed), the floodgates open. He reports polishing off pints of ice cream, scarfing down bags of cookies, inhaling trays of brownies. No carbohydrate is off limits to him once he steps off the Metro North train and crosses the threshold from work to home.
Does Adam simply lack the desire or common-sense willpower to make the necessary changes in his lifestyle or is there something more complicated at play?
I would argue that Adam’s ADHD triggered a binge-eating disorder (BED) that festered unchecked over the past 20 years. Patients with BED typically eat massive quantities of food over short periods of time – often when they’re not even hungry. Adam admitted that he would generally continue to eat well after feeling stuffed to the brim.
The answer probably lies with dopamine, a neurotransmitter produced in the reward centers of the brain that regulates how people experience pleasure and control impulses. We believe that people with ADHD have low levels of dopamine (it’s actually a bit more complicated, but this is the general idea). These low levels of dopamine lead people to self-medicate with sugars, salt, and fats to increase dopamine levels.
Lisdexamfetamine (Vyvanse) is a Food and Drug Administration–approved treatment option for both ADHD and binge eating. It raises the levels of dopamine (as well as norepinephrine) in the brain’s reward center. Often, the strong urge to binge subsides rapidly once ADHD is properly treated.
Rather than starting Adam on a semaglutide or similar agent, I opted to start him on lisdexamfetamine. When I spoke to him 1 week later, he confided that the world suddenly shifted into focus, and he was able to plan his meals throughout the day and resist the urge to binge late at night.
I may eventually add a semaglutide-like medication if his weight loss plateaus, but for now, I will focus on raising his dopamine levels to tackle the underlying cause of his weight gain.
Dr. Messer is a clinical assistant professor at the Icahn School of Medicine at Mount Sinai, New York. She disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
In medical school, we were repeatedly advised that there is both a science and an art to the practice of medicine. In these days of doc-in-a-box online consultations for obesity, it’s tempting to think that there’s a one-size-fits-all purely scientific approach for these new weight loss medications. Yet, for every nine patients who lose weight seemingly effortlessly on this class of medication, there is always one whose body stubbornly refuses to submit.
Adam is a 58-year-old man who came to me recently because he was having difficulty losing weight. Over the past 20 years, he’d been steadily gaining weight and now, technically has morbid obesity (a term which should arguably be obsolete). His weight gain is complicated by high blood pressure, high cholesterol, and obstructive sleep apnea. His sleep apnea has caused such profound exhaustion that he no longer has the energy to work out. He also has significant ADHD, which has been left untreated because of his ability to white-knuckle it through his many daily meetings and calls. A married father of three, he is a successful portfolio manager at a high-yield bond fund.
Adam tends to eat minimally during the day, thereby baffling his colleagues with the stark contrast between his minimal caloric intake and his large belly. However, when he returns from work late at night (kids safely tucked into bed), the floodgates open. He reports polishing off pints of ice cream, scarfing down bags of cookies, inhaling trays of brownies. No carbohydrate is off limits to him once he steps off the Metro North train and crosses the threshold from work to home.
Does Adam simply lack the desire or common-sense willpower to make the necessary changes in his lifestyle or is there something more complicated at play?
I would argue that Adam’s ADHD triggered a binge-eating disorder (BED) that festered unchecked over the past 20 years. Patients with BED typically eat massive quantities of food over short periods of time – often when they’re not even hungry. Adam admitted that he would generally continue to eat well after feeling stuffed to the brim.
The answer probably lies with dopamine, a neurotransmitter produced in the reward centers of the brain that regulates how people experience pleasure and control impulses. We believe that people with ADHD have low levels of dopamine (it’s actually a bit more complicated, but this is the general idea). These low levels of dopamine lead people to self-medicate with sugars, salt, and fats to increase dopamine levels.
Lisdexamfetamine (Vyvanse) is a Food and Drug Administration–approved treatment option for both ADHD and binge eating. It raises the levels of dopamine (as well as norepinephrine) in the brain’s reward center. Often, the strong urge to binge subsides rapidly once ADHD is properly treated.
Rather than starting Adam on a semaglutide or similar agent, I opted to start him on lisdexamfetamine. When I spoke to him 1 week later, he confided that the world suddenly shifted into focus, and he was able to plan his meals throughout the day and resist the urge to binge late at night.
I may eventually add a semaglutide-like medication if his weight loss plateaus, but for now, I will focus on raising his dopamine levels to tackle the underlying cause of his weight gain.
Dr. Messer is a clinical assistant professor at the Icahn School of Medicine at Mount Sinai, New York. She disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
The most important study from ESC: FRAIL-AF
One of the hardest tasks of a clinician is applying evidence from trials to the person in your office. At the annual congress of the European Society of Cardiology, the surprising and unexpected results of the FRAIL-AF trial confirm the massive challenge of evidence translation.
FRAIL-AF investigators set out to study the question of whether frail, elderly patients with atrial fibrillation who were doing well with vitamin K antagonists (VKA) should be switched to direct-acting oral anticoagulants (DOAC).
Senior author Geert-Jan Geersing, MD, PhD, from the University Medical Center Utrecht (the Netherlands), told me that frustration led him to design this study. He was frustrated that colleagues assumed that evidence in nonfrail patients can always be translated to frail patients.
Dr. Geersing offered two reasons why common wisdom may be wrong. First was that the large DOAC versus warfarin trials included few elderly patients with frailty. Second, first author Linda Joosten, MD, made it clear in her presentation that frailty is a lot more than aging. It is a clinical syndrome, which entails a “high burden of comorbidities, dependency on others, and a reduced ability to resist stressors.”
The FRAIL-AF trial
The investigators recruited elderly, frail patients with fibrillation who were treated with VKAs and had stable international normalized ratios from outpatient clinics throughout the Netherlands. They screened about 2,600 patients and enrolled nearly 1,400. Most were excluded for not being frail.
Half the group was randomized to switching to a DOAC – drug choice was left to the treating clinician – and the other half remained on VKAs. Patients were 83 years of age on average with a mean CHA2DS2-VASc score of 4. All four classes of DOAC were used in the switching arm.
The primary endpoint was major or clinically relevant nonmajor bleeding, whichever came first, accounting for death as a competing risk. Follow-up was 1 year.
The results for switching to DOAC vs. VKA
Dr. Joosten started her presentation with this: “The results turned out to be different than we expected.” The authors designed the trial with the idea that switching to DOACs would be superior in safety to remaining on VKAs.
But the trial was halted after an interim analysis found a rate of major bleeding in the switching arm of 15.3% versus 9.4% in the arm staying on VKA (hazard ratio, 1.69; 95% confidence interval, 1.23-2.32; P = .0012).
The Kaplan-Meier event curves reveal that the excess risk of bleeding occurred after 100 days and increased with time. This argued against an early effect from transitioning the drugs.
An analysis looking at specific DOAC drugs revealed similar hazards for the two most common ones used – apixaban and rivaroxaban.
Thrombotic events were a secondary endpoint and were low in absolute numbers, 2.4% versus 2.0%, for remaining on VKA and switching to DOAC, respectively (HR, 1.26; 95% CI, 0.60-2.61).
The time in therapeutic range in FRAIL-AF was similar to that in the seminal DOAC trials.
Comments
Three reasons lead me to choose FRAIL-AF as the most important study from the 2023 ESC congress.
First is the specific lesson about switching drugs. Note that FRAIL-AF did not address the question of starting anticoagulation. The trial results show that if you have a frail older patient who is doing well on VKA, don’t change to a DOAC. That is important to know, but it is not what gives this study its heft.
The second reason centers on the investigators choice to do this trial. Dr. Geersing had a feeling that common wisdom was wrong. He did not try to persuade colleagues with anecdote or plausibility or meta-analyses of observational studies. He set out to answer a question in the correct way – with a randomized trial.
This is the path forward in medicine. I’ve often heard proponents of observational research declare that many topics in medicine cannot be studied with trials. I could hear people arguing that it’s not feasible to study mostly home-bound, elderly frail patients. And the fact that there exist so few trials in this space would support that argument.
But the FRAIL-AF authors showed that it is possible. This is the kind of science that medicine should celebrate. There were no soft endpoints, financial conflicts, or spin. If medical science had science as its incentive, rather than attention, FRAIL-AF easily wins top honors.
The third reason FRAIL-AF is so important is that it teaches us the humility required in translating evidence in our clinics. I like to say evidence is what separates doctors from palm readers. But using this evidence requires thinking hard about how average effects in trial environments apply to our patient.
Yes, of course, there is clear evidence from tens of thousands of patients in the DOAC versus warfarin trials, that, for those patients, on average, DOACs compare favorably with VKA. The average age of patients in these trials was 70-73 years; the average age in FRAIL-AF was 83 years. And that is just age. A substudy of the ENGAGE AF-TIMI 48 trial found that only 360 of more than 20,000 patients in the trial had severe frailty.
That lesson extends to nearly every common therapy in medicine today. It also casts great doubt on the soft-thinking idea of using evidence from trials to derive quality metrics. As if the nuance of evidence translation can be captured in an electronic health record.
The skillful use of evidence will be one of the main challenges of the next generation of clinicians. Thanks to advances in medical science, more patients will live long enough to become frail. And the so-called “guideline-directed” therapies may not apply to them.
Dr. Joosten, Dr. Geersing, and the FRAIL-AF team have taught us specific lessons about anticoagulation, but their greatest contribution has been to demonstrate the value of humility in science and the practice of evidence-based medicine.
If you treat patients, no trial at this meeting is more important.
Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
One of the hardest tasks of a clinician is applying evidence from trials to the person in your office. At the annual congress of the European Society of Cardiology, the surprising and unexpected results of the FRAIL-AF trial confirm the massive challenge of evidence translation.
FRAIL-AF investigators set out to study the question of whether frail, elderly patients with atrial fibrillation who were doing well with vitamin K antagonists (VKA) should be switched to direct-acting oral anticoagulants (DOAC).
Senior author Geert-Jan Geersing, MD, PhD, from the University Medical Center Utrecht (the Netherlands), told me that frustration led him to design this study. He was frustrated that colleagues assumed that evidence in nonfrail patients can always be translated to frail patients.
Dr. Geersing offered two reasons why common wisdom may be wrong. First was that the large DOAC versus warfarin trials included few elderly patients with frailty. Second, first author Linda Joosten, MD, made it clear in her presentation that frailty is a lot more than aging. It is a clinical syndrome, which entails a “high burden of comorbidities, dependency on others, and a reduced ability to resist stressors.”
The FRAIL-AF trial
The investigators recruited elderly, frail patients with fibrillation who were treated with VKAs and had stable international normalized ratios from outpatient clinics throughout the Netherlands. They screened about 2,600 patients and enrolled nearly 1,400. Most were excluded for not being frail.
Half the group was randomized to switching to a DOAC – drug choice was left to the treating clinician – and the other half remained on VKAs. Patients were 83 years of age on average with a mean CHA2DS2-VASc score of 4. All four classes of DOAC were used in the switching arm.
The primary endpoint was major or clinically relevant nonmajor bleeding, whichever came first, accounting for death as a competing risk. Follow-up was 1 year.
The results for switching to DOAC vs. VKA
Dr. Joosten started her presentation with this: “The results turned out to be different than we expected.” The authors designed the trial with the idea that switching to DOACs would be superior in safety to remaining on VKAs.
But the trial was halted after an interim analysis found a rate of major bleeding in the switching arm of 15.3% versus 9.4% in the arm staying on VKA (hazard ratio, 1.69; 95% confidence interval, 1.23-2.32; P = .0012).
The Kaplan-Meier event curves reveal that the excess risk of bleeding occurred after 100 days and increased with time. This argued against an early effect from transitioning the drugs.
An analysis looking at specific DOAC drugs revealed similar hazards for the two most common ones used – apixaban and rivaroxaban.
Thrombotic events were a secondary endpoint and were low in absolute numbers, 2.4% versus 2.0%, for remaining on VKA and switching to DOAC, respectively (HR, 1.26; 95% CI, 0.60-2.61).
The time in therapeutic range in FRAIL-AF was similar to that in the seminal DOAC trials.
Comments
Three reasons lead me to choose FRAIL-AF as the most important study from the 2023 ESC congress.
First is the specific lesson about switching drugs. Note that FRAIL-AF did not address the question of starting anticoagulation. The trial results show that if you have a frail older patient who is doing well on VKA, don’t change to a DOAC. That is important to know, but it is not what gives this study its heft.
The second reason centers on the investigators choice to do this trial. Dr. Geersing had a feeling that common wisdom was wrong. He did not try to persuade colleagues with anecdote or plausibility or meta-analyses of observational studies. He set out to answer a question in the correct way – with a randomized trial.
This is the path forward in medicine. I’ve often heard proponents of observational research declare that many topics in medicine cannot be studied with trials. I could hear people arguing that it’s not feasible to study mostly home-bound, elderly frail patients. And the fact that there exist so few trials in this space would support that argument.
But the FRAIL-AF authors showed that it is possible. This is the kind of science that medicine should celebrate. There were no soft endpoints, financial conflicts, or spin. If medical science had science as its incentive, rather than attention, FRAIL-AF easily wins top honors.
The third reason FRAIL-AF is so important is that it teaches us the humility required in translating evidence in our clinics. I like to say evidence is what separates doctors from palm readers. But using this evidence requires thinking hard about how average effects in trial environments apply to our patient.
Yes, of course, there is clear evidence from tens of thousands of patients in the DOAC versus warfarin trials, that, for those patients, on average, DOACs compare favorably with VKA. The average age of patients in these trials was 70-73 years; the average age in FRAIL-AF was 83 years. And that is just age. A substudy of the ENGAGE AF-TIMI 48 trial found that only 360 of more than 20,000 patients in the trial had severe frailty.
That lesson extends to nearly every common therapy in medicine today. It also casts great doubt on the soft-thinking idea of using evidence from trials to derive quality metrics. As if the nuance of evidence translation can be captured in an electronic health record.
The skillful use of evidence will be one of the main challenges of the next generation of clinicians. Thanks to advances in medical science, more patients will live long enough to become frail. And the so-called “guideline-directed” therapies may not apply to them.
Dr. Joosten, Dr. Geersing, and the FRAIL-AF team have taught us specific lessons about anticoagulation, but their greatest contribution has been to demonstrate the value of humility in science and the practice of evidence-based medicine.
If you treat patients, no trial at this meeting is more important.
Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
One of the hardest tasks of a clinician is applying evidence from trials to the person in your office. At the annual congress of the European Society of Cardiology, the surprising and unexpected results of the FRAIL-AF trial confirm the massive challenge of evidence translation.
FRAIL-AF investigators set out to study the question of whether frail, elderly patients with atrial fibrillation who were doing well with vitamin K antagonists (VKA) should be switched to direct-acting oral anticoagulants (DOAC).
Senior author Geert-Jan Geersing, MD, PhD, from the University Medical Center Utrecht (the Netherlands), told me that frustration led him to design this study. He was frustrated that colleagues assumed that evidence in nonfrail patients can always be translated to frail patients.
Dr. Geersing offered two reasons why common wisdom may be wrong. First was that the large DOAC versus warfarin trials included few elderly patients with frailty. Second, first author Linda Joosten, MD, made it clear in her presentation that frailty is a lot more than aging. It is a clinical syndrome, which entails a “high burden of comorbidities, dependency on others, and a reduced ability to resist stressors.”
The FRAIL-AF trial
The investigators recruited elderly, frail patients with fibrillation who were treated with VKAs and had stable international normalized ratios from outpatient clinics throughout the Netherlands. They screened about 2,600 patients and enrolled nearly 1,400. Most were excluded for not being frail.
Half the group was randomized to switching to a DOAC – drug choice was left to the treating clinician – and the other half remained on VKAs. Patients were 83 years of age on average with a mean CHA2DS2-VASc score of 4. All four classes of DOAC were used in the switching arm.
The primary endpoint was major or clinically relevant nonmajor bleeding, whichever came first, accounting for death as a competing risk. Follow-up was 1 year.
The results for switching to DOAC vs. VKA
Dr. Joosten started her presentation with this: “The results turned out to be different than we expected.” The authors designed the trial with the idea that switching to DOACs would be superior in safety to remaining on VKAs.
But the trial was halted after an interim analysis found a rate of major bleeding in the switching arm of 15.3% versus 9.4% in the arm staying on VKA (hazard ratio, 1.69; 95% confidence interval, 1.23-2.32; P = .0012).
The Kaplan-Meier event curves reveal that the excess risk of bleeding occurred after 100 days and increased with time. This argued against an early effect from transitioning the drugs.
An analysis looking at specific DOAC drugs revealed similar hazards for the two most common ones used – apixaban and rivaroxaban.
Thrombotic events were a secondary endpoint and were low in absolute numbers, 2.4% versus 2.0%, for remaining on VKA and switching to DOAC, respectively (HR, 1.26; 95% CI, 0.60-2.61).
The time in therapeutic range in FRAIL-AF was similar to that in the seminal DOAC trials.
Comments
Three reasons lead me to choose FRAIL-AF as the most important study from the 2023 ESC congress.
First is the specific lesson about switching drugs. Note that FRAIL-AF did not address the question of starting anticoagulation. The trial results show that if you have a frail older patient who is doing well on VKA, don’t change to a DOAC. That is important to know, but it is not what gives this study its heft.
The second reason centers on the investigators choice to do this trial. Dr. Geersing had a feeling that common wisdom was wrong. He did not try to persuade colleagues with anecdote or plausibility or meta-analyses of observational studies. He set out to answer a question in the correct way – with a randomized trial.
This is the path forward in medicine. I’ve often heard proponents of observational research declare that many topics in medicine cannot be studied with trials. I could hear people arguing that it’s not feasible to study mostly home-bound, elderly frail patients. And the fact that there exist so few trials in this space would support that argument.
But the FRAIL-AF authors showed that it is possible. This is the kind of science that medicine should celebrate. There were no soft endpoints, financial conflicts, or spin. If medical science had science as its incentive, rather than attention, FRAIL-AF easily wins top honors.
The third reason FRAIL-AF is so important is that it teaches us the humility required in translating evidence in our clinics. I like to say evidence is what separates doctors from palm readers. But using this evidence requires thinking hard about how average effects in trial environments apply to our patient.
Yes, of course, there is clear evidence from tens of thousands of patients in the DOAC versus warfarin trials, that, for those patients, on average, DOACs compare favorably with VKA. The average age of patients in these trials was 70-73 years; the average age in FRAIL-AF was 83 years. And that is just age. A substudy of the ENGAGE AF-TIMI 48 trial found that only 360 of more than 20,000 patients in the trial had severe frailty.
That lesson extends to nearly every common therapy in medicine today. It also casts great doubt on the soft-thinking idea of using evidence from trials to derive quality metrics. As if the nuance of evidence translation can be captured in an electronic health record.
The skillful use of evidence will be one of the main challenges of the next generation of clinicians. Thanks to advances in medical science, more patients will live long enough to become frail. And the so-called “guideline-directed” therapies may not apply to them.
Dr. Joosten, Dr. Geersing, and the FRAIL-AF team have taught us specific lessons about anticoagulation, but their greatest contribution has been to demonstrate the value of humility in science and the practice of evidence-based medicine.
If you treat patients, no trial at this meeting is more important.
Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
‘Decapitated’ boy saved by surgery team
This transcript has been edited for clarity.
F. Perry Wilson, MD, MSCE: I am joined today by Dr. Ohad Einav. He’s a staff surgeon in orthopedics at Hadassah Medical Center in Jerusalem. He’s with me to talk about an absolutely incredible surgical case, something that is terrifying to most non–orthopedic surgeons and I imagine is fairly scary for spine surgeons like him as well. But what we don’t have is information about how this works from a medical perspective. So, first of all, Dr. Einav, thank you for taking time to speak with me today.
Ohad Einav, MD: Thank you for having me.
Dr. Wilson: Can you tell us about Suleiman Hassan and what happened to him before he came into your care?
Dr. Einav: Hassan is a 12-year-old child who was riding his bicycle on the West Bank, about 40 minutes from here. Unfortunately, he was involved in a motor vehicle accident and he suffered injuries to his abdomen and cervical spine. He was transported to our service by helicopter from the scene of the accident.
Dr. Wilson: “Injury to the cervical spine” might be something of an understatement. He had what’s called atlanto-occipital dislocation, colloquially often referred to as internal decapitation. Can you tell us what that means? It sounds terrifying.
Dr. Einav: It’s an injury to the ligaments between the occiput and the upper cervical spine, with or without bony fracture. The atlanto-occipital joint is formed by the superior articular facet of the atlas and the occipital condyle, stabilized by an articular capsule between the head and neck, and is supported by various ligaments around it that stabilize the joint and allow joint movements, including flexion, extension, and some rotation in the lower levels.
Dr. Wilson: This joint has several degrees of freedom, which means it needs a lot of support. With this type of injury, where essentially you have severing of the ligaments, is it usually survivable? How dangerous is this?
Dr. Einav: The mortality rate is 50%-60%, depending on the primary impact, the injury, transportation later on, and then the surgery and surgical management.
Dr. Wilson: Tell us a bit about this patient’s status when he came to your medical center. I assume he was in bad shape.
Dr. Einav: Hassan arrived at our medical center with a Glasgow Coma Scale score of 15. He was fully conscious. He was hemodynamically stable except for a bad laceration on his abdomen. He had a Philadelphia collar around his neck. He was transported by chopper because the paramedics suspected that he had a cervical spine injury and decided to bring him to a Level 1 trauma center.
He was monitored and we treated him according to the ATLS [advanced trauma life support] protocol. He didn’t have any gross sensory deficits, but he was a little confused about the whole situation and the accident. Therefore, we could do a general examination but we couldn’t rely on that regarding any sensory deficit that he may or may not have. We decided as a team that it would be better to slow down and control the situation. We decided not to operate on him immediately. We basically stabilized him and made sure that he didn’t have any traumatic internal organ damage. Later on we took him to the OR and performed surgery.
Dr. Wilson: It’s amazing that he had intact motor function, considering the extent of his injury. The spinal cord was spared somewhat during the injury. There must have been a moment when you realized that this kid, who was conscious and could move all four extremities, had a very severe neck injury. Was that due to a CT scan or physical exam? And what was your feeling when you saw that he had atlanto-occipital dislocation?
Dr. Einav: As a surgeon, you have a gut feeling in regard to the general examination of the patient. But I never rely on gut feelings. On the CT, I understood exactly what he had, what we needed to do, and the time frame.
Dr. Wilson: You’ve done these types of surgeries before, right? Obviously, no one has done a lot of them because this isn’t very common. But you knew what to do. Did you have a plan? Where does your experience come into play in a situation like this?
Dr. Einav: I graduated from the spine program of Toronto University, where I did a fellowship in trauma of the spine and complex spine surgery. I had very good teachers, and during my fellowship I treated a few cases in older patients that were similar but not the same. Therefore, I knew exactly what needed to be done.
Dr. Wilson: For those of us who aren’t surgeons, take us into the OR with you. This is obviously an incredibly delicate procedure. You are high up in the spinal cord at the base of the brain. The slightest mistake could have devastating consequences. What are the key elements of this procedure? What can go wrong here? What is the number-one thing you have to look out for when you’re trying to fix an internal decapitation?
Dr. Einav: The key element in surgeries of the cervical spine – trauma and complex spine surgery – is planning. I never go to the OR without knowing what I’m going to do. I have a few plans – plan A, plan B, plan C – in case something fails. So, I definitely know what the next step will be. I always think about the surgery a few hours before, if I have time to prepare.
The second thing that is very important is teamwork. The team needs to be coordinated. Everybody needs to know what their job is. With these types of injuries, it’s not the time for rookies. If you are new, please stand back and let the more experienced people do that job. I’m talking about surgeons, nurses, anesthesiologists – everyone.
Another important thing in planning is choosing the right hardware. For example, in this case we had a problem because most of the hardware is designed for adults, and we had to improvise because there isn’t a lot of hardware on the market for the pediatric population. The adult plates and screws are too big, so we had to improvise.
Dr. Wilson: Tell us more about that. How do you improvise spinal hardware for a 12-year-old?
Dr. Einav: In this case, I chose to use hardware from one of the companies that works with us.
You can see in this model the area of the injury, and the area that we worked on. To perform the surgery, I had to use some plates and rods from a different company. This company’s (NuVasive) hardware has a small attachment to the skull, which was helpful for affixing the skull to the cervical spine, instead of using a big plate that would sit at the base of the skull and would not be very good for him. Most of the hardware is made for adults and not for kids.
Dr. Wilson: Will that hardware preserve the motor function of his neck? Will he be able to turn his head and extend and flex it?
Dr. Einav: The injury leads to instability and destruction of both articulations between the head and neck. Therefore, those articulations won’t be able to function the same way in the future. There is a decrease of something like 50% of the flexion and extension of Hassan’s cervical spine. Therefore, I decided that in this case there would be no chance of saving Hassan’s motor function unless we performed a fusion between the head and the neck, and therefore I decided that this would be the best procedure with the best survival rate. So, in the future, he will have some diminished flexion, extension, and rotation of his head.
Dr. Wilson: How long did his surgery take?
Dr. Einav: To be honest, I don’t remember. But I can tell you that it took us time. It was very challenging to coordinate with everyone. The most problematic part of the surgery to perform is what we call “flip-over.”
The anesthesiologist intubated the patient when he was supine, and later on, we flipped him prone to operate on the spine. This maneuver can actually lead to injury by itself, and injury at this level is fatal. So, we took our time and got Hassan into the OR. The anesthesiologist did a great job with the GlideScope – inserting the endotracheal tube. Later on, we neuromonitored him. Basically, we connected Hassan’s peripheral nerves to a computer and monitored his motor function. Gently we flipped him over, and after that we saw a little change in his motor function, so we had to modify his position so we could preserve his motor function. We then started the procedure, which took a few hours. I don’t know exactly how many.
Dr. Wilson: That just speaks to how delicate this is for everything from the intubation, where typically you’re manipulating the head, to the repositioning. Clearly this requires a lot of teamwork.
What happened after the operation? How is he doing?
Dr. Einav: After the operation, Hassan had a great recovery. He’s doing well. He doesn’t have any motor or sensory deficits. He’s able to ambulate without any aid. He had no signs of infection, which can happen after a car accident, neither from his abdominal wound nor from the occipital cervical surgery. He feels well. We saw him in the clinic. We removed his collar. We monitored him at the clinic. He looked amazing.
Dr. Wilson: That’s incredible. Are there long-term risks for him that you need to be looking out for?
Dr. Einav: Yes, and that’s the reason that we are monitoring him post surgery. While he was in the hospital, we monitored his motor and sensory functions, as well as his wound healing. Later on, in the clinic, for a few weeks after surgery we monitored for any failure of the hardware and bone graft. We check for healing of the bone graft and bone substitutes we put in to heal those bones.
Dr. Wilson: He will grow, right? He’s only 12, so he still has some years of growth in him. Is he going to need more surgery or any kind of hardware upgrade?
Dr. Einav: I hope not. In my surgeries, I never rely on the hardware for long durations. If I decide to do, for example, fusion, I rely on the hardware for a certain amount of time. And then I plan that the biology will do the work. If I plan for fusion, I put bone grafts in the preferred area for a fusion. Then if the hardware fails, I wouldn’t need to take out the hardware, and there would be no change in the condition of the patient.
Dr. Wilson: What an incredible story. It’s clear that you and your team kept your cool despite a very high-acuity situation with a ton of risk. What a tremendous outcome that this boy is not only alive but fully functional. So, congratulations to you and your team. That was very strong work.
Dr. Einav: Thank you very much. I would like to thank our team. We have to remember that the surgeon is not standing alone in the war. Hassan’s story is a success story of a very big group of people from various backgrounds and religions. They work day and night to help people and save lives. To the paramedics, the physiologists, the traumatologists, the pediatricians, the nurses, the physiotherapists, and obviously the surgeons, a big thank you. His story is our success story.
Dr. Wilson: It’s inspiring to see so many people come together to do what we all are here for, which is to fight against suffering, disease, and death. Thank you for keeping up that fight. And thank you for joining me here.
Dr. Einav: Thank you very much.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
F. Perry Wilson, MD, MSCE: I am joined today by Dr. Ohad Einav. He’s a staff surgeon in orthopedics at Hadassah Medical Center in Jerusalem. He’s with me to talk about an absolutely incredible surgical case, something that is terrifying to most non–orthopedic surgeons and I imagine is fairly scary for spine surgeons like him as well. But what we don’t have is information about how this works from a medical perspective. So, first of all, Dr. Einav, thank you for taking time to speak with me today.
Ohad Einav, MD: Thank you for having me.
Dr. Wilson: Can you tell us about Suleiman Hassan and what happened to him before he came into your care?
Dr. Einav: Hassan is a 12-year-old child who was riding his bicycle on the West Bank, about 40 minutes from here. Unfortunately, he was involved in a motor vehicle accident and he suffered injuries to his abdomen and cervical spine. He was transported to our service by helicopter from the scene of the accident.
Dr. Wilson: “Injury to the cervical spine” might be something of an understatement. He had what’s called atlanto-occipital dislocation, colloquially often referred to as internal decapitation. Can you tell us what that means? It sounds terrifying.
Dr. Einav: It’s an injury to the ligaments between the occiput and the upper cervical spine, with or without bony fracture. The atlanto-occipital joint is formed by the superior articular facet of the atlas and the occipital condyle, stabilized by an articular capsule between the head and neck, and is supported by various ligaments around it that stabilize the joint and allow joint movements, including flexion, extension, and some rotation in the lower levels.
Dr. Wilson: This joint has several degrees of freedom, which means it needs a lot of support. With this type of injury, where essentially you have severing of the ligaments, is it usually survivable? How dangerous is this?
Dr. Einav: The mortality rate is 50%-60%, depending on the primary impact, the injury, transportation later on, and then the surgery and surgical management.
Dr. Wilson: Tell us a bit about this patient’s status when he came to your medical center. I assume he was in bad shape.
Dr. Einav: Hassan arrived at our medical center with a Glasgow Coma Scale score of 15. He was fully conscious. He was hemodynamically stable except for a bad laceration on his abdomen. He had a Philadelphia collar around his neck. He was transported by chopper because the paramedics suspected that he had a cervical spine injury and decided to bring him to a Level 1 trauma center.
He was monitored and we treated him according to the ATLS [advanced trauma life support] protocol. He didn’t have any gross sensory deficits, but he was a little confused about the whole situation and the accident. Therefore, we could do a general examination but we couldn’t rely on that regarding any sensory deficit that he may or may not have. We decided as a team that it would be better to slow down and control the situation. We decided not to operate on him immediately. We basically stabilized him and made sure that he didn’t have any traumatic internal organ damage. Later on we took him to the OR and performed surgery.
Dr. Wilson: It’s amazing that he had intact motor function, considering the extent of his injury. The spinal cord was spared somewhat during the injury. There must have been a moment when you realized that this kid, who was conscious and could move all four extremities, had a very severe neck injury. Was that due to a CT scan or physical exam? And what was your feeling when you saw that he had atlanto-occipital dislocation?
Dr. Einav: As a surgeon, you have a gut feeling in regard to the general examination of the patient. But I never rely on gut feelings. On the CT, I understood exactly what he had, what we needed to do, and the time frame.
Dr. Wilson: You’ve done these types of surgeries before, right? Obviously, no one has done a lot of them because this isn’t very common. But you knew what to do. Did you have a plan? Where does your experience come into play in a situation like this?
Dr. Einav: I graduated from the spine program of Toronto University, where I did a fellowship in trauma of the spine and complex spine surgery. I had very good teachers, and during my fellowship I treated a few cases in older patients that were similar but not the same. Therefore, I knew exactly what needed to be done.
Dr. Wilson: For those of us who aren’t surgeons, take us into the OR with you. This is obviously an incredibly delicate procedure. You are high up in the spinal cord at the base of the brain. The slightest mistake could have devastating consequences. What are the key elements of this procedure? What can go wrong here? What is the number-one thing you have to look out for when you’re trying to fix an internal decapitation?
Dr. Einav: The key element in surgeries of the cervical spine – trauma and complex spine surgery – is planning. I never go to the OR without knowing what I’m going to do. I have a few plans – plan A, plan B, plan C – in case something fails. So, I definitely know what the next step will be. I always think about the surgery a few hours before, if I have time to prepare.
The second thing that is very important is teamwork. The team needs to be coordinated. Everybody needs to know what their job is. With these types of injuries, it’s not the time for rookies. If you are new, please stand back and let the more experienced people do that job. I’m talking about surgeons, nurses, anesthesiologists – everyone.
Another important thing in planning is choosing the right hardware. For example, in this case we had a problem because most of the hardware is designed for adults, and we had to improvise because there isn’t a lot of hardware on the market for the pediatric population. The adult plates and screws are too big, so we had to improvise.
Dr. Wilson: Tell us more about that. How do you improvise spinal hardware for a 12-year-old?
Dr. Einav: In this case, I chose to use hardware from one of the companies that works with us.
You can see in this model the area of the injury, and the area that we worked on. To perform the surgery, I had to use some plates and rods from a different company. This company’s (NuVasive) hardware has a small attachment to the skull, which was helpful for affixing the skull to the cervical spine, instead of using a big plate that would sit at the base of the skull and would not be very good for him. Most of the hardware is made for adults and not for kids.
Dr. Wilson: Will that hardware preserve the motor function of his neck? Will he be able to turn his head and extend and flex it?
Dr. Einav: The injury leads to instability and destruction of both articulations between the head and neck. Therefore, those articulations won’t be able to function the same way in the future. There is a decrease of something like 50% of the flexion and extension of Hassan’s cervical spine. Therefore, I decided that in this case there would be no chance of saving Hassan’s motor function unless we performed a fusion between the head and the neck, and therefore I decided that this would be the best procedure with the best survival rate. So, in the future, he will have some diminished flexion, extension, and rotation of his head.
Dr. Wilson: How long did his surgery take?
Dr. Einav: To be honest, I don’t remember. But I can tell you that it took us time. It was very challenging to coordinate with everyone. The most problematic part of the surgery to perform is what we call “flip-over.”
The anesthesiologist intubated the patient when he was supine, and later on, we flipped him prone to operate on the spine. This maneuver can actually lead to injury by itself, and injury at this level is fatal. So, we took our time and got Hassan into the OR. The anesthesiologist did a great job with the GlideScope – inserting the endotracheal tube. Later on, we neuromonitored him. Basically, we connected Hassan’s peripheral nerves to a computer and monitored his motor function. Gently we flipped him over, and after that we saw a little change in his motor function, so we had to modify his position so we could preserve his motor function. We then started the procedure, which took a few hours. I don’t know exactly how many.
Dr. Wilson: That just speaks to how delicate this is for everything from the intubation, where typically you’re manipulating the head, to the repositioning. Clearly this requires a lot of teamwork.
What happened after the operation? How is he doing?
Dr. Einav: After the operation, Hassan had a great recovery. He’s doing well. He doesn’t have any motor or sensory deficits. He’s able to ambulate without any aid. He had no signs of infection, which can happen after a car accident, neither from his abdominal wound nor from the occipital cervical surgery. He feels well. We saw him in the clinic. We removed his collar. We monitored him at the clinic. He looked amazing.
Dr. Wilson: That’s incredible. Are there long-term risks for him that you need to be looking out for?
Dr. Einav: Yes, and that’s the reason that we are monitoring him post surgery. While he was in the hospital, we monitored his motor and sensory functions, as well as his wound healing. Later on, in the clinic, for a few weeks after surgery we monitored for any failure of the hardware and bone graft. We check for healing of the bone graft and bone substitutes we put in to heal those bones.
Dr. Wilson: He will grow, right? He’s only 12, so he still has some years of growth in him. Is he going to need more surgery or any kind of hardware upgrade?
Dr. Einav: I hope not. In my surgeries, I never rely on the hardware for long durations. If I decide to do, for example, fusion, I rely on the hardware for a certain amount of time. And then I plan that the biology will do the work. If I plan for fusion, I put bone grafts in the preferred area for a fusion. Then if the hardware fails, I wouldn’t need to take out the hardware, and there would be no change in the condition of the patient.
Dr. Wilson: What an incredible story. It’s clear that you and your team kept your cool despite a very high-acuity situation with a ton of risk. What a tremendous outcome that this boy is not only alive but fully functional. So, congratulations to you and your team. That was very strong work.
Dr. Einav: Thank you very much. I would like to thank our team. We have to remember that the surgeon is not standing alone in the war. Hassan’s story is a success story of a very big group of people from various backgrounds and religions. They work day and night to help people and save lives. To the paramedics, the physiologists, the traumatologists, the pediatricians, the nurses, the physiotherapists, and obviously the surgeons, a big thank you. His story is our success story.
Dr. Wilson: It’s inspiring to see so many people come together to do what we all are here for, which is to fight against suffering, disease, and death. Thank you for keeping up that fight. And thank you for joining me here.
Dr. Einav: Thank you very much.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
F. Perry Wilson, MD, MSCE: I am joined today by Dr. Ohad Einav. He’s a staff surgeon in orthopedics at Hadassah Medical Center in Jerusalem. He’s with me to talk about an absolutely incredible surgical case, something that is terrifying to most non–orthopedic surgeons and I imagine is fairly scary for spine surgeons like him as well. But what we don’t have is information about how this works from a medical perspective. So, first of all, Dr. Einav, thank you for taking time to speak with me today.
Ohad Einav, MD: Thank you for having me.
Dr. Wilson: Can you tell us about Suleiman Hassan and what happened to him before he came into your care?
Dr. Einav: Hassan is a 12-year-old child who was riding his bicycle on the West Bank, about 40 minutes from here. Unfortunately, he was involved in a motor vehicle accident and he suffered injuries to his abdomen and cervical spine. He was transported to our service by helicopter from the scene of the accident.
Dr. Wilson: “Injury to the cervical spine” might be something of an understatement. He had what’s called atlanto-occipital dislocation, colloquially often referred to as internal decapitation. Can you tell us what that means? It sounds terrifying.
Dr. Einav: It’s an injury to the ligaments between the occiput and the upper cervical spine, with or without bony fracture. The atlanto-occipital joint is formed by the superior articular facet of the atlas and the occipital condyle, stabilized by an articular capsule between the head and neck, and is supported by various ligaments around it that stabilize the joint and allow joint movements, including flexion, extension, and some rotation in the lower levels.
Dr. Wilson: This joint has several degrees of freedom, which means it needs a lot of support. With this type of injury, where essentially you have severing of the ligaments, is it usually survivable? How dangerous is this?
Dr. Einav: The mortality rate is 50%-60%, depending on the primary impact, the injury, transportation later on, and then the surgery and surgical management.
Dr. Wilson: Tell us a bit about this patient’s status when he came to your medical center. I assume he was in bad shape.
Dr. Einav: Hassan arrived at our medical center with a Glasgow Coma Scale score of 15. He was fully conscious. He was hemodynamically stable except for a bad laceration on his abdomen. He had a Philadelphia collar around his neck. He was transported by chopper because the paramedics suspected that he had a cervical spine injury and decided to bring him to a Level 1 trauma center.
He was monitored and we treated him according to the ATLS [advanced trauma life support] protocol. He didn’t have any gross sensory deficits, but he was a little confused about the whole situation and the accident. Therefore, we could do a general examination but we couldn’t rely on that regarding any sensory deficit that he may or may not have. We decided as a team that it would be better to slow down and control the situation. We decided not to operate on him immediately. We basically stabilized him and made sure that he didn’t have any traumatic internal organ damage. Later on we took him to the OR and performed surgery.
Dr. Wilson: It’s amazing that he had intact motor function, considering the extent of his injury. The spinal cord was spared somewhat during the injury. There must have been a moment when you realized that this kid, who was conscious and could move all four extremities, had a very severe neck injury. Was that due to a CT scan or physical exam? And what was your feeling when you saw that he had atlanto-occipital dislocation?
Dr. Einav: As a surgeon, you have a gut feeling in regard to the general examination of the patient. But I never rely on gut feelings. On the CT, I understood exactly what he had, what we needed to do, and the time frame.
Dr. Wilson: You’ve done these types of surgeries before, right? Obviously, no one has done a lot of them because this isn’t very common. But you knew what to do. Did you have a plan? Where does your experience come into play in a situation like this?
Dr. Einav: I graduated from the spine program of Toronto University, where I did a fellowship in trauma of the spine and complex spine surgery. I had very good teachers, and during my fellowship I treated a few cases in older patients that were similar but not the same. Therefore, I knew exactly what needed to be done.
Dr. Wilson: For those of us who aren’t surgeons, take us into the OR with you. This is obviously an incredibly delicate procedure. You are high up in the spinal cord at the base of the brain. The slightest mistake could have devastating consequences. What are the key elements of this procedure? What can go wrong here? What is the number-one thing you have to look out for when you’re trying to fix an internal decapitation?
Dr. Einav: The key element in surgeries of the cervical spine – trauma and complex spine surgery – is planning. I never go to the OR without knowing what I’m going to do. I have a few plans – plan A, plan B, plan C – in case something fails. So, I definitely know what the next step will be. I always think about the surgery a few hours before, if I have time to prepare.
The second thing that is very important is teamwork. The team needs to be coordinated. Everybody needs to know what their job is. With these types of injuries, it’s not the time for rookies. If you are new, please stand back and let the more experienced people do that job. I’m talking about surgeons, nurses, anesthesiologists – everyone.
Another important thing in planning is choosing the right hardware. For example, in this case we had a problem because most of the hardware is designed for adults, and we had to improvise because there isn’t a lot of hardware on the market for the pediatric population. The adult plates and screws are too big, so we had to improvise.
Dr. Wilson: Tell us more about that. How do you improvise spinal hardware for a 12-year-old?
Dr. Einav: In this case, I chose to use hardware from one of the companies that works with us.
You can see in this model the area of the injury, and the area that we worked on. To perform the surgery, I had to use some plates and rods from a different company. This company’s (NuVasive) hardware has a small attachment to the skull, which was helpful for affixing the skull to the cervical spine, instead of using a big plate that would sit at the base of the skull and would not be very good for him. Most of the hardware is made for adults and not for kids.
Dr. Wilson: Will that hardware preserve the motor function of his neck? Will he be able to turn his head and extend and flex it?
Dr. Einav: The injury leads to instability and destruction of both articulations between the head and neck. Therefore, those articulations won’t be able to function the same way in the future. There is a decrease of something like 50% of the flexion and extension of Hassan’s cervical spine. Therefore, I decided that in this case there would be no chance of saving Hassan’s motor function unless we performed a fusion between the head and the neck, and therefore I decided that this would be the best procedure with the best survival rate. So, in the future, he will have some diminished flexion, extension, and rotation of his head.
Dr. Wilson: How long did his surgery take?
Dr. Einav: To be honest, I don’t remember. But I can tell you that it took us time. It was very challenging to coordinate with everyone. The most problematic part of the surgery to perform is what we call “flip-over.”
The anesthesiologist intubated the patient when he was supine, and later on, we flipped him prone to operate on the spine. This maneuver can actually lead to injury by itself, and injury at this level is fatal. So, we took our time and got Hassan into the OR. The anesthesiologist did a great job with the GlideScope – inserting the endotracheal tube. Later on, we neuromonitored him. Basically, we connected Hassan’s peripheral nerves to a computer and monitored his motor function. Gently we flipped him over, and after that we saw a little change in his motor function, so we had to modify his position so we could preserve his motor function. We then started the procedure, which took a few hours. I don’t know exactly how many.
Dr. Wilson: That just speaks to how delicate this is for everything from the intubation, where typically you’re manipulating the head, to the repositioning. Clearly this requires a lot of teamwork.
What happened after the operation? How is he doing?
Dr. Einav: After the operation, Hassan had a great recovery. He’s doing well. He doesn’t have any motor or sensory deficits. He’s able to ambulate without any aid. He had no signs of infection, which can happen after a car accident, neither from his abdominal wound nor from the occipital cervical surgery. He feels well. We saw him in the clinic. We removed his collar. We monitored him at the clinic. He looked amazing.
Dr. Wilson: That’s incredible. Are there long-term risks for him that you need to be looking out for?
Dr. Einav: Yes, and that’s the reason that we are monitoring him post surgery. While he was in the hospital, we monitored his motor and sensory functions, as well as his wound healing. Later on, in the clinic, for a few weeks after surgery we monitored for any failure of the hardware and bone graft. We check for healing of the bone graft and bone substitutes we put in to heal those bones.
Dr. Wilson: He will grow, right? He’s only 12, so he still has some years of growth in him. Is he going to need more surgery or any kind of hardware upgrade?
Dr. Einav: I hope not. In my surgeries, I never rely on the hardware for long durations. If I decide to do, for example, fusion, I rely on the hardware for a certain amount of time. And then I plan that the biology will do the work. If I plan for fusion, I put bone grafts in the preferred area for a fusion. Then if the hardware fails, I wouldn’t need to take out the hardware, and there would be no change in the condition of the patient.
Dr. Wilson: What an incredible story. It’s clear that you and your team kept your cool despite a very high-acuity situation with a ton of risk. What a tremendous outcome that this boy is not only alive but fully functional. So, congratulations to you and your team. That was very strong work.
Dr. Einav: Thank you very much. I would like to thank our team. We have to remember that the surgeon is not standing alone in the war. Hassan’s story is a success story of a very big group of people from various backgrounds and religions. They work day and night to help people and save lives. To the paramedics, the physiologists, the traumatologists, the pediatricians, the nurses, the physiotherapists, and obviously the surgeons, a big thank you. His story is our success story.
Dr. Wilson: It’s inspiring to see so many people come together to do what we all are here for, which is to fight against suffering, disease, and death. Thank you for keeping up that fight. And thank you for joining me here.
Dr. Einav: Thank you very much.
A version of this article first appeared on Medscape.com.
Treatments for Hidradenitis Suppurativa Comorbidities Help With Pain Management
Hidradenitis suppurativa (HS) has an unpredictable disease course and poses substantial therapeutic challenges. It carries an increased risk for adverse cardiovascular outcomes and all-cause mortality. It also is associated with comorbidities including mood disorders, tobacco smoking, obesity, diabetes mellitus, sleep disorders, sexual dysfunction, and autoimmune diseases, which can complicate its management and considerably affect patients’ quality of life (QOL).1 Hidradenitis suppurativa also disproportionately affects minority groups and has far-reaching inequities; for example, the condition has a notable economic impact on patients, including higher unemployment and disability rates, lower-paying jobs, less paid time off, and other indirect costs.2,3 Race can impact how pain itself is treated. In one study (N = 217), Black patients with extremity fractures presenting to anemergency department were significantly less likely to receive analgesia compared to White patients despite reporting similar pain (57% vs 74%, respectively; P = .01).4 In another study, Hispanic patients were 7-times less likely to be treated with opioids compared to non-Hispanic patients with long-bone fractures.5 Herein, we highlight pain management disparities in HS patients.
Treating HS Comorbidities Helps Improve Pain
Pain is reported by almost all HS patients and is the symptom most associated with QOL impairment.6,7 Pain in HS is multifactorial, with other symptoms and comorbidities affecting its severity. Treatment of acute flares often is painful and procedural, including intralesional steroid injections or incision and drainage.8 Algorithms for addressing pain through the treatment of comorbidities also have been developed.6 Although there are few studies on the medications that treat related comorbidities in HS, there is evidence of their benefits in similar diseases; for example, treating depression in patients with irritable bowel disease (IBD) improved pain perception, cognitive function, and sexual dysfunction.9
Depression exacerbates pain, and higher levels of depression have been observed in severe HS.10,11 Additionally, more than 80% of individuals with HS report tobacco smoking.1 Nicotine not only increases pain sensitivity and decreases pain tolerance but also worsens neuropathic, nociceptive, and psychosocial pain, as well as mood disorders and sleep disturbances.12 Given the higher prevalence of depression and smoking in HS patients and the impact on pain, addressing these comorbidities is crucial. Additionally, poor sleep amplifies pain sensitivity and affects neurologic pain modulation.13 Chronic pain also is associated with obesity and sleep dysfunction.14
Treatments Targeting Pain and Comorbidities
Treatments that target comorbidities and other symptoms of HS also may improve pain. Bupropion is a well-studied antidepressant and first-line option to aid in smoking cessation. It provides acute and chronic pain relief associated with IBD and may perform similarly in patients with HS.15-18 Bupropion also demonstrated dose-dependent weight reduction in obese and overweight individuals.19,20 Additionally, varenicline is a first-line option to aid in smoking cessation and can be combined with bupropion to increase long-term efficacy.21,22
Other antidepressants may alleviate HS pain. The selective norepinephrine reuptake inhibitors duloxetine and venlafaxine are recommended for chronic pain in HS.6 Selective serotonin reuptake inhibitors such as citalopram, escitalopram, and paroxetine are inexpensive and widely available antidepressants. Citalopram is as efficacious as duloxetine for chronic pain with fewer side effects.23 Paroxetine has been shown to improve pain and pruritus, QOL, and depression in patients with IBD.24 Benefits such as improved weight and sexual dysfunction also have been reported.25
Metformin is well studied in Black patients, and greater glycemic response supports its efficacy for diabetes as well as HS, which disproportionately affects individuals with skin of color.26 Metformin also targets other comorbidities of HS, such as improving insulin resistance, polycystic ovary syndrome, acne vulgaris, weight loss, hyperlipidemia, cardiovascular risk, and neuropsychologic conditions.27 Growing evidence supports the use of metformin as a new agent in chronic pain management, specifically for patients with HS.28,29
Final Thoughts
Hidradenitis suppurativa is a complex medical condition seen disproportionately in minority groups. Understanding common comorbidities as well as the biases associated with pain management will allow providers to treat HS patients more effectively. Dermatologists who see many HS patients should become more familiar with treating these associated comorbidities to provide patient care that is more holistic and effective.
- Garg A, Malviya N, Strunk A, et al. Comorbidity screening in hidradenitis suppurativa: evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations. J Am Acad Dermatol. 2022;86:1092-1101. doi:10.1016/j.jaad.2021.01.059
- Tzellos T, Yang H, Mu F, et al. Impact of hidradenitis suppurativa on work loss, indirect costs and income. Br J Dermatol. 2019;181:147-154. doi:10.1111/bjd.17101
- Udechukwu NS, Fleischer AB. Higher risk of care for hidradenitis suppurativa in African American and non-Hispanic patients in the United States. J Natl Med Assoc. 2017;109:44-48. doi:10.1016/j.jnma.2016.09.002
- Todd KH, Deaton C, D’Adamo AP, et al. Ethnicity and analgesic practice. Ann Emerg Med. 2000;35:11-16. doi:10.1016/s0196-0644(00)70099-0
- Todd KH, Samaroo N, Hoffman JR. Ethnicity as a risk factor for inadequate emergency department analgesia. JAMA. 1993;269:1537-1539.
- Savage KT, Singh V, Patel ZS, et al. Pain management in hidradenitis suppurativa and a proposed treatment algorithm. J Am Acad Dermatol. 2021;85:187-199. doi:10.1016/j.jaad.2020.09.039
- Matusiak Ł, Szcze˛ch J, Kaaz K, et al. Clinical characteristics of pruritus and pain in patients with hidradenitis suppurativa. Acta Derm Venereol. 2018;98:191-194. doi:10.2340/00015555-2815
- Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations: part I: diagnosis, evaluation, and the use of complementary and procedural management. J Am Acad Dermatol. 2019;81:76-90. doi:10.1016/j.jaad.2019.02.067
- Walker EA, Gelfand MD, Gelfand AN, et al. The relationship of current psychiatric disorder to functional disability and distress in patients with inflammatory bowel disease. Gen Hosp Psychiatry. 1996;18:220-229. doi:10.1016/0163-8343(96)00036-9
- Phan K, Huo YR, Smith SD. Hidradenitis suppurativa and psychiatric comorbidities, suicides and substance abuse: systematic review and meta-analysis. Ann Transl Med. 2020;8:821. doi:10.21037/atm-20-1028
- Woo AK. Depression and anxiety in pain. Rev Pain. 2010;4:8-12. doi:10.1177/204946371000400103
- Iida H, Yamaguchi S, Goyagi T, et al. Consensus statement on smoking cessation in patients with pain. J Anesth. 2022;36:671-687. doi:10.1007/s00540-022-03097-w
- Krause AJ, Prather AA, Wager TD, et al. The pain of sleep loss: a brain characterization in humans. J Neurosci. 2019;39:2291-2300. doi:10.1523/JNEUROSCI.2408-18.2018
- Mundal I, Gråwe RW, Bjørngaard JH, et al. Prevalence and long-term predictors of persistent chronic widespread pain in the general population in an 11-year prospective study: the HUNT study. BMC Musculoskelet Disord. 2014;15:213. doi:10.1186/1471-2474-15-213
- Aubin H-J. Tolerability and safety of sustained-release bupropion in the management of smoking cessation. Drugs. 2002;(62 suppl 2):45-52. doi:10.2165/00003495-200262002-00005
- Shah TH, Moradimehr A. Bupropion for the treatment of neuropathic pain. Am J Hosp Palliat Care. 2010;27:333-336. doi:10.1177/1049909110361229
- Baune BT, Renger L. Pharmacological and non-pharmacological interventions to improve cognitive dysfunction and functional ability in clinical depression—a systematic review. Psychiatry Res. 2014;219:25-50. doi:10.1016/j.psychres.2014.05.013
- Walker PW, Cole JO, Gardner EA, et al. Improvement in fluoxetine-associated sexual dysfunction in patients switched to bupropion. J Clin Psychiatry. 1993;54:459-465.
- Sherman MM, Ungureanu S, Rey JA. Naltrexone/bupropion ER (contrave): newly approved treatment option for chronic weight management in obese adults. P T. 2016;41:164-172.
- Anderson JW, Greenway FL, Fujioka K, et al. Bupropion SR enhances weight loss: a 48-week double-blind, placebo-controlled trial. Obes Res. 2002;10:633-641. doi:10.1038/oby.2002.86
- Kalkhoran S, Benowitz NL, Rigotti NA. Prevention and treatment of tobacco use: JACC health promotion series. J Am Coll Cardiol. 2018;72:1030-1045. doi:10.1016/j.jacc.2018.06.036
- Singh D, Saadabadi A. Varenicline. StatPearls Publishing; 2023.
- Mazza M, Mazza O, Pazzaglia C, et al. Escitalopram 20 mg versus duloxetine 60 mg for the treatment of chronic low back pain. Expert Opin Pharmacother. 2010;11:1049-1052. doi:10.1517/14656561003730413
- Docherty MJ, Jones RCW, Wallace MS. Managing pain in inflammatory bowel disease. Gastroenterol Hepatol (N Y). 2011;7:592-601.
- Shrestha P, Fariba KA, Abdijadid S. Paroxetine. StatPearls Publishing; 2022.
- Williams LK, Padhukasahasram B, Ahmedani BK, et al. Differing effects of metformin on glycemic control by race-ethnicity. J Clin Endocrinol Metab. 2014;99:3160-3168. doi:10.1210/jc.2014-1539
- Sharma S, Mathur DK, Paliwal V, et al. Efficacy of metformin in the treatment of acne in women with polycystic ovarian syndrome: a newer approach to acne therapy. J Clin Aesthet Dermatol. 2019;12:34-38.
- Scheinfeld N. Hidradenitis suppurativa: a practical review of possible medical treatments based on over 350 hidradenitis patients. Dermatol Online J. 2013;19:1. doi:10.5070/D35VW402NF
- Baeza-Flores GDC, Guzmán-Priego CG, Parra-Flores LI, et al. Metformin: a prospective alternative for the treatment of chronic pain. Front Pharmacol. 2020;11:558474. doi:10.3389/fphar.2020.558474
Hidradenitis suppurativa (HS) has an unpredictable disease course and poses substantial therapeutic challenges. It carries an increased risk for adverse cardiovascular outcomes and all-cause mortality. It also is associated with comorbidities including mood disorders, tobacco smoking, obesity, diabetes mellitus, sleep disorders, sexual dysfunction, and autoimmune diseases, which can complicate its management and considerably affect patients’ quality of life (QOL).1 Hidradenitis suppurativa also disproportionately affects minority groups and has far-reaching inequities; for example, the condition has a notable economic impact on patients, including higher unemployment and disability rates, lower-paying jobs, less paid time off, and other indirect costs.2,3 Race can impact how pain itself is treated. In one study (N = 217), Black patients with extremity fractures presenting to anemergency department were significantly less likely to receive analgesia compared to White patients despite reporting similar pain (57% vs 74%, respectively; P = .01).4 In another study, Hispanic patients were 7-times less likely to be treated with opioids compared to non-Hispanic patients with long-bone fractures.5 Herein, we highlight pain management disparities in HS patients.
Treating HS Comorbidities Helps Improve Pain
Pain is reported by almost all HS patients and is the symptom most associated with QOL impairment.6,7 Pain in HS is multifactorial, with other symptoms and comorbidities affecting its severity. Treatment of acute flares often is painful and procedural, including intralesional steroid injections or incision and drainage.8 Algorithms for addressing pain through the treatment of comorbidities also have been developed.6 Although there are few studies on the medications that treat related comorbidities in HS, there is evidence of their benefits in similar diseases; for example, treating depression in patients with irritable bowel disease (IBD) improved pain perception, cognitive function, and sexual dysfunction.9
Depression exacerbates pain, and higher levels of depression have been observed in severe HS.10,11 Additionally, more than 80% of individuals with HS report tobacco smoking.1 Nicotine not only increases pain sensitivity and decreases pain tolerance but also worsens neuropathic, nociceptive, and psychosocial pain, as well as mood disorders and sleep disturbances.12 Given the higher prevalence of depression and smoking in HS patients and the impact on pain, addressing these comorbidities is crucial. Additionally, poor sleep amplifies pain sensitivity and affects neurologic pain modulation.13 Chronic pain also is associated with obesity and sleep dysfunction.14
Treatments Targeting Pain and Comorbidities
Treatments that target comorbidities and other symptoms of HS also may improve pain. Bupropion is a well-studied antidepressant and first-line option to aid in smoking cessation. It provides acute and chronic pain relief associated with IBD and may perform similarly in patients with HS.15-18 Bupropion also demonstrated dose-dependent weight reduction in obese and overweight individuals.19,20 Additionally, varenicline is a first-line option to aid in smoking cessation and can be combined with bupropion to increase long-term efficacy.21,22
Other antidepressants may alleviate HS pain. The selective norepinephrine reuptake inhibitors duloxetine and venlafaxine are recommended for chronic pain in HS.6 Selective serotonin reuptake inhibitors such as citalopram, escitalopram, and paroxetine are inexpensive and widely available antidepressants. Citalopram is as efficacious as duloxetine for chronic pain with fewer side effects.23 Paroxetine has been shown to improve pain and pruritus, QOL, and depression in patients with IBD.24 Benefits such as improved weight and sexual dysfunction also have been reported.25
Metformin is well studied in Black patients, and greater glycemic response supports its efficacy for diabetes as well as HS, which disproportionately affects individuals with skin of color.26 Metformin also targets other comorbidities of HS, such as improving insulin resistance, polycystic ovary syndrome, acne vulgaris, weight loss, hyperlipidemia, cardiovascular risk, and neuropsychologic conditions.27 Growing evidence supports the use of metformin as a new agent in chronic pain management, specifically for patients with HS.28,29
Final Thoughts
Hidradenitis suppurativa is a complex medical condition seen disproportionately in minority groups. Understanding common comorbidities as well as the biases associated with pain management will allow providers to treat HS patients more effectively. Dermatologists who see many HS patients should become more familiar with treating these associated comorbidities to provide patient care that is more holistic and effective.
Hidradenitis suppurativa (HS) has an unpredictable disease course and poses substantial therapeutic challenges. It carries an increased risk for adverse cardiovascular outcomes and all-cause mortality. It also is associated with comorbidities including mood disorders, tobacco smoking, obesity, diabetes mellitus, sleep disorders, sexual dysfunction, and autoimmune diseases, which can complicate its management and considerably affect patients’ quality of life (QOL).1 Hidradenitis suppurativa also disproportionately affects minority groups and has far-reaching inequities; for example, the condition has a notable economic impact on patients, including higher unemployment and disability rates, lower-paying jobs, less paid time off, and other indirect costs.2,3 Race can impact how pain itself is treated. In one study (N = 217), Black patients with extremity fractures presenting to anemergency department were significantly less likely to receive analgesia compared to White patients despite reporting similar pain (57% vs 74%, respectively; P = .01).4 In another study, Hispanic patients were 7-times less likely to be treated with opioids compared to non-Hispanic patients with long-bone fractures.5 Herein, we highlight pain management disparities in HS patients.
Treating HS Comorbidities Helps Improve Pain
Pain is reported by almost all HS patients and is the symptom most associated with QOL impairment.6,7 Pain in HS is multifactorial, with other symptoms and comorbidities affecting its severity. Treatment of acute flares often is painful and procedural, including intralesional steroid injections or incision and drainage.8 Algorithms for addressing pain through the treatment of comorbidities also have been developed.6 Although there are few studies on the medications that treat related comorbidities in HS, there is evidence of their benefits in similar diseases; for example, treating depression in patients with irritable bowel disease (IBD) improved pain perception, cognitive function, and sexual dysfunction.9
Depression exacerbates pain, and higher levels of depression have been observed in severe HS.10,11 Additionally, more than 80% of individuals with HS report tobacco smoking.1 Nicotine not only increases pain sensitivity and decreases pain tolerance but also worsens neuropathic, nociceptive, and psychosocial pain, as well as mood disorders and sleep disturbances.12 Given the higher prevalence of depression and smoking in HS patients and the impact on pain, addressing these comorbidities is crucial. Additionally, poor sleep amplifies pain sensitivity and affects neurologic pain modulation.13 Chronic pain also is associated with obesity and sleep dysfunction.14
Treatments Targeting Pain and Comorbidities
Treatments that target comorbidities and other symptoms of HS also may improve pain. Bupropion is a well-studied antidepressant and first-line option to aid in smoking cessation. It provides acute and chronic pain relief associated with IBD and may perform similarly in patients with HS.15-18 Bupropion also demonstrated dose-dependent weight reduction in obese and overweight individuals.19,20 Additionally, varenicline is a first-line option to aid in smoking cessation and can be combined with bupropion to increase long-term efficacy.21,22
Other antidepressants may alleviate HS pain. The selective norepinephrine reuptake inhibitors duloxetine and venlafaxine are recommended for chronic pain in HS.6 Selective serotonin reuptake inhibitors such as citalopram, escitalopram, and paroxetine are inexpensive and widely available antidepressants. Citalopram is as efficacious as duloxetine for chronic pain with fewer side effects.23 Paroxetine has been shown to improve pain and pruritus, QOL, and depression in patients with IBD.24 Benefits such as improved weight and sexual dysfunction also have been reported.25
Metformin is well studied in Black patients, and greater glycemic response supports its efficacy for diabetes as well as HS, which disproportionately affects individuals with skin of color.26 Metformin also targets other comorbidities of HS, such as improving insulin resistance, polycystic ovary syndrome, acne vulgaris, weight loss, hyperlipidemia, cardiovascular risk, and neuropsychologic conditions.27 Growing evidence supports the use of metformin as a new agent in chronic pain management, specifically for patients with HS.28,29
Final Thoughts
Hidradenitis suppurativa is a complex medical condition seen disproportionately in minority groups. Understanding common comorbidities as well as the biases associated with pain management will allow providers to treat HS patients more effectively. Dermatologists who see many HS patients should become more familiar with treating these associated comorbidities to provide patient care that is more holistic and effective.
- Garg A, Malviya N, Strunk A, et al. Comorbidity screening in hidradenitis suppurativa: evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations. J Am Acad Dermatol. 2022;86:1092-1101. doi:10.1016/j.jaad.2021.01.059
- Tzellos T, Yang H, Mu F, et al. Impact of hidradenitis suppurativa on work loss, indirect costs and income. Br J Dermatol. 2019;181:147-154. doi:10.1111/bjd.17101
- Udechukwu NS, Fleischer AB. Higher risk of care for hidradenitis suppurativa in African American and non-Hispanic patients in the United States. J Natl Med Assoc. 2017;109:44-48. doi:10.1016/j.jnma.2016.09.002
- Todd KH, Deaton C, D’Adamo AP, et al. Ethnicity and analgesic practice. Ann Emerg Med. 2000;35:11-16. doi:10.1016/s0196-0644(00)70099-0
- Todd KH, Samaroo N, Hoffman JR. Ethnicity as a risk factor for inadequate emergency department analgesia. JAMA. 1993;269:1537-1539.
- Savage KT, Singh V, Patel ZS, et al. Pain management in hidradenitis suppurativa and a proposed treatment algorithm. J Am Acad Dermatol. 2021;85:187-199. doi:10.1016/j.jaad.2020.09.039
- Matusiak Ł, Szcze˛ch J, Kaaz K, et al. Clinical characteristics of pruritus and pain in patients with hidradenitis suppurativa. Acta Derm Venereol. 2018;98:191-194. doi:10.2340/00015555-2815
- Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations: part I: diagnosis, evaluation, and the use of complementary and procedural management. J Am Acad Dermatol. 2019;81:76-90. doi:10.1016/j.jaad.2019.02.067
- Walker EA, Gelfand MD, Gelfand AN, et al. The relationship of current psychiatric disorder to functional disability and distress in patients with inflammatory bowel disease. Gen Hosp Psychiatry. 1996;18:220-229. doi:10.1016/0163-8343(96)00036-9
- Phan K, Huo YR, Smith SD. Hidradenitis suppurativa and psychiatric comorbidities, suicides and substance abuse: systematic review and meta-analysis. Ann Transl Med. 2020;8:821. doi:10.21037/atm-20-1028
- Woo AK. Depression and anxiety in pain. Rev Pain. 2010;4:8-12. doi:10.1177/204946371000400103
- Iida H, Yamaguchi S, Goyagi T, et al. Consensus statement on smoking cessation in patients with pain. J Anesth. 2022;36:671-687. doi:10.1007/s00540-022-03097-w
- Krause AJ, Prather AA, Wager TD, et al. The pain of sleep loss: a brain characterization in humans. J Neurosci. 2019;39:2291-2300. doi:10.1523/JNEUROSCI.2408-18.2018
- Mundal I, Gråwe RW, Bjørngaard JH, et al. Prevalence and long-term predictors of persistent chronic widespread pain in the general population in an 11-year prospective study: the HUNT study. BMC Musculoskelet Disord. 2014;15:213. doi:10.1186/1471-2474-15-213
- Aubin H-J. Tolerability and safety of sustained-release bupropion in the management of smoking cessation. Drugs. 2002;(62 suppl 2):45-52. doi:10.2165/00003495-200262002-00005
- Shah TH, Moradimehr A. Bupropion for the treatment of neuropathic pain. Am J Hosp Palliat Care. 2010;27:333-336. doi:10.1177/1049909110361229
- Baune BT, Renger L. Pharmacological and non-pharmacological interventions to improve cognitive dysfunction and functional ability in clinical depression—a systematic review. Psychiatry Res. 2014;219:25-50. doi:10.1016/j.psychres.2014.05.013
- Walker PW, Cole JO, Gardner EA, et al. Improvement in fluoxetine-associated sexual dysfunction in patients switched to bupropion. J Clin Psychiatry. 1993;54:459-465.
- Sherman MM, Ungureanu S, Rey JA. Naltrexone/bupropion ER (contrave): newly approved treatment option for chronic weight management in obese adults. P T. 2016;41:164-172.
- Anderson JW, Greenway FL, Fujioka K, et al. Bupropion SR enhances weight loss: a 48-week double-blind, placebo-controlled trial. Obes Res. 2002;10:633-641. doi:10.1038/oby.2002.86
- Kalkhoran S, Benowitz NL, Rigotti NA. Prevention and treatment of tobacco use: JACC health promotion series. J Am Coll Cardiol. 2018;72:1030-1045. doi:10.1016/j.jacc.2018.06.036
- Singh D, Saadabadi A. Varenicline. StatPearls Publishing; 2023.
- Mazza M, Mazza O, Pazzaglia C, et al. Escitalopram 20 mg versus duloxetine 60 mg for the treatment of chronic low back pain. Expert Opin Pharmacother. 2010;11:1049-1052. doi:10.1517/14656561003730413
- Docherty MJ, Jones RCW, Wallace MS. Managing pain in inflammatory bowel disease. Gastroenterol Hepatol (N Y). 2011;7:592-601.
- Shrestha P, Fariba KA, Abdijadid S. Paroxetine. StatPearls Publishing; 2022.
- Williams LK, Padhukasahasram B, Ahmedani BK, et al. Differing effects of metformin on glycemic control by race-ethnicity. J Clin Endocrinol Metab. 2014;99:3160-3168. doi:10.1210/jc.2014-1539
- Sharma S, Mathur DK, Paliwal V, et al. Efficacy of metformin in the treatment of acne in women with polycystic ovarian syndrome: a newer approach to acne therapy. J Clin Aesthet Dermatol. 2019;12:34-38.
- Scheinfeld N. Hidradenitis suppurativa: a practical review of possible medical treatments based on over 350 hidradenitis patients. Dermatol Online J. 2013;19:1. doi:10.5070/D35VW402NF
- Baeza-Flores GDC, Guzmán-Priego CG, Parra-Flores LI, et al. Metformin: a prospective alternative for the treatment of chronic pain. Front Pharmacol. 2020;11:558474. doi:10.3389/fphar.2020.558474
- Garg A, Malviya N, Strunk A, et al. Comorbidity screening in hidradenitis suppurativa: evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations. J Am Acad Dermatol. 2022;86:1092-1101. doi:10.1016/j.jaad.2021.01.059
- Tzellos T, Yang H, Mu F, et al. Impact of hidradenitis suppurativa on work loss, indirect costs and income. Br J Dermatol. 2019;181:147-154. doi:10.1111/bjd.17101
- Udechukwu NS, Fleischer AB. Higher risk of care for hidradenitis suppurativa in African American and non-Hispanic patients in the United States. J Natl Med Assoc. 2017;109:44-48. doi:10.1016/j.jnma.2016.09.002
- Todd KH, Deaton C, D’Adamo AP, et al. Ethnicity and analgesic practice. Ann Emerg Med. 2000;35:11-16. doi:10.1016/s0196-0644(00)70099-0
- Todd KH, Samaroo N, Hoffman JR. Ethnicity as a risk factor for inadequate emergency department analgesia. JAMA. 1993;269:1537-1539.
- Savage KT, Singh V, Patel ZS, et al. Pain management in hidradenitis suppurativa and a proposed treatment algorithm. J Am Acad Dermatol. 2021;85:187-199. doi:10.1016/j.jaad.2020.09.039
- Matusiak Ł, Szcze˛ch J, Kaaz K, et al. Clinical characteristics of pruritus and pain in patients with hidradenitis suppurativa. Acta Derm Venereol. 2018;98:191-194. doi:10.2340/00015555-2815
- Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations: part I: diagnosis, evaluation, and the use of complementary and procedural management. J Am Acad Dermatol. 2019;81:76-90. doi:10.1016/j.jaad.2019.02.067
- Walker EA, Gelfand MD, Gelfand AN, et al. The relationship of current psychiatric disorder to functional disability and distress in patients with inflammatory bowel disease. Gen Hosp Psychiatry. 1996;18:220-229. doi:10.1016/0163-8343(96)00036-9
- Phan K, Huo YR, Smith SD. Hidradenitis suppurativa and psychiatric comorbidities, suicides and substance abuse: systematic review and meta-analysis. Ann Transl Med. 2020;8:821. doi:10.21037/atm-20-1028
- Woo AK. Depression and anxiety in pain. Rev Pain. 2010;4:8-12. doi:10.1177/204946371000400103
- Iida H, Yamaguchi S, Goyagi T, et al. Consensus statement on smoking cessation in patients with pain. J Anesth. 2022;36:671-687. doi:10.1007/s00540-022-03097-w
- Krause AJ, Prather AA, Wager TD, et al. The pain of sleep loss: a brain characterization in humans. J Neurosci. 2019;39:2291-2300. doi:10.1523/JNEUROSCI.2408-18.2018
- Mundal I, Gråwe RW, Bjørngaard JH, et al. Prevalence and long-term predictors of persistent chronic widespread pain in the general population in an 11-year prospective study: the HUNT study. BMC Musculoskelet Disord. 2014;15:213. doi:10.1186/1471-2474-15-213
- Aubin H-J. Tolerability and safety of sustained-release bupropion in the management of smoking cessation. Drugs. 2002;(62 suppl 2):45-52. doi:10.2165/00003495-200262002-00005
- Shah TH, Moradimehr A. Bupropion for the treatment of neuropathic pain. Am J Hosp Palliat Care. 2010;27:333-336. doi:10.1177/1049909110361229
- Baune BT, Renger L. Pharmacological and non-pharmacological interventions to improve cognitive dysfunction and functional ability in clinical depression—a systematic review. Psychiatry Res. 2014;219:25-50. doi:10.1016/j.psychres.2014.05.013
- Walker PW, Cole JO, Gardner EA, et al. Improvement in fluoxetine-associated sexual dysfunction in patients switched to bupropion. J Clin Psychiatry. 1993;54:459-465.
- Sherman MM, Ungureanu S, Rey JA. Naltrexone/bupropion ER (contrave): newly approved treatment option for chronic weight management in obese adults. P T. 2016;41:164-172.
- Anderson JW, Greenway FL, Fujioka K, et al. Bupropion SR enhances weight loss: a 48-week double-blind, placebo-controlled trial. Obes Res. 2002;10:633-641. doi:10.1038/oby.2002.86
- Kalkhoran S, Benowitz NL, Rigotti NA. Prevention and treatment of tobacco use: JACC health promotion series. J Am Coll Cardiol. 2018;72:1030-1045. doi:10.1016/j.jacc.2018.06.036
- Singh D, Saadabadi A. Varenicline. StatPearls Publishing; 2023.
- Mazza M, Mazza O, Pazzaglia C, et al. Escitalopram 20 mg versus duloxetine 60 mg for the treatment of chronic low back pain. Expert Opin Pharmacother. 2010;11:1049-1052. doi:10.1517/14656561003730413
- Docherty MJ, Jones RCW, Wallace MS. Managing pain in inflammatory bowel disease. Gastroenterol Hepatol (N Y). 2011;7:592-601.
- Shrestha P, Fariba KA, Abdijadid S. Paroxetine. StatPearls Publishing; 2022.
- Williams LK, Padhukasahasram B, Ahmedani BK, et al. Differing effects of metformin on glycemic control by race-ethnicity. J Clin Endocrinol Metab. 2014;99:3160-3168. doi:10.1210/jc.2014-1539
- Sharma S, Mathur DK, Paliwal V, et al. Efficacy of metformin in the treatment of acne in women with polycystic ovarian syndrome: a newer approach to acne therapy. J Clin Aesthet Dermatol. 2019;12:34-38.
- Scheinfeld N. Hidradenitis suppurativa: a practical review of possible medical treatments based on over 350 hidradenitis patients. Dermatol Online J. 2013;19:1. doi:10.5070/D35VW402NF
- Baeza-Flores GDC, Guzmán-Priego CG, Parra-Flores LI, et al. Metformin: a prospective alternative for the treatment of chronic pain. Front Pharmacol. 2020;11:558474. doi:10.3389/fphar.2020.558474
Mammography breast density reporting: What it means for clinicians
This transcript has been edited for clarity.
Today, I’m going to talk about the 2023 Food and Drug Administration regulation that requires breast density to be reported on all mammogram results nationwide, and for that report to go to both clinicians and patients. Previously this was the rule in some states, but not in others. This is important because 40%-50% of women have dense breasts. I’m going to discuss what that means for you, and for our patients.
First
Breast density describes the appearance of the breast on mammography. Appearance varies on the basis of breast tissue composition, with fibroglandular tissue being more dense than fatty tissue. Breast density is important because it relates to both the risk for cancer and the ability of mammography to detect cancer.
Breast density is defined and classified according to the American College of Radiology’s BI-RADS four-category scale. Categories 1 and 2 refer to breast tissue that is not dense, accounting for about 50% of the population. Categories 3 and 4 describe heterogeneously dense and extremely dense breast tissue, which occur in approximately 40% and 50% of women, respectively. When speaking about dense breast tissue readings on mammography, we are referring to categories 3 and 4.
Women with dense breast tissue have an increased risk of developing breast cancer and are less likely to have early breast cancer detected on mammography.
Let’s go over the details by category:
For women in categories 1 and 2 (considered not dense breast tissue), the sensitivity of mammography for detecting early breast cancer is 80%-90%. In categories 3 and 4, the sensitivity of mammography drops to 60%-70%.
Compared with women with average breast density, the risk of developing breast cancer is 20% higher in women with BI-RADS category 3 breasts, and more than twice as high (relative risk, 2.1) in those with BI-RADS category 4 breasts. Thus, the risk of developing breast cancer is higher, but the sensitivity of the test is lower.
The clinical question is, what should we do about this? For women who have a normal mammogram with dense breasts, should follow-up testing be done, and if so, what test? The main follow-up testing options are either ultrasound or MRI, usually ultrasound. Additional testing will detect additional cancers that were not picked up on the initial mammogram and will also lead to additional biopsies for false-positive tests from the additional testing.
An American College of Gynecology and Obstetrics practice advisory nicely summarizes the evidence and clarifies that this decision is made in the context of a lack of published evidence demonstrating improved outcomes, specifically no reduction in breast cancer mortality, with supplemental testing. The official ACOG stance is that they “do not recommend routine use of alternative or adjunctive tests to screening mammography in women with dense breasts who are asymptomatic and have no additional risk factors.”
This is an area where it is important to understand the data. We are all going to be getting test results back that indicate level of breast density, and those test results will also be sent to our patients, so we are going to be asked about this by interested patients. Should this be something that we talk to patients about, utilizing shared decision-making to decide about whether follow-up testing is necessary in women with dense breasts? That is something each clinician will need to decide, and knowing the data is a critically important step in that decision.
Neil Skolnik, MD, is a professor, department of family medicine, at Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director, department of family medicine, Abington (Pennsylvania) Jefferson Health.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Today, I’m going to talk about the 2023 Food and Drug Administration regulation that requires breast density to be reported on all mammogram results nationwide, and for that report to go to both clinicians and patients. Previously this was the rule in some states, but not in others. This is important because 40%-50% of women have dense breasts. I’m going to discuss what that means for you, and for our patients.
First
Breast density describes the appearance of the breast on mammography. Appearance varies on the basis of breast tissue composition, with fibroglandular tissue being more dense than fatty tissue. Breast density is important because it relates to both the risk for cancer and the ability of mammography to detect cancer.
Breast density is defined and classified according to the American College of Radiology’s BI-RADS four-category scale. Categories 1 and 2 refer to breast tissue that is not dense, accounting for about 50% of the population. Categories 3 and 4 describe heterogeneously dense and extremely dense breast tissue, which occur in approximately 40% and 50% of women, respectively. When speaking about dense breast tissue readings on mammography, we are referring to categories 3 and 4.
Women with dense breast tissue have an increased risk of developing breast cancer and are less likely to have early breast cancer detected on mammography.
Let’s go over the details by category:
For women in categories 1 and 2 (considered not dense breast tissue), the sensitivity of mammography for detecting early breast cancer is 80%-90%. In categories 3 and 4, the sensitivity of mammography drops to 60%-70%.
Compared with women with average breast density, the risk of developing breast cancer is 20% higher in women with BI-RADS category 3 breasts, and more than twice as high (relative risk, 2.1) in those with BI-RADS category 4 breasts. Thus, the risk of developing breast cancer is higher, but the sensitivity of the test is lower.
The clinical question is, what should we do about this? For women who have a normal mammogram with dense breasts, should follow-up testing be done, and if so, what test? The main follow-up testing options are either ultrasound or MRI, usually ultrasound. Additional testing will detect additional cancers that were not picked up on the initial mammogram and will also lead to additional biopsies for false-positive tests from the additional testing.
An American College of Gynecology and Obstetrics practice advisory nicely summarizes the evidence and clarifies that this decision is made in the context of a lack of published evidence demonstrating improved outcomes, specifically no reduction in breast cancer mortality, with supplemental testing. The official ACOG stance is that they “do not recommend routine use of alternative or adjunctive tests to screening mammography in women with dense breasts who are asymptomatic and have no additional risk factors.”
This is an area where it is important to understand the data. We are all going to be getting test results back that indicate level of breast density, and those test results will also be sent to our patients, so we are going to be asked about this by interested patients. Should this be something that we talk to patients about, utilizing shared decision-making to decide about whether follow-up testing is necessary in women with dense breasts? That is something each clinician will need to decide, and knowing the data is a critically important step in that decision.
Neil Skolnik, MD, is a professor, department of family medicine, at Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director, department of family medicine, Abington (Pennsylvania) Jefferson Health.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Today, I’m going to talk about the 2023 Food and Drug Administration regulation that requires breast density to be reported on all mammogram results nationwide, and for that report to go to both clinicians and patients. Previously this was the rule in some states, but not in others. This is important because 40%-50% of women have dense breasts. I’m going to discuss what that means for you, and for our patients.
First
Breast density describes the appearance of the breast on mammography. Appearance varies on the basis of breast tissue composition, with fibroglandular tissue being more dense than fatty tissue. Breast density is important because it relates to both the risk for cancer and the ability of mammography to detect cancer.
Breast density is defined and classified according to the American College of Radiology’s BI-RADS four-category scale. Categories 1 and 2 refer to breast tissue that is not dense, accounting for about 50% of the population. Categories 3 and 4 describe heterogeneously dense and extremely dense breast tissue, which occur in approximately 40% and 50% of women, respectively. When speaking about dense breast tissue readings on mammography, we are referring to categories 3 and 4.
Women with dense breast tissue have an increased risk of developing breast cancer and are less likely to have early breast cancer detected on mammography.
Let’s go over the details by category:
For women in categories 1 and 2 (considered not dense breast tissue), the sensitivity of mammography for detecting early breast cancer is 80%-90%. In categories 3 and 4, the sensitivity of mammography drops to 60%-70%.
Compared with women with average breast density, the risk of developing breast cancer is 20% higher in women with BI-RADS category 3 breasts, and more than twice as high (relative risk, 2.1) in those with BI-RADS category 4 breasts. Thus, the risk of developing breast cancer is higher, but the sensitivity of the test is lower.
The clinical question is, what should we do about this? For women who have a normal mammogram with dense breasts, should follow-up testing be done, and if so, what test? The main follow-up testing options are either ultrasound or MRI, usually ultrasound. Additional testing will detect additional cancers that were not picked up on the initial mammogram and will also lead to additional biopsies for false-positive tests from the additional testing.
An American College of Gynecology and Obstetrics practice advisory nicely summarizes the evidence and clarifies that this decision is made in the context of a lack of published evidence demonstrating improved outcomes, specifically no reduction in breast cancer mortality, with supplemental testing. The official ACOG stance is that they “do not recommend routine use of alternative or adjunctive tests to screening mammography in women with dense breasts who are asymptomatic and have no additional risk factors.”
This is an area where it is important to understand the data. We are all going to be getting test results back that indicate level of breast density, and those test results will also be sent to our patients, so we are going to be asked about this by interested patients. Should this be something that we talk to patients about, utilizing shared decision-making to decide about whether follow-up testing is necessary in women with dense breasts? That is something each clinician will need to decide, and knowing the data is a critically important step in that decision.
Neil Skolnik, MD, is a professor, department of family medicine, at Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director, department of family medicine, Abington (Pennsylvania) Jefferson Health.
A version of this article first appeared on Medscape.com.
A toxic and fractured political system can breed angst and PTSD
As psychiatrists know, many of our severely traumatized adult patients were victims of abuse during childhood. We routinely ask every new patient about physical, emotional, or sexual abuse when they were growing up because of the well-established, serious neurobiological and mental repercussions.1,2
Perhaps one of the worst experiences for a child is to witness bitterly adversarial parents (their vital role models) who argue viciously, despise each other, and hurl insults (and even punches) at each other. Such a chronically and emotionally traumatic upbringing can haunt kids well into adulthood, disrupting their hypothalamic-pituitary-adrenal axis and triggering anxiety, depression, and even psychosis due to epigenetic changes that ultimately lead to abnormal brain development.3
It often feels that the governance of our country, or the national “political family,” is seriously fractured like a hopelessly dysfunctional family. Could that be negatively impacting the mental health of the citizenry? Having 2 antagonistic political parties expressing visceral hatred and undisguised contempt for each other 24/7 (thanks to the enabling era of cable TV, the internet, and social media) has transformed each party’s fanatic followers from fellow citizens to ideological combatants. In this poisonous societal zeitgeist of bidirectional acrimony and mutual detestation, the opposing parties and their “intellectual militias” label each other as “extremists” or “radicals.” They become completely blind to any redeeming social value in the ideas or principles of their political opponents. They spend enormous time and energy on undermining each other instead of attending to the myriad vital issues involved in the governance of a massive and complex country.
Winston Churchill said, “Democracy is the worst form of government, except for all the others that have been tried.”4 The current toxic cloud of intense “hyperpartisanship” is emblematic of the dark Machiavellian side of democracy. But those who lament the current distorted version of democracy should contemplate living in a dictatorship or totalitarian regime, where a despot would execute any dissenter or invade and destroy an adjacent country at a whim.
Churchill made that statement in 1947. The internet, social media, and smartphones were science fiction back then. Those technological advances have added fuel to the political process and significantly stoked the flames of hyperpartisanship. It’s now democracy on steroids, where freedom of expression goes to extremes, highlighting the warts and pitfalls of the democratic system. Political rivals can now communicate their ferocious disagreements to millions of their disciples instantaneously, triggering immediate rebuttals and counterattacks by their adversaries. This “virtual guerilla warfare” is mentally and emotionally exhausting to all involved, especially to the subset of neutral bystanders who are unaffiliated with either political party, which, due to the “religification” of politics, have become like secular religions.5 Chronic, unremitting, inescapable stress is a sure pathway for anxiety, depression, posttraumatic stress disorder, and even brain atrophy.
Optimists may point out that the United States has weathered and emerged stronger from many serious traumas, including the Civil War (with its lethal divisiveness), World War I, the deadly 1918 influenza pandemic, the Great Depression, Pearl Harbor, World War II, the Cold War, the Vietnam War, the Watergate political scandal, the 9/11 terrorist attacks, the banking collapse and recession, and most recently the COVID-19 pandemic, which brought society to a standstill and induced so much anxiety and uncertainty.
On the other hand, pessimists would insist those sequential crises left indelible scars that cumulatively altered the mindset of political rivals, predisposing them to extreme views of each other. Alienation inevitably leads to fanaticism. It’s perplexing but fascinating how the fierce bidirectional missives of weaponized ideas can be as virulent and destructive as a traditional physical war. Perhaps in this era, the pen is mightier than the sword after all.
Continue to: From a psychiatric perspective...
From a psychiatric perspective, the intransigent groupthink of political partisanship eerily resembles folie en masse, a psychiatric syndrome for which there is no established treatment. It has become a serious threat to our modern democracy. So I decided to ask the “know-it-all” artificial intelligence ChatGPT, whom I previously had “invited” to write a “guest editorial” about myths surrounding psychiatry,6 to answer 3 burning questions:
1. Is there toxic hyperpartisanship in the USA today? (Box 1)
Box 1
Yes, there is toxic hyperpartisanship in the United States today. Political polarization has been on the rise for several decades, and in recent years, it has become increasingly toxic and divisive. This toxic hyperpartisanship has contributed to a breakdown in civil discourse and a lack of cooperation and compromise in government.
The toxic hyperpartisanship is evident in many aspects of American society, including politics, media, and social media. Political leaders often engage in divisive rhetoric and focus on winning at all costs, rather than working towards solutions that benefit the country as a whole. Media outlets often present news in a partisan manner, further fueling political polarization. Social media platforms have also played a role in exacerbating toxic hyperpartisanship by allowing the spread of misinformation and creating echo chambers where people are only exposed to like-minded viewpoints.
The consequences of toxic hyperpartisanship are significant, as it can hinder progress on important issues and erode trust in institutions and government. It also makes it difficult for people to engage in productive dialogue and find common ground, leading to a lack of cooperation and compromise.
It is important for individuals to be aware of the impact of toxic hyperpartisanship and work towards finding ways to bridge the political divide and engage in constructive dialogue.
2. How can severe hyperpartisanship be corrected? (Supplemental Box 1)
Supplemental Box 1
Severe hyperpartisanship, characterized by intense and entrenched divisions between political parties, can be a challenging issue to address, but there are several steps that can be taken to work towards correcting it. Here are some potential approaches:
1. Promote civil discourse: Encourage respectful and constructive conversations between individuals with differing political views. This can be achieved through education programs, media campaigns, and initiatives to foster open dialogue.
2. Electoral reforms: Consider implementing electoral reforms that can reduce the influence of extreme partisanship. For example, ranked-choice voting or nonpartisan primaries may encourage candidates to appeal to a broader base of voters rather than just their party’s base.
3. Campaign finance reform: Limit the influence of money in politics, as it can exacerbate hyperpartisanship by allowing wealthy donors to have undue influence over candidates and parties.
4. Independent redistricting: Ensure that electoral district boundaries are drawn in a fair and nonpartisan manner. Gerrymandering, the manipulation of district lines to favor one party, can contribute to hyperpartisanship by creating “safe” districts where extreme candidates are more likely to be elected.
5. Promote media literacy: Encourage media literacy education to help citizens critically evaluate information sources and avoid echo chambers. A well-informed electorate is less susceptible to extreme partisanship.
6. Encourage bipartisan collaboration: Highlight and support instances of successful bipartisan collaboration. Elected officials who work across the aisle can serve as positive examples and encourage others to follow suit.
7. Address economic inequality: Tackling economic disparities can alleviate some of the underlying factors that contribute to polarization. When people feel economically secure, they may be more willing to seek common ground.
8. Civics education: Improve civics education in schools to foster a deeper understanding of democratic values, the political process, and the importance of civic engagement.
9. Leadership example: Encourage political leaders to model cooperation and compromise rather than relying on divisive rhetoric. Voters often take cues from their leaders’ behavior.
10. Promote third parties: Support and encourage the emergence of viable thirdparty candidates. A more diverse political landscape can provide alternatives to extreme partisanship.
11. Focus on common ground: Identify and prioritize issues where there is potential for bipartisan consensus and progress. Building success on these issues can create momentum for further cooperation.
12. Encourage grassroots activism: Support grassroots movements that seek to bridge divides and foster understanding between individuals and communities with different political perspectives.
It’s essential to recognize that addressing severe hyperpartisanship is a complex and long-term process that requires collective effort from citizens, political leaders, educators, and institutions. It won’t be achieved overnight, but through sustained and committed actions, progress can be made toward a more collaborative and less divisive political climate.
3. What can cause the collapse of a democracy? (Supplemental Box 2).
Supplemental Box 2
The collapse of a democracy can be a complex and multifaceted process, influenced by various factors and circumstances. Some of the common causes that can lead to the erosion or breakdown of a democratic system include:
1. Authoritarianism and power concentration: When leaders or institutions become increasingly authoritarian, centralizing power and weakening checks and balances, it can undermine democratic principles.
2. Corruption and lack of accountability: Rampant corruption among political leaders and institutions can erode public trust in the democratic system, leading to disillusionment and disengagement.
3. Economic instability: Prolonged economic crises or severe inequality can lead to social unrest, increasing the appeal of populist or extremist movements that may challenge democratic norms.
4. Weakening of rule of law: If the rule of law is weakened, and there is a lack of respect for judicial independence and constitutional principles, democratic institutions can become vulnerable to manipulation.
5. Erosion of civil liberties: Suppression of freedom of speech, media, assembly, and association can limit citizens’ ability to express their opinions and participate in the democratic process.
6. Polarization and divisive politics: Extreme political polarization and a breakdown of civil discourse can hinder cooperation and compromise essential for a functioning democracy.
7. External interference: Foreign intervention, propaganda, or cyberattacks can influence electoral processes and undermine democratic institutions.
8. Rise of populism and nationalism: Populist movements that challenge democratic norms, demonize minorities, or advocate for a strongman leadership can pose a threat to democracy.
9. Demographic and social shifts: Demographic changes and social tensions can exacerbate political divisions and weaken the fabric of democratic societies.
10. Lack of civic education and participation: A lack of civic education and low voter turnout can lead to reduced civic engagement and undermine the democratic process.
It is crucial to understand that no democracy is immune to these challenges, and the strength of a democratic system depends on the vigilance and engagement of its citizens, the integrity of its institutions, and the commitment to upholding democratic values. Safeguarding and strengthening democracy requires ongoing efforts to address these issues and protect the principles that underpin democratic governance.
Judge for yourself, but I believe the ChatGPT responses were spot-on.
1. Lippard ETC, Nemeroff CB. The devastating clinical consequences of child abuse and neglect: increased disease vulnerability and poor treatment response in mood disorders. Am J Psychiatry. 2023;180(8):548-564.
2. Nemeroff CB. Paradise lost: the neurobiological and clinical consequences of child abuse and neglect. Neuron. 2016;89(5):892-909.
3. Zhang ZZ, Moeckel C, Mustafa M, et al. The association of epigenetic age acceleration and depressive and anxiety symptom severity among children recently exposed to substantiated maltreatment. J Psychiatr Res. 2023;165:7-13.
4. International Churchill Society. The worst form of government. Accessed August 8, 2023. https://winstonchurchill.org/resources/quotes/the-worst-form-of-government/
5. Nasrallah HA. From ideology to articles of faith: the ‘religification’ of political beliefs. Current Psychiatry. 2021;20(7):4-5,19.
6. Nasrallah HA. A ‘guest editorial’ … generated by ChatGPT? Current Psychiatry. 2023;22(4):22:6-7.
As psychiatrists know, many of our severely traumatized adult patients were victims of abuse during childhood. We routinely ask every new patient about physical, emotional, or sexual abuse when they were growing up because of the well-established, serious neurobiological and mental repercussions.1,2
Perhaps one of the worst experiences for a child is to witness bitterly adversarial parents (their vital role models) who argue viciously, despise each other, and hurl insults (and even punches) at each other. Such a chronically and emotionally traumatic upbringing can haunt kids well into adulthood, disrupting their hypothalamic-pituitary-adrenal axis and triggering anxiety, depression, and even psychosis due to epigenetic changes that ultimately lead to abnormal brain development.3
It often feels that the governance of our country, or the national “political family,” is seriously fractured like a hopelessly dysfunctional family. Could that be negatively impacting the mental health of the citizenry? Having 2 antagonistic political parties expressing visceral hatred and undisguised contempt for each other 24/7 (thanks to the enabling era of cable TV, the internet, and social media) has transformed each party’s fanatic followers from fellow citizens to ideological combatants. In this poisonous societal zeitgeist of bidirectional acrimony and mutual detestation, the opposing parties and their “intellectual militias” label each other as “extremists” or “radicals.” They become completely blind to any redeeming social value in the ideas or principles of their political opponents. They spend enormous time and energy on undermining each other instead of attending to the myriad vital issues involved in the governance of a massive and complex country.
Winston Churchill said, “Democracy is the worst form of government, except for all the others that have been tried.”4 The current toxic cloud of intense “hyperpartisanship” is emblematic of the dark Machiavellian side of democracy. But those who lament the current distorted version of democracy should contemplate living in a dictatorship or totalitarian regime, where a despot would execute any dissenter or invade and destroy an adjacent country at a whim.
Churchill made that statement in 1947. The internet, social media, and smartphones were science fiction back then. Those technological advances have added fuel to the political process and significantly stoked the flames of hyperpartisanship. It’s now democracy on steroids, where freedom of expression goes to extremes, highlighting the warts and pitfalls of the democratic system. Political rivals can now communicate their ferocious disagreements to millions of their disciples instantaneously, triggering immediate rebuttals and counterattacks by their adversaries. This “virtual guerilla warfare” is mentally and emotionally exhausting to all involved, especially to the subset of neutral bystanders who are unaffiliated with either political party, which, due to the “religification” of politics, have become like secular religions.5 Chronic, unremitting, inescapable stress is a sure pathway for anxiety, depression, posttraumatic stress disorder, and even brain atrophy.
Optimists may point out that the United States has weathered and emerged stronger from many serious traumas, including the Civil War (with its lethal divisiveness), World War I, the deadly 1918 influenza pandemic, the Great Depression, Pearl Harbor, World War II, the Cold War, the Vietnam War, the Watergate political scandal, the 9/11 terrorist attacks, the banking collapse and recession, and most recently the COVID-19 pandemic, which brought society to a standstill and induced so much anxiety and uncertainty.
On the other hand, pessimists would insist those sequential crises left indelible scars that cumulatively altered the mindset of political rivals, predisposing them to extreme views of each other. Alienation inevitably leads to fanaticism. It’s perplexing but fascinating how the fierce bidirectional missives of weaponized ideas can be as virulent and destructive as a traditional physical war. Perhaps in this era, the pen is mightier than the sword after all.
Continue to: From a psychiatric perspective...
From a psychiatric perspective, the intransigent groupthink of political partisanship eerily resembles folie en masse, a psychiatric syndrome for which there is no established treatment. It has become a serious threat to our modern democracy. So I decided to ask the “know-it-all” artificial intelligence ChatGPT, whom I previously had “invited” to write a “guest editorial” about myths surrounding psychiatry,6 to answer 3 burning questions:
1. Is there toxic hyperpartisanship in the USA today? (Box 1)
Box 1
Yes, there is toxic hyperpartisanship in the United States today. Political polarization has been on the rise for several decades, and in recent years, it has become increasingly toxic and divisive. This toxic hyperpartisanship has contributed to a breakdown in civil discourse and a lack of cooperation and compromise in government.
The toxic hyperpartisanship is evident in many aspects of American society, including politics, media, and social media. Political leaders often engage in divisive rhetoric and focus on winning at all costs, rather than working towards solutions that benefit the country as a whole. Media outlets often present news in a partisan manner, further fueling political polarization. Social media platforms have also played a role in exacerbating toxic hyperpartisanship by allowing the spread of misinformation and creating echo chambers where people are only exposed to like-minded viewpoints.
The consequences of toxic hyperpartisanship are significant, as it can hinder progress on important issues and erode trust in institutions and government. It also makes it difficult for people to engage in productive dialogue and find common ground, leading to a lack of cooperation and compromise.
It is important for individuals to be aware of the impact of toxic hyperpartisanship and work towards finding ways to bridge the political divide and engage in constructive dialogue.
2. How can severe hyperpartisanship be corrected? (Supplemental Box 1)
Supplemental Box 1
Severe hyperpartisanship, characterized by intense and entrenched divisions between political parties, can be a challenging issue to address, but there are several steps that can be taken to work towards correcting it. Here are some potential approaches:
1. Promote civil discourse: Encourage respectful and constructive conversations between individuals with differing political views. This can be achieved through education programs, media campaigns, and initiatives to foster open dialogue.
2. Electoral reforms: Consider implementing electoral reforms that can reduce the influence of extreme partisanship. For example, ranked-choice voting or nonpartisan primaries may encourage candidates to appeal to a broader base of voters rather than just their party’s base.
3. Campaign finance reform: Limit the influence of money in politics, as it can exacerbate hyperpartisanship by allowing wealthy donors to have undue influence over candidates and parties.
4. Independent redistricting: Ensure that electoral district boundaries are drawn in a fair and nonpartisan manner. Gerrymandering, the manipulation of district lines to favor one party, can contribute to hyperpartisanship by creating “safe” districts where extreme candidates are more likely to be elected.
5. Promote media literacy: Encourage media literacy education to help citizens critically evaluate information sources and avoid echo chambers. A well-informed electorate is less susceptible to extreme partisanship.
6. Encourage bipartisan collaboration: Highlight and support instances of successful bipartisan collaboration. Elected officials who work across the aisle can serve as positive examples and encourage others to follow suit.
7. Address economic inequality: Tackling economic disparities can alleviate some of the underlying factors that contribute to polarization. When people feel economically secure, they may be more willing to seek common ground.
8. Civics education: Improve civics education in schools to foster a deeper understanding of democratic values, the political process, and the importance of civic engagement.
9. Leadership example: Encourage political leaders to model cooperation and compromise rather than relying on divisive rhetoric. Voters often take cues from their leaders’ behavior.
10. Promote third parties: Support and encourage the emergence of viable thirdparty candidates. A more diverse political landscape can provide alternatives to extreme partisanship.
11. Focus on common ground: Identify and prioritize issues where there is potential for bipartisan consensus and progress. Building success on these issues can create momentum for further cooperation.
12. Encourage grassroots activism: Support grassroots movements that seek to bridge divides and foster understanding between individuals and communities with different political perspectives.
It’s essential to recognize that addressing severe hyperpartisanship is a complex and long-term process that requires collective effort from citizens, political leaders, educators, and institutions. It won’t be achieved overnight, but through sustained and committed actions, progress can be made toward a more collaborative and less divisive political climate.
3. What can cause the collapse of a democracy? (Supplemental Box 2).
Supplemental Box 2
The collapse of a democracy can be a complex and multifaceted process, influenced by various factors and circumstances. Some of the common causes that can lead to the erosion or breakdown of a democratic system include:
1. Authoritarianism and power concentration: When leaders or institutions become increasingly authoritarian, centralizing power and weakening checks and balances, it can undermine democratic principles.
2. Corruption and lack of accountability: Rampant corruption among political leaders and institutions can erode public trust in the democratic system, leading to disillusionment and disengagement.
3. Economic instability: Prolonged economic crises or severe inequality can lead to social unrest, increasing the appeal of populist or extremist movements that may challenge democratic norms.
4. Weakening of rule of law: If the rule of law is weakened, and there is a lack of respect for judicial independence and constitutional principles, democratic institutions can become vulnerable to manipulation.
5. Erosion of civil liberties: Suppression of freedom of speech, media, assembly, and association can limit citizens’ ability to express their opinions and participate in the democratic process.
6. Polarization and divisive politics: Extreme political polarization and a breakdown of civil discourse can hinder cooperation and compromise essential for a functioning democracy.
7. External interference: Foreign intervention, propaganda, or cyberattacks can influence electoral processes and undermine democratic institutions.
8. Rise of populism and nationalism: Populist movements that challenge democratic norms, demonize minorities, or advocate for a strongman leadership can pose a threat to democracy.
9. Demographic and social shifts: Demographic changes and social tensions can exacerbate political divisions and weaken the fabric of democratic societies.
10. Lack of civic education and participation: A lack of civic education and low voter turnout can lead to reduced civic engagement and undermine the democratic process.
It is crucial to understand that no democracy is immune to these challenges, and the strength of a democratic system depends on the vigilance and engagement of its citizens, the integrity of its institutions, and the commitment to upholding democratic values. Safeguarding and strengthening democracy requires ongoing efforts to address these issues and protect the principles that underpin democratic governance.
Judge for yourself, but I believe the ChatGPT responses were spot-on.
As psychiatrists know, many of our severely traumatized adult patients were victims of abuse during childhood. We routinely ask every new patient about physical, emotional, or sexual abuse when they were growing up because of the well-established, serious neurobiological and mental repercussions.1,2
Perhaps one of the worst experiences for a child is to witness bitterly adversarial parents (their vital role models) who argue viciously, despise each other, and hurl insults (and even punches) at each other. Such a chronically and emotionally traumatic upbringing can haunt kids well into adulthood, disrupting their hypothalamic-pituitary-adrenal axis and triggering anxiety, depression, and even psychosis due to epigenetic changes that ultimately lead to abnormal brain development.3
It often feels that the governance of our country, or the national “political family,” is seriously fractured like a hopelessly dysfunctional family. Could that be negatively impacting the mental health of the citizenry? Having 2 antagonistic political parties expressing visceral hatred and undisguised contempt for each other 24/7 (thanks to the enabling era of cable TV, the internet, and social media) has transformed each party’s fanatic followers from fellow citizens to ideological combatants. In this poisonous societal zeitgeist of bidirectional acrimony and mutual detestation, the opposing parties and their “intellectual militias” label each other as “extremists” or “radicals.” They become completely blind to any redeeming social value in the ideas or principles of their political opponents. They spend enormous time and energy on undermining each other instead of attending to the myriad vital issues involved in the governance of a massive and complex country.
Winston Churchill said, “Democracy is the worst form of government, except for all the others that have been tried.”4 The current toxic cloud of intense “hyperpartisanship” is emblematic of the dark Machiavellian side of democracy. But those who lament the current distorted version of democracy should contemplate living in a dictatorship or totalitarian regime, where a despot would execute any dissenter or invade and destroy an adjacent country at a whim.
Churchill made that statement in 1947. The internet, social media, and smartphones were science fiction back then. Those technological advances have added fuel to the political process and significantly stoked the flames of hyperpartisanship. It’s now democracy on steroids, where freedom of expression goes to extremes, highlighting the warts and pitfalls of the democratic system. Political rivals can now communicate their ferocious disagreements to millions of their disciples instantaneously, triggering immediate rebuttals and counterattacks by their adversaries. This “virtual guerilla warfare” is mentally and emotionally exhausting to all involved, especially to the subset of neutral bystanders who are unaffiliated with either political party, which, due to the “religification” of politics, have become like secular religions.5 Chronic, unremitting, inescapable stress is a sure pathway for anxiety, depression, posttraumatic stress disorder, and even brain atrophy.
Optimists may point out that the United States has weathered and emerged stronger from many serious traumas, including the Civil War (with its lethal divisiveness), World War I, the deadly 1918 influenza pandemic, the Great Depression, Pearl Harbor, World War II, the Cold War, the Vietnam War, the Watergate political scandal, the 9/11 terrorist attacks, the banking collapse and recession, and most recently the COVID-19 pandemic, which brought society to a standstill and induced so much anxiety and uncertainty.
On the other hand, pessimists would insist those sequential crises left indelible scars that cumulatively altered the mindset of political rivals, predisposing them to extreme views of each other. Alienation inevitably leads to fanaticism. It’s perplexing but fascinating how the fierce bidirectional missives of weaponized ideas can be as virulent and destructive as a traditional physical war. Perhaps in this era, the pen is mightier than the sword after all.
Continue to: From a psychiatric perspective...
From a psychiatric perspective, the intransigent groupthink of political partisanship eerily resembles folie en masse, a psychiatric syndrome for which there is no established treatment. It has become a serious threat to our modern democracy. So I decided to ask the “know-it-all” artificial intelligence ChatGPT, whom I previously had “invited” to write a “guest editorial” about myths surrounding psychiatry,6 to answer 3 burning questions:
1. Is there toxic hyperpartisanship in the USA today? (Box 1)
Box 1
Yes, there is toxic hyperpartisanship in the United States today. Political polarization has been on the rise for several decades, and in recent years, it has become increasingly toxic and divisive. This toxic hyperpartisanship has contributed to a breakdown in civil discourse and a lack of cooperation and compromise in government.
The toxic hyperpartisanship is evident in many aspects of American society, including politics, media, and social media. Political leaders often engage in divisive rhetoric and focus on winning at all costs, rather than working towards solutions that benefit the country as a whole. Media outlets often present news in a partisan manner, further fueling political polarization. Social media platforms have also played a role in exacerbating toxic hyperpartisanship by allowing the spread of misinformation and creating echo chambers where people are only exposed to like-minded viewpoints.
The consequences of toxic hyperpartisanship are significant, as it can hinder progress on important issues and erode trust in institutions and government. It also makes it difficult for people to engage in productive dialogue and find common ground, leading to a lack of cooperation and compromise.
It is important for individuals to be aware of the impact of toxic hyperpartisanship and work towards finding ways to bridge the political divide and engage in constructive dialogue.
2. How can severe hyperpartisanship be corrected? (Supplemental Box 1)
Supplemental Box 1
Severe hyperpartisanship, characterized by intense and entrenched divisions between political parties, can be a challenging issue to address, but there are several steps that can be taken to work towards correcting it. Here are some potential approaches:
1. Promote civil discourse: Encourage respectful and constructive conversations between individuals with differing political views. This can be achieved through education programs, media campaigns, and initiatives to foster open dialogue.
2. Electoral reforms: Consider implementing electoral reforms that can reduce the influence of extreme partisanship. For example, ranked-choice voting or nonpartisan primaries may encourage candidates to appeal to a broader base of voters rather than just their party’s base.
3. Campaign finance reform: Limit the influence of money in politics, as it can exacerbate hyperpartisanship by allowing wealthy donors to have undue influence over candidates and parties.
4. Independent redistricting: Ensure that electoral district boundaries are drawn in a fair and nonpartisan manner. Gerrymandering, the manipulation of district lines to favor one party, can contribute to hyperpartisanship by creating “safe” districts where extreme candidates are more likely to be elected.
5. Promote media literacy: Encourage media literacy education to help citizens critically evaluate information sources and avoid echo chambers. A well-informed electorate is less susceptible to extreme partisanship.
6. Encourage bipartisan collaboration: Highlight and support instances of successful bipartisan collaboration. Elected officials who work across the aisle can serve as positive examples and encourage others to follow suit.
7. Address economic inequality: Tackling economic disparities can alleviate some of the underlying factors that contribute to polarization. When people feel economically secure, they may be more willing to seek common ground.
8. Civics education: Improve civics education in schools to foster a deeper understanding of democratic values, the political process, and the importance of civic engagement.
9. Leadership example: Encourage political leaders to model cooperation and compromise rather than relying on divisive rhetoric. Voters often take cues from their leaders’ behavior.
10. Promote third parties: Support and encourage the emergence of viable thirdparty candidates. A more diverse political landscape can provide alternatives to extreme partisanship.
11. Focus on common ground: Identify and prioritize issues where there is potential for bipartisan consensus and progress. Building success on these issues can create momentum for further cooperation.
12. Encourage grassroots activism: Support grassroots movements that seek to bridge divides and foster understanding between individuals and communities with different political perspectives.
It’s essential to recognize that addressing severe hyperpartisanship is a complex and long-term process that requires collective effort from citizens, political leaders, educators, and institutions. It won’t be achieved overnight, but through sustained and committed actions, progress can be made toward a more collaborative and less divisive political climate.
3. What can cause the collapse of a democracy? (Supplemental Box 2).
Supplemental Box 2
The collapse of a democracy can be a complex and multifaceted process, influenced by various factors and circumstances. Some of the common causes that can lead to the erosion or breakdown of a democratic system include:
1. Authoritarianism and power concentration: When leaders or institutions become increasingly authoritarian, centralizing power and weakening checks and balances, it can undermine democratic principles.
2. Corruption and lack of accountability: Rampant corruption among political leaders and institutions can erode public trust in the democratic system, leading to disillusionment and disengagement.
3. Economic instability: Prolonged economic crises or severe inequality can lead to social unrest, increasing the appeal of populist or extremist movements that may challenge democratic norms.
4. Weakening of rule of law: If the rule of law is weakened, and there is a lack of respect for judicial independence and constitutional principles, democratic institutions can become vulnerable to manipulation.
5. Erosion of civil liberties: Suppression of freedom of speech, media, assembly, and association can limit citizens’ ability to express their opinions and participate in the democratic process.
6. Polarization and divisive politics: Extreme political polarization and a breakdown of civil discourse can hinder cooperation and compromise essential for a functioning democracy.
7. External interference: Foreign intervention, propaganda, or cyberattacks can influence electoral processes and undermine democratic institutions.
8. Rise of populism and nationalism: Populist movements that challenge democratic norms, demonize minorities, or advocate for a strongman leadership can pose a threat to democracy.
9. Demographic and social shifts: Demographic changes and social tensions can exacerbate political divisions and weaken the fabric of democratic societies.
10. Lack of civic education and participation: A lack of civic education and low voter turnout can lead to reduced civic engagement and undermine the democratic process.
It is crucial to understand that no democracy is immune to these challenges, and the strength of a democratic system depends on the vigilance and engagement of its citizens, the integrity of its institutions, and the commitment to upholding democratic values. Safeguarding and strengthening democracy requires ongoing efforts to address these issues and protect the principles that underpin democratic governance.
Judge for yourself, but I believe the ChatGPT responses were spot-on.
1. Lippard ETC, Nemeroff CB. The devastating clinical consequences of child abuse and neglect: increased disease vulnerability and poor treatment response in mood disorders. Am J Psychiatry. 2023;180(8):548-564.
2. Nemeroff CB. Paradise lost: the neurobiological and clinical consequences of child abuse and neglect. Neuron. 2016;89(5):892-909.
3. Zhang ZZ, Moeckel C, Mustafa M, et al. The association of epigenetic age acceleration and depressive and anxiety symptom severity among children recently exposed to substantiated maltreatment. J Psychiatr Res. 2023;165:7-13.
4. International Churchill Society. The worst form of government. Accessed August 8, 2023. https://winstonchurchill.org/resources/quotes/the-worst-form-of-government/
5. Nasrallah HA. From ideology to articles of faith: the ‘religification’ of political beliefs. Current Psychiatry. 2021;20(7):4-5,19.
6. Nasrallah HA. A ‘guest editorial’ … generated by ChatGPT? Current Psychiatry. 2023;22(4):22:6-7.
1. Lippard ETC, Nemeroff CB. The devastating clinical consequences of child abuse and neglect: increased disease vulnerability and poor treatment response in mood disorders. Am J Psychiatry. 2023;180(8):548-564.
2. Nemeroff CB. Paradise lost: the neurobiological and clinical consequences of child abuse and neglect. Neuron. 2016;89(5):892-909.
3. Zhang ZZ, Moeckel C, Mustafa M, et al. The association of epigenetic age acceleration and depressive and anxiety symptom severity among children recently exposed to substantiated maltreatment. J Psychiatr Res. 2023;165:7-13.
4. International Churchill Society. The worst form of government. Accessed August 8, 2023. https://winstonchurchill.org/resources/quotes/the-worst-form-of-government/
5. Nasrallah HA. From ideology to articles of faith: the ‘religification’ of political beliefs. Current Psychiatry. 2021;20(7):4-5,19.
6. Nasrallah HA. A ‘guest editorial’ … generated by ChatGPT? Current Psychiatry. 2023;22(4):22:6-7.
