Commentary

Changing behavior is hard. And at nearly every clinical encounter, we counsel/encourage/remind/help (choose a verb) our patients to make a change—to do something hard. We tell them they need to increase their physical activity, get more sleep, or alter their eating habits. We know that if they make the needed changes, they can improve their health and possibly lengthen their lives. But we also know (from the systematic reviews the US Preventive Services Task Force [USPSTF] uses to make its recommendations) that brief counseling in our offices is largely ineffective unless we connect patients to resources to support the recommended change.

As examples, the USPSTF currently recommends the following (both grade “B”):

• offer or refer adults with cardiovascular disease risk factors to behavioral counseling interventions to promote a healthy diet and physical activity.¹
• offer or refer adults with a body mass index of 30 or higher to intensive, multicomponent behavioral interventions.²

This 2-step rule is tech-free and can be applied by patients in a few seconds to make healthier food choices.

To support our patients when making recommendations such as these, we might refer them to a dietitian for intensive counseling and meal-planning guidance. The American Diabetes Association says that patients seeking to manage their diabetes and prediabetes “can start by working with a registered dietitian nutritionist … to make an eating plan that works for [them].”³ However, this kind of resource is unavailable to many of our patients.

So what else can we do?

We can help patients decide what to buy in the grocery aisle. Nutrition labels are useful, but they are limited by their complexity and requisite level of health literacy.⁴ Even the concept of “calories” is not so intuitive. This challenge with interpreting calories led me (in some of my prior work) to explore a potentially more useful approach: conveying calorie information as physical activity equivalents.⁵

In this issue of The Journal of Family Practice, Dong and colleagues present their findings on whether a simple equation (the Altman Rule) that uses information on nutrition labels may be a reasonable proxy for an even more difficult concept—­glycemic load.⁶ The idea is that consumers (eg, patients with diabetes) can use this rule to help them in their decision-making at the grocery store (or the convenience store or gas station, for that matter, where the high-glycemic-load carbohydrates may be even more tempting). The 2-step rule is tech-free and can be applied in a few seconds. Their research demonstrated that the rule is a reasonable proxy for glycemic load for packaged carbohydrates (eg, chips, cereals, crackers, granola bars). Caveats acknowledged, foods that meet the rule are likely to be healthier choices.

Looking ahead, I would like to see whether counseling patients about the Altman Rule leads to their use of it, and how that translates into healthier eating, lower A1C, and ideally better health. For now, the Altman Rule is worth learning about. It may serve as another tool that you can use to support your patients when you ask them to do the hard work of making healthier food choices. 

Changing behavior is hard. And at nearly every clinical encounter, we counsel/encourage/remind/help (choose a verb) our patients to make a change—to do something hard. We tell them they need to increase their physical activity, get more sleep, or alter their eating habits. We know that if they make the needed changes, they can improve their health and possibly lengthen their lives. But we also know (from the systematic reviews the US Preventive Services Task Force [USPSTF] uses to make its recommendations) that brief counseling in our offices is largely ineffective unless we connect patients to resources to support the recommended change.

As examples, the USPSTF currently recommends the following (both grade “B”):

• offer or refer adults with cardiovascular disease risk factors to behavioral counseling interventions to promote a healthy diet and physical activity.¹
• offer or refer adults with a body mass index of 30 or higher to intensive, multicomponent behavioral interventions.²

This 2-step rule is tech-free and can be applied by patients in a few seconds to make healthier food choices.

To support our patients when making recommendations such as these, we might refer them to a dietitian for intensive counseling and meal-planning guidance. The American Diabetes Association says that patients seeking to manage their diabetes and prediabetes “can start by working with a registered dietitian nutritionist … to make an eating plan that works for [them].”³ However, this kind of resource is unavailable to many of our patients.

So what else can we do?

We can help patients decide what to buy in the grocery aisle. Nutrition labels are useful, but they are limited by their complexity and requisite level of health literacy.⁴ Even the concept of “calories” is not so intuitive. This challenge with interpreting calories led me (in some of my prior work) to explore a potentially more useful approach: conveying calorie information as physical activity equivalents.⁵

In this issue of The Journal of Family Practice, Dong and colleagues present their findings on whether a simple equation (the Altman Rule) that uses information on nutrition labels may be a reasonable proxy for an even more difficult concept—­glycemic load.⁶ The idea is that consumers (eg, patients with diabetes) can use this rule to help them in their decision-making at the grocery store (or the convenience store or gas station, for that matter, where the high-glycemic-load carbohydrates may be even more tempting). The 2-step rule is tech-free and can be applied in a few seconds. Their research demonstrated that the rule is a reasonable proxy for glycemic load for packaged carbohydrates (eg, chips, cereals, crackers, granola bars). Caveats acknowledged, foods that meet the rule are likely to be healthier choices.

Looking ahead, I would like to see whether counseling patients about the Altman Rule leads to their use of it, and how that translates into healthier eating, lower A1C, and ideally better health. For now, the Altman Rule is worth learning about. It may serve as another tool that you can use to support your patients when you ask them to do the hard work of making healthier food choices. 

Changing behavior is hard. And at nearly every clinical encounter, we counsel/encourage/remind/help (choose a verb) our patients to make a change—to do something hard. We tell them they need to increase their physical activity, get more sleep, or alter their eating habits. We know that if they make the needed changes, they can improve their health and possibly lengthen their lives. But we also know (from the systematic reviews the US Preventive Services Task Force [USPSTF] uses to make its recommendations) that brief counseling in our offices is largely ineffective unless we connect patients to resources to support the recommended change.

As examples, the USPSTF currently recommends the following (both grade “B”):

• offer or refer adults with cardiovascular disease risk factors to behavioral counseling interventions to promote a healthy diet and physical activity.¹
• offer or refer adults with a body mass index of 30 or higher to intensive, multicomponent behavioral interventions.²

This 2-step rule is tech-free and can be applied by patients in a few seconds to make healthier food choices.

To support our patients when making recommendations such as these, we might refer them to a dietitian for intensive counseling and meal-planning guidance. The American Diabetes Association says that patients seeking to manage their diabetes and prediabetes “can start by working with a registered dietitian nutritionist … to make an eating plan that works for [them].”³ However, this kind of resource is unavailable to many of our patients.

So what else can we do?

We can help patients decide what to buy in the grocery aisle. Nutrition labels are useful, but they are limited by their complexity and requisite level of health literacy.⁴ Even the concept of “calories” is not so intuitive. This challenge with interpreting calories led me (in some of my prior work) to explore a potentially more useful approach: conveying calorie information as physical activity equivalents.⁵

In this issue of The Journal of Family Practice, Dong and colleagues present their findings on whether a simple equation (the Altman Rule) that uses information on nutrition labels may be a reasonable proxy for an even more difficult concept—­glycemic load.⁶ The idea is that consumers (eg, patients with diabetes) can use this rule to help them in their decision-making at the grocery store (or the convenience store or gas station, for that matter, where the high-glycemic-load carbohydrates may be even more tempting). The 2-step rule is tech-free and can be applied in a few seconds. Their research demonstrated that the rule is a reasonable proxy for glycemic load for packaged carbohydrates (eg, chips, cereals, crackers, granola bars). Caveats acknowledged, foods that meet the rule are likely to be healthier choices.

Looking ahead, I would like to see whether counseling patients about the Altman Rule leads to their use of it, and how that translates into healthier eating, lower A1C, and ideally better health. For now, the Altman Rule is worth learning about. It may serve as another tool that you can use to support your patients when you ask them to do the hard work of making healthier food choices. 

This transcript has been edited for clarity.

If you’re anywhere near Seattle, anywhere near Florida, or anywhere where it might be not oppressively hot outside but encouraging some people who might want to go out and get a little exercise, you’ve undoubtedly seen or heard of pickleball.

This took off, I think, out of Bainbridge Island, Wash. It was meant as a gentlemanly game where people didn’t exert themselves too much. The joke is you could play it while holding a drink in one hand. It’s gotten more popular and more competitive. It’s kind of a miniature version of tennis, with a smaller court, a plastic ball, and a wooden paddle. The ball can go back and forth rapidly, but you’re always playing doubles and it doesn’t take as much energy, exertion, and, if you will, fitness as a game like singles tennis.

Pickleball has a downside. The upside is it’s gotten many people outdoors getting some exercise and socializing. That’s all to the good. But a recent study suggested that there are about $500 million worth of injuries coming into the health care system associated with pickleball. There have been leg sprains, broken bones, people getting hit in the eye, hamstring pulls, and many other problems. I’ve been told that many of the spectators who show up for pickleball matches are there with a cast or have some kind of a wrap on because they were injured.

Well, many people have argued in the past about what we are going to do about health care costs. Some suggest if you voluntarily incur health care damage, you ought to pay for that yourself and you ought to have a big copay.

If you decide you’re going to do cross-country skiing or downhill skiing and you injure yourself, you chose to do it, so you pay. If you’re not going to maintain your weight, you’re going to smoke, or you’re going to ride around without a helmet, that’s your choice. You ought to pay.

I think the pickleball example is really a good challenge to these views. You obviously want people to go out and get some exercise. Here, we’re talking about a population that’s a little older and oftentimes doesn’t get out there as much as doctors would like to get the exercise that’s still important that they need, and yet it does incur injuries and problems.

My suggestion would be to make the game a little safer. Let’s try to encourage people to warm up more before they get out there and jump out of the car and engage in their pickleball battles. Goggles might be important to prevent the eye injuries in a game that’s played up close. Maybe we want to make sure that people look out for one another out there. If they think they’re getting dehydrated or tired, they should say, “Let’s sit down.”

I’m not willing to put a tax or a copay on the pickleball players of America. I know they choose to do it. It’s got an upside and benefits, as many things like skiing and other behaviors that have some risk do, but I think we want to be encouraging, not discouraging, of it.

I don’t like a society where anybody who tries to do something that takes risk winds up bearing extra cost for doing that. I understand that that gets people irritated when it comes to dangerous, hyper-risky behavior like smoking and not wearing a motorcycle helmet. I think the way to engage is not to call out the sinner or to try and punish those who are trying to do things that bring them enjoyment, reward, or in some of these cases, physical fitness, but to try to make things safer and try to gradually improve and get rid of the risk side to capture the full benefit side.

I’m not sure I’ve come up with all the best ways to make pickleball safer, but I think that’s where our thinking in health care should go. My view is to get out there and play pickleball. If you do pull your hamstring, raise my insurance premium a little bit. I’ll help to pay for it. Better you get some enjoyment and some exercise.

I get the downside, but come on, folks, we ought to be, as a community, somewhat supportive of the fun and recreation that our fellow citizens engage in.
 

Dr. Caplan is director, division of medical ethics, New York University Langone Medical Center. He disclosed serving as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position); and as a contributing author and adviser for Medscape.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

If you’re anywhere near Seattle, anywhere near Florida, or anywhere where it might be not oppressively hot outside but encouraging some people who might want to go out and get a little exercise, you’ve undoubtedly seen or heard of pickleball.

This took off, I think, out of Bainbridge Island, Wash. It was meant as a gentlemanly game where people didn’t exert themselves too much. The joke is you could play it while holding a drink in one hand. It’s gotten more popular and more competitive. It’s kind of a miniature version of tennis, with a smaller court, a plastic ball, and a wooden paddle. The ball can go back and forth rapidly, but you’re always playing doubles and it doesn’t take as much energy, exertion, and, if you will, fitness as a game like singles tennis.

Pickleball has a downside. The upside is it’s gotten many people outdoors getting some exercise and socializing. That’s all to the good. But a recent study suggested that there are about $500 million worth of injuries coming into the health care system associated with pickleball. There have been leg sprains, broken bones, people getting hit in the eye, hamstring pulls, and many other problems. I’ve been told that many of the spectators who show up for pickleball matches are there with a cast or have some kind of a wrap on because they were injured.

Well, many people have argued in the past about what we are going to do about health care costs. Some suggest if you voluntarily incur health care damage, you ought to pay for that yourself and you ought to have a big copay.

If you decide you’re going to do cross-country skiing or downhill skiing and you injure yourself, you chose to do it, so you pay. If you’re not going to maintain your weight, you’re going to smoke, or you’re going to ride around without a helmet, that’s your choice. You ought to pay.

I think the pickleball example is really a good challenge to these views. You obviously want people to go out and get some exercise. Here, we’re talking about a population that’s a little older and oftentimes doesn’t get out there as much as doctors would like to get the exercise that’s still important that they need, and yet it does incur injuries and problems.

My suggestion would be to make the game a little safer. Let’s try to encourage people to warm up more before they get out there and jump out of the car and engage in their pickleball battles. Goggles might be important to prevent the eye injuries in a game that’s played up close. Maybe we want to make sure that people look out for one another out there. If they think they’re getting dehydrated or tired, they should say, “Let’s sit down.”

I’m not willing to put a tax or a copay on the pickleball players of America. I know they choose to do it. It’s got an upside and benefits, as many things like skiing and other behaviors that have some risk do, but I think we want to be encouraging, not discouraging, of it.

I don’t like a society where anybody who tries to do something that takes risk winds up bearing extra cost for doing that. I understand that that gets people irritated when it comes to dangerous, hyper-risky behavior like smoking and not wearing a motorcycle helmet. I think the way to engage is not to call out the sinner or to try and punish those who are trying to do things that bring them enjoyment, reward, or in some of these cases, physical fitness, but to try to make things safer and try to gradually improve and get rid of the risk side to capture the full benefit side.

I’m not sure I’ve come up with all the best ways to make pickleball safer, but I think that’s where our thinking in health care should go. My view is to get out there and play pickleball. If you do pull your hamstring, raise my insurance premium a little bit. I’ll help to pay for it. Better you get some enjoyment and some exercise.

I get the downside, but come on, folks, we ought to be, as a community, somewhat supportive of the fun and recreation that our fellow citizens engage in.
 

Dr. Caplan is director, division of medical ethics, New York University Langone Medical Center. He disclosed serving as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position); and as a contributing author and adviser for Medscape.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

If you’re anywhere near Seattle, anywhere near Florida, or anywhere where it might be not oppressively hot outside but encouraging some people who might want to go out and get a little exercise, you’ve undoubtedly seen or heard of pickleball.

This took off, I think, out of Bainbridge Island, Wash. It was meant as a gentlemanly game where people didn’t exert themselves too much. The joke is you could play it while holding a drink in one hand. It’s gotten more popular and more competitive. It’s kind of a miniature version of tennis, with a smaller court, a plastic ball, and a wooden paddle. The ball can go back and forth rapidly, but you’re always playing doubles and it doesn’t take as much energy, exertion, and, if you will, fitness as a game like singles tennis.

Pickleball has a downside. The upside is it’s gotten many people outdoors getting some exercise and socializing. That’s all to the good. But a recent study suggested that there are about $500 million worth of injuries coming into the health care system associated with pickleball. There have been leg sprains, broken bones, people getting hit in the eye, hamstring pulls, and many other problems. I’ve been told that many of the spectators who show up for pickleball matches are there with a cast or have some kind of a wrap on because they were injured.

Well, many people have argued in the past about what we are going to do about health care costs. Some suggest if you voluntarily incur health care damage, you ought to pay for that yourself and you ought to have a big copay.

If you decide you’re going to do cross-country skiing or downhill skiing and you injure yourself, you chose to do it, so you pay. If you’re not going to maintain your weight, you’re going to smoke, or you’re going to ride around without a helmet, that’s your choice. You ought to pay.

I think the pickleball example is really a good challenge to these views. You obviously want people to go out and get some exercise. Here, we’re talking about a population that’s a little older and oftentimes doesn’t get out there as much as doctors would like to get the exercise that’s still important that they need, and yet it does incur injuries and problems.

My suggestion would be to make the game a little safer. Let’s try to encourage people to warm up more before they get out there and jump out of the car and engage in their pickleball battles. Goggles might be important to prevent the eye injuries in a game that’s played up close. Maybe we want to make sure that people look out for one another out there. If they think they’re getting dehydrated or tired, they should say, “Let’s sit down.”

I’m not willing to put a tax or a copay on the pickleball players of America. I know they choose to do it. It’s got an upside and benefits, as many things like skiing and other behaviors that have some risk do, but I think we want to be encouraging, not discouraging, of it.

I don’t like a society where anybody who tries to do something that takes risk winds up bearing extra cost for doing that. I understand that that gets people irritated when it comes to dangerous, hyper-risky behavior like smoking and not wearing a motorcycle helmet. I think the way to engage is not to call out the sinner or to try and punish those who are trying to do things that bring them enjoyment, reward, or in some of these cases, physical fitness, but to try to make things safer and try to gradually improve and get rid of the risk side to capture the full benefit side.

I’m not sure I’ve come up with all the best ways to make pickleball safer, but I think that’s where our thinking in health care should go. My view is to get out there and play pickleball. If you do pull your hamstring, raise my insurance premium a little bit. I’ll help to pay for it. Better you get some enjoyment and some exercise.

I get the downside, but come on, folks, we ought to be, as a community, somewhat supportive of the fun and recreation that our fellow citizens engage in.
 

Dr. Caplan is director, division of medical ethics, New York University Langone Medical Center. He disclosed serving as a director, officer, partner, employee, adviser, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position); and as a contributing author and adviser for Medscape.

A version of this article appeared on Medscape.com.

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.

Eva Ritvo

“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.

There has never been a better time to be (or become!) a mental health professional. 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.

Eva Ritvo

“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.

There has never been a better time to be (or become!) a mental health professional. 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.

Eva Ritvo

“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.

There has never been a better time to be (or become!) a mental health professional. 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.

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.

JAMA Internal Medicine

JAMA Internal Medicine

Dr. Wilson

JAMA Internal Medicine

JAMA Internal Medicine

JAMA Internal Medicine

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.

JAMA Internal Medicine

JAMA Internal Medicine

Dr. Wilson

JAMA Internal Medicine

JAMA Internal Medicine

JAMA Internal Medicine

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.

JAMA Internal Medicine

JAMA Internal Medicine

Dr. Wilson

JAMA Internal Medicine

JAMA Internal Medicine

JAMA Internal Medicine

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.

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, the field of psychiatry is seemingly doubling down on efforts to predict and prevent suicide deaths, and the way it is doing so has very questionable validity.

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, the field of psychiatry is seemingly doubling down on efforts to predict and prevent suicide deaths, and the way it is doing so has very questionable validity.

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, the field of psychiatry is seemingly doubling down on efforts to predict and prevent suicide deaths, and the way it is doing so has very questionable validity.

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 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.¹The focus of this column is to provide an update on the use of almonds and almond oil for skincare since covering the topic in July 2014.

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 dermnews@mdedge.com.

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.¹The focus of this column is to provide an update on the use of almonds and almond oil for skincare since covering the topic in July 2014.

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 dermnews@mdedge.com.

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.¹The focus of this column is to provide an update on the use of almonds and almond oil for skincare since covering the topic in July 2014.

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 dermnews@mdedge.com.

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.
 

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. It is well known that ADHD is a leading cause of binge-eating tendencies. So, what is the link between these two seemingly unrelated disorders?

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. It is well known that ADHD is a leading cause of binge-eating tendencies. So, what is the link between these two seemingly unrelated disorders?

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. It is well known that ADHD is a leading cause of binge-eating tendencies. So, what is the link between these two seemingly unrelated disorders?

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.

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.

FRAIL-AF clearly shows how cautious we should be in applying evidence gathered in younger, healthier patients to older, more vulnerable patients. 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.

FRAIL-AF clearly shows how cautious we should be in applying evidence gathered in younger, healthier patients to older, more vulnerable patients. 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.

FRAIL-AF clearly shows how cautious we should be in applying evidence gathered in younger, healthier patients to older, more vulnerable patients. 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.

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. It’s a case of internal decapitation that has generated a lot of news around the world because it happened to a young boy. 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.

Hadassah Medical Center

Hadassah Medical Center

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. It’s a case of internal decapitation that has generated a lot of news around the world because it happened to a young boy. 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.

Hadassah Medical Center

Hadassah Medical Center

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. It’s a case of internal decapitation that has generated a lot of news around the world because it happened to a young boy. 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.

Hadassah Medical Center

Hadassah Medical Center

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