Opinion

Since the November 2022 release of a much-discussed artificial intelligence (AI)-based chatbot, I have been curious what all the buzz is about. I decided to engage my well-connected software-savvy son-in-law to hear where he thought things were going.

He started by suggesting that I pose a question to the chatbot about something of which I had some current knowledge. I had recently researched the concept of primal beliefs and so we asked the chatbot to write a short essay about when an individual develops his/her primal beliefs.

In a matter of seconds the “machine” spit out a very readable document that included all the information that had taken me several hours to unearth and digest. And ... it included the references that I had determined to be valid and appropriate. It was an impressive performance to say the least.

Obviously, a technological development with this capability is sending tremors through the educational establishment. One can easily think of several human skills that an AI like this might eventually make superfluous. It will also make it increasingly difficult for educators to determine a students’ true abilities – research, synthesis, and writing to name just a few. But, of course, one could question whether we will need to teach and then test for these skills that the chatbot can perform more quickly. I’m going to leave it to the educators to struggle with that question.

In the long term you and I may find that AI is a serious threat to our existence as health care providers. In the meantime I’ve decided to focus on how we in primary care can take advantage of the wonders of the current AI technology.

My first thought is that if I were having trouble arriving at a diagnosis, I might appreciate having a chatbot to ask for help. Of course this would require that I had already taken a history, done a good exam, and ordered some obvious lab and imaging studies. It would also mean that I had decent knowledge and understanding of basic pathophysiology and was capable of thinking broadly enough to ask a question that would give me the greatest chance of getting the correct answer.

Knowing how to ask the right question is a skill that can be taught. For example, my wife is a successful and experienced online shopper but she acknowledges that when we have medical questions, I can often find the answer more quickly than she can. My relative success usually hinges on my choice of the key word(s) to begin the search, clearly the result of my medical training.

Once I have received a list of possible diagnoses from the chatbot, I must then be able to evaluate the validity and applicability of the references it has supplied. That too is a skill that can be taught. And, for the moment the critical importance of having these two skills suggests that graduating from medical school will continue to give us some job security in the face of expanding AI.

The same process I could used to coax the chatbot to arrive at a diagnosis could be applied when faced with a therapeutic question. Is surgery better than a pharmacological approach? If I need help with a dosage regimen, I could find this information online now. But, wouldn’t it be quicker and maybe better if I asked the chatbot to do the research for me and print a short essay on the pros and cons of different management approaches?

Once I’ve made the diagnosis, crafted a management plan, and now want to hand the patient a document in his/her primary language and at his/her reading skill level describing the diagnosis and giving detailed instructions to follow, this would seem to be a piece of cake for a chatbot given the appropriate commands. Hopefully I would remember to include the disclaimer that “This document was created with the help of a chatbot.”

Clearly, there is nothing to prevent our patients from asking the chatbot the same questions I have posed. And, no doubt, this will happen. It is already happening in a more cumbersome fashion when patients research their own symptoms. However, in the short term I believe we will retain the upper hand.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

Since the November 2022 release of a much-discussed artificial intelligence (AI)-based chatbot, I have been curious what all the buzz is about. I decided to engage my well-connected software-savvy son-in-law to hear where he thought things were going.

He started by suggesting that I pose a question to the chatbot about something of which I had some current knowledge. I had recently researched the concept of primal beliefs and so we asked the chatbot to write a short essay about when an individual develops his/her primal beliefs.

In a matter of seconds the “machine” spit out a very readable document that included all the information that had taken me several hours to unearth and digest. And ... it included the references that I had determined to be valid and appropriate. It was an impressive performance to say the least.

Obviously, a technological development with this capability is sending tremors through the educational establishment. One can easily think of several human skills that an AI like this might eventually make superfluous. It will also make it increasingly difficult for educators to determine a students’ true abilities – research, synthesis, and writing to name just a few. But, of course, one could question whether we will need to teach and then test for these skills that the chatbot can perform more quickly. I’m going to leave it to the educators to struggle with that question.

In the long term you and I may find that AI is a serious threat to our existence as health care providers. In the meantime I’ve decided to focus on how we in primary care can take advantage of the wonders of the current AI technology.

My first thought is that if I were having trouble arriving at a diagnosis, I might appreciate having a chatbot to ask for help. Of course this would require that I had already taken a history, done a good exam, and ordered some obvious lab and imaging studies. It would also mean that I had decent knowledge and understanding of basic pathophysiology and was capable of thinking broadly enough to ask a question that would give me the greatest chance of getting the correct answer.

Knowing how to ask the right question is a skill that can be taught. For example, my wife is a successful and experienced online shopper but she acknowledges that when we have medical questions, I can often find the answer more quickly than she can. My relative success usually hinges on my choice of the key word(s) to begin the search, clearly the result of my medical training.

Once I have received a list of possible diagnoses from the chatbot, I must then be able to evaluate the validity and applicability of the references it has supplied. That too is a skill that can be taught. And, for the moment the critical importance of having these two skills suggests that graduating from medical school will continue to give us some job security in the face of expanding AI.

The same process I could used to coax the chatbot to arrive at a diagnosis could be applied when faced with a therapeutic question. Is surgery better than a pharmacological approach? If I need help with a dosage regimen, I could find this information online now. But, wouldn’t it be quicker and maybe better if I asked the chatbot to do the research for me and print a short essay on the pros and cons of different management approaches?

Once I’ve made the diagnosis, crafted a management plan, and now want to hand the patient a document in his/her primary language and at his/her reading skill level describing the diagnosis and giving detailed instructions to follow, this would seem to be a piece of cake for a chatbot given the appropriate commands. Hopefully I would remember to include the disclaimer that “This document was created with the help of a chatbot.”

Clearly, there is nothing to prevent our patients from asking the chatbot the same questions I have posed. And, no doubt, this will happen. It is already happening in a more cumbersome fashion when patients research their own symptoms. However, in the short term I believe we will retain the upper hand.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

Since the November 2022 release of a much-discussed artificial intelligence (AI)-based chatbot, I have been curious what all the buzz is about. I decided to engage my well-connected software-savvy son-in-law to hear where he thought things were going.

He started by suggesting that I pose a question to the chatbot about something of which I had some current knowledge. I had recently researched the concept of primal beliefs and so we asked the chatbot to write a short essay about when an individual develops his/her primal beliefs.

In a matter of seconds the “machine” spit out a very readable document that included all the information that had taken me several hours to unearth and digest. And ... it included the references that I had determined to be valid and appropriate. It was an impressive performance to say the least.

Obviously, a technological development with this capability is sending tremors through the educational establishment. One can easily think of several human skills that an AI like this might eventually make superfluous. It will also make it increasingly difficult for educators to determine a students’ true abilities – research, synthesis, and writing to name just a few. But, of course, one could question whether we will need to teach and then test for these skills that the chatbot can perform more quickly. I’m going to leave it to the educators to struggle with that question.

In the long term you and I may find that AI is a serious threat to our existence as health care providers. In the meantime I’ve decided to focus on how we in primary care can take advantage of the wonders of the current AI technology.

My first thought is that if I were having trouble arriving at a diagnosis, I might appreciate having a chatbot to ask for help. Of course this would require that I had already taken a history, done a good exam, and ordered some obvious lab and imaging studies. It would also mean that I had decent knowledge and understanding of basic pathophysiology and was capable of thinking broadly enough to ask a question that would give me the greatest chance of getting the correct answer.

Knowing how to ask the right question is a skill that can be taught. For example, my wife is a successful and experienced online shopper but she acknowledges that when we have medical questions, I can often find the answer more quickly than she can. My relative success usually hinges on my choice of the key word(s) to begin the search, clearly the result of my medical training.

Once I have received a list of possible diagnoses from the chatbot, I must then be able to evaluate the validity and applicability of the references it has supplied. That too is a skill that can be taught. And, for the moment the critical importance of having these two skills suggests that graduating from medical school will continue to give us some job security in the face of expanding AI.

The same process I could used to coax the chatbot to arrive at a diagnosis could be applied when faced with a therapeutic question. Is surgery better than a pharmacological approach? If I need help with a dosage regimen, I could find this information online now. But, wouldn’t it be quicker and maybe better if I asked the chatbot to do the research for me and print a short essay on the pros and cons of different management approaches?

Once I’ve made the diagnosis, crafted a management plan, and now want to hand the patient a document in his/her primary language and at his/her reading skill level describing the diagnosis and giving detailed instructions to follow, this would seem to be a piece of cake for a chatbot given the appropriate commands. Hopefully I would remember to include the disclaimer that “This document was created with the help of a chatbot.”

Clearly, there is nothing to prevent our patients from asking the chatbot the same questions I have posed. And, no doubt, this will happen. It is already happening in a more cumbersome fashion when patients research their own symptoms. However, in the short term I believe we will retain the upper hand.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

The old man was restrained at the last moment from jumping off the hospital’s fifth floor atrium parapet. He was suffering from terminal cancer and had been racked with chronic, severe pain for months.

The consult recognized symptoms of depression arising from his continuous physical suffering, advising that a male aide be dispatched to sit with the man and that he be put on a regimen of 10 mg of methadone twice a day to alleviate the pain. The following day the man was calm; he no longer wanted to kill himself. He expressed a strong desire to go home, return to gardening, and to play with his grandchildren.

Dr. Behar

Most of the 47,000 suicides that occur in the United States every year are preventable.¹ Our national policy on this front has been nothing short of an abject failure. The government implemented a system with limited effect on completed suicides – a telephone hotline. This hotline is not called by the most common suicide victims: male, old, and quiet.²

The consequences of this national policy disaster have been profound, resulting in the biggest loss of productive years of life for any fatal condition.³ The grief experienced by the families of those who commit suicide is far greater than normal bereavement: The cause of death of their loved ones was not an unfortunate accident or a disease, it was an intentional act, and families take it personally.

One of the greatest achievements of psychiatry during the 20th century was the lowering of suicide rates in prisons by 70% with no treatment, no additional staffing, and no additional expenditures of funds. Today if inmates threaten suicide, they are immediately placed under eyesight supervision by guards. The federal pamphlet that describes this protocol was published in 1995 and is freely available online.⁴

Half of all suicide attempts are made by individuals who are legally drunk.⁵ Watch them for 6 hours and then ask them if they want to kill themselves and the response will almost invariably be “Of course not,” with the risk of further attempts dissipating in step with their blood alcohol level. The best resources to provide this kind of intervention are responsible adult family members, at no cost to the government. Indeed, in many cases family supervision is superior to that provided by a locked psychiatric ward with three staff members chasing after 20 agitated people all night long. The one-on-one attention that a family member can provide is free as well as far more personal and insightful, and more sincerely caring.

Guarantees in the field of medicine are rare. But, one such guarantee is that after their mood has improved, 100% of people will be thankful that they did not hurt themselves.⁶ This means that successful treatment will prevent 100% of all suicides.⁷ Not all treatments are successful, but 95% can be.⁸ At autopsy, few successful suicide victims have psychiatric medications in their system.⁹ The urge to kill oneself might best be characterized as a temporary chemical alteration of the brain causing delusional thoughts, including the ultimate delusion that life is not worth living.¹⁰ This alteration suppresses the strongest, most fundamental urge of all, namely, the survival instinct.

We must overturn the catastrophic decision of the U.S. Supreme Court that requires the showing of a dangerous act and the holding of a trial employing at least three lawyers for involuntary commitment to be authorized. Rather, involuntary treatment is justified by medical necessity as determined by two licensed professionals with no conflicts of interest. It can be outpatient.

The Supreme Court’s decision in O’Connor v. Donaldson in 1975 remedied an illusory wrong, addressing an act of blatant malpractice, not policy inequity.¹¹ The superintendent of the state facility in that case was not even a doctor. He kept O’Connor prisoner for more than a decade, perhaps to keep a bed filled. Over the past half-century, this one decision has resulted in 1 million preventable suicides¹² and half a million senseless murders by paranoid individuals, including many rampage shootings.¹³

More than two-thirds of homeless individuals suffer from an untreated mental condition.¹⁴ The vast majority of them will refuse all offers of treatment because they also have anosognosia, a brain-based disorder causing denial of illness.¹⁵ By referring to these individuals as “homeless,” we are also lowering real estate values for a square block around where they happen to be camped out. That cost has never been calculated, but it is another real consequence of this devastating Supreme Court decision.¹⁶

Detractors and mental health rights activists may argue that individual rights cannot be infringed. In that case, those same detractors and mental health rights activists must take responsibility for the thousands of lives and billions of dollars in economic damage caused by their refusal to allow an effective solution to the suicide epidemic to be implemented. Enforced outpatient treatment by the U.S. Air Force dropped its suicide rate by 60%. As an unintended benefit, the murder rate dropped by 50%.¹⁷

Through the adoption of well-established, indisputably effective approaches, suicide and its horrible and painful costs can be ended. It is high time we did so.

Dr. Behar is a psychiatrist in Lower Merion, Pa. He graduated from Hahnemann Medical College, Philadelphia, in 1975, and has had postgraduate training at SUNY Stony Brook, University of Iowa, the National Institute of Mental Health, and Columbia University. His practice focuses on difficult, treatment-resistant cases.

References

1. U.S. Centers for Disease Control and Prevention. Suicide Prevention. 2020.

2. Luoma JB et al. Contact with mental health and primary care providers before suicide: A review of the evidence. Am J Psychiatry. 2002 Jun 1. doi: 10.1176/appi.ajp.159.6.909.

3. World Health Organization. Suicide. 2021 Jun 17.

4. National Institute of Corrections. Correctional suicide prevention: Policies and procedures. 1995.

5. Hufford MR. Alcohol and suicidal behavior. Clin Psychol Rev. 2001 Jul;21(5):797-811.

6. Stanley B and Brown GK. Safety planning intervention: A brief intervention to mitigate suicide risk. Cogn Behav Pract. 2012 May;19(2):256-64.

7. Ibid.

8. Brown GK and Jager-Hyman S. Evidence-based psychotherapies for suicide prevention: Future directions. Am J Prev Med. 2014 Sep;47(3 Suppl 2):S186-94.

9. Isometsä ET. Psychological autopsy studies – A review. Eur Psychiatry. 2001 Nov;16(7):379-85.

10. Van Orden KA et al. The interpersonal theory of suicide. Psychol Rev. 2010 Apr; 117(2):575-600.

11. O’Connor v. Donaldson, 422 U.S. 563 (1975).

12. Calculated based on annual suicide statistics from the CDC and the time elapsed since the Supreme Court decision in O’Connor v. Donaldson.

13. Metzl JM and MacLeish KT. Mental illness, mass shootings, and the politics of American firearms. Am J Public Health. 2015 Feb;105(2):240-9.

14. Fazel S et al. The prevalence of mental disorders among the homeless in western countries: Systematic review and meta-regression analysis. PLoS Med. 2008 Dec 2;5(12):e225.

15. Amador XF and David AS. (eds.) Insight and psychosis: Awareness of illness in schizophrenia and related disorders (2nd ed.). Oxford Univ Press. 2004.

16. Calculated based on the potential impact of homelessness on property values and the relationship between untreated mental illness and homelessness.

17. Armed Forces Health Surveillance Branch. Surveillance snapshot: Manner and cause of death, active component, U.S. Armed Forces, 1998-2015. Medical Surveillance Monthly Report. 2016 Apr;23(4):19.

The old man was restrained at the last moment from jumping off the hospital’s fifth floor atrium parapet. He was suffering from terminal cancer and had been racked with chronic, severe pain for months.

The consult recognized symptoms of depression arising from his continuous physical suffering, advising that a male aide be dispatched to sit with the man and that he be put on a regimen of 10 mg of methadone twice a day to alleviate the pain. The following day the man was calm; he no longer wanted to kill himself. He expressed a strong desire to go home, return to gardening, and to play with his grandchildren.

Dr. Behar

Most of the 47,000 suicides that occur in the United States every year are preventable.¹ Our national policy on this front has been nothing short of an abject failure. The government implemented a system with limited effect on completed suicides – a telephone hotline. This hotline is not called by the most common suicide victims: male, old, and quiet.²

The consequences of this national policy disaster have been profound, resulting in the biggest loss of productive years of life for any fatal condition.³ The grief experienced by the families of those who commit suicide is far greater than normal bereavement: The cause of death of their loved ones was not an unfortunate accident or a disease, it was an intentional act, and families take it personally.

One of the greatest achievements of psychiatry during the 20th century was the lowering of suicide rates in prisons by 70% with no treatment, no additional staffing, and no additional expenditures of funds. Today if inmates threaten suicide, they are immediately placed under eyesight supervision by guards. The federal pamphlet that describes this protocol was published in 1995 and is freely available online.⁴

Half of all suicide attempts are made by individuals who are legally drunk.⁵ Watch them for 6 hours and then ask them if they want to kill themselves and the response will almost invariably be “Of course not,” with the risk of further attempts dissipating in step with their blood alcohol level. The best resources to provide this kind of intervention are responsible adult family members, at no cost to the government. Indeed, in many cases family supervision is superior to that provided by a locked psychiatric ward with three staff members chasing after 20 agitated people all night long. The one-on-one attention that a family member can provide is free as well as far more personal and insightful, and more sincerely caring.

Guarantees in the field of medicine are rare. But, one such guarantee is that after their mood has improved, 100% of people will be thankful that they did not hurt themselves.⁶ This means that successful treatment will prevent 100% of all suicides.⁷ Not all treatments are successful, but 95% can be.⁸ At autopsy, few successful suicide victims have psychiatric medications in their system.⁹ The urge to kill oneself might best be characterized as a temporary chemical alteration of the brain causing delusional thoughts, including the ultimate delusion that life is not worth living.¹⁰ This alteration suppresses the strongest, most fundamental urge of all, namely, the survival instinct.

We must overturn the catastrophic decision of the U.S. Supreme Court that requires the showing of a dangerous act and the holding of a trial employing at least three lawyers for involuntary commitment to be authorized. Rather, involuntary treatment is justified by medical necessity as determined by two licensed professionals with no conflicts of interest. It can be outpatient.

The Supreme Court’s decision in O’Connor v. Donaldson in 1975 remedied an illusory wrong, addressing an act of blatant malpractice, not policy inequity.¹¹ The superintendent of the state facility in that case was not even a doctor. He kept O’Connor prisoner for more than a decade, perhaps to keep a bed filled. Over the past half-century, this one decision has resulted in 1 million preventable suicides¹² and half a million senseless murders by paranoid individuals, including many rampage shootings.¹³

More than two-thirds of homeless individuals suffer from an untreated mental condition.¹⁴ The vast majority of them will refuse all offers of treatment because they also have anosognosia, a brain-based disorder causing denial of illness.¹⁵ By referring to these individuals as “homeless,” we are also lowering real estate values for a square block around where they happen to be camped out. That cost has never been calculated, but it is another real consequence of this devastating Supreme Court decision.¹⁶

Detractors and mental health rights activists may argue that individual rights cannot be infringed. In that case, those same detractors and mental health rights activists must take responsibility for the thousands of lives and billions of dollars in economic damage caused by their refusal to allow an effective solution to the suicide epidemic to be implemented. Enforced outpatient treatment by the U.S. Air Force dropped its suicide rate by 60%. As an unintended benefit, the murder rate dropped by 50%.¹⁷

Through the adoption of well-established, indisputably effective approaches, suicide and its horrible and painful costs can be ended. It is high time we did so.

Dr. Behar is a psychiatrist in Lower Merion, Pa. He graduated from Hahnemann Medical College, Philadelphia, in 1975, and has had postgraduate training at SUNY Stony Brook, University of Iowa, the National Institute of Mental Health, and Columbia University. His practice focuses on difficult, treatment-resistant cases.

References

1. U.S. Centers for Disease Control and Prevention. Suicide Prevention. 2020.

2. Luoma JB et al. Contact with mental health and primary care providers before suicide: A review of the evidence. Am J Psychiatry. 2002 Jun 1. doi: 10.1176/appi.ajp.159.6.909.

3. World Health Organization. Suicide. 2021 Jun 17.

4. National Institute of Corrections. Correctional suicide prevention: Policies and procedures. 1995.

5. Hufford MR. Alcohol and suicidal behavior. Clin Psychol Rev. 2001 Jul;21(5):797-811.

6. Stanley B and Brown GK. Safety planning intervention: A brief intervention to mitigate suicide risk. Cogn Behav Pract. 2012 May;19(2):256-64.

7. Ibid.

8. Brown GK and Jager-Hyman S. Evidence-based psychotherapies for suicide prevention: Future directions. Am J Prev Med. 2014 Sep;47(3 Suppl 2):S186-94.

9. Isometsä ET. Psychological autopsy studies – A review. Eur Psychiatry. 2001 Nov;16(7):379-85.

10. Van Orden KA et al. The interpersonal theory of suicide. Psychol Rev. 2010 Apr; 117(2):575-600.

11. O’Connor v. Donaldson, 422 U.S. 563 (1975).

12. Calculated based on annual suicide statistics from the CDC and the time elapsed since the Supreme Court decision in O’Connor v. Donaldson.

13. Metzl JM and MacLeish KT. Mental illness, mass shootings, and the politics of American firearms. Am J Public Health. 2015 Feb;105(2):240-9.

14. Fazel S et al. The prevalence of mental disorders among the homeless in western countries: Systematic review and meta-regression analysis. PLoS Med. 2008 Dec 2;5(12):e225.

15. Amador XF and David AS. (eds.) Insight and psychosis: Awareness of illness in schizophrenia and related disorders (2nd ed.). Oxford Univ Press. 2004.

16. Calculated based on the potential impact of homelessness on property values and the relationship between untreated mental illness and homelessness.

17. Armed Forces Health Surveillance Branch. Surveillance snapshot: Manner and cause of death, active component, U.S. Armed Forces, 1998-2015. Medical Surveillance Monthly Report. 2016 Apr;23(4):19.

The old man was restrained at the last moment from jumping off the hospital’s fifth floor atrium parapet. He was suffering from terminal cancer and had been racked with chronic, severe pain for months.

The consult recognized symptoms of depression arising from his continuous physical suffering, advising that a male aide be dispatched to sit with the man and that he be put on a regimen of 10 mg of methadone twice a day to alleviate the pain. The following day the man was calm; he no longer wanted to kill himself. He expressed a strong desire to go home, return to gardening, and to play with his grandchildren.

Dr. Behar

Most of the 47,000 suicides that occur in the United States every year are preventable.¹ Our national policy on this front has been nothing short of an abject failure. The government implemented a system with limited effect on completed suicides – a telephone hotline. This hotline is not called by the most common suicide victims: male, old, and quiet.²

The consequences of this national policy disaster have been profound, resulting in the biggest loss of productive years of life for any fatal condition.³ The grief experienced by the families of those who commit suicide is far greater than normal bereavement: The cause of death of their loved ones was not an unfortunate accident or a disease, it was an intentional act, and families take it personally.

One of the greatest achievements of psychiatry during the 20th century was the lowering of suicide rates in prisons by 70% with no treatment, no additional staffing, and no additional expenditures of funds. Today if inmates threaten suicide, they are immediately placed under eyesight supervision by guards. The federal pamphlet that describes this protocol was published in 1995 and is freely available online.⁴

Half of all suicide attempts are made by individuals who are legally drunk.⁵ Watch them for 6 hours and then ask them if they want to kill themselves and the response will almost invariably be “Of course not,” with the risk of further attempts dissipating in step with their blood alcohol level. The best resources to provide this kind of intervention are responsible adult family members, at no cost to the government. Indeed, in many cases family supervision is superior to that provided by a locked psychiatric ward with three staff members chasing after 20 agitated people all night long. The one-on-one attention that a family member can provide is free as well as far more personal and insightful, and more sincerely caring.

Guarantees in the field of medicine are rare. But, one such guarantee is that after their mood has improved, 100% of people will be thankful that they did not hurt themselves.⁶ This means that successful treatment will prevent 100% of all suicides.⁷ Not all treatments are successful, but 95% can be.⁸ At autopsy, few successful suicide victims have psychiatric medications in their system.⁹ The urge to kill oneself might best be characterized as a temporary chemical alteration of the brain causing delusional thoughts, including the ultimate delusion that life is not worth living.¹⁰ This alteration suppresses the strongest, most fundamental urge of all, namely, the survival instinct.

We must overturn the catastrophic decision of the U.S. Supreme Court that requires the showing of a dangerous act and the holding of a trial employing at least three lawyers for involuntary commitment to be authorized. Rather, involuntary treatment is justified by medical necessity as determined by two licensed professionals with no conflicts of interest. It can be outpatient.

The Supreme Court’s decision in O’Connor v. Donaldson in 1975 remedied an illusory wrong, addressing an act of blatant malpractice, not policy inequity.¹¹ The superintendent of the state facility in that case was not even a doctor. He kept O’Connor prisoner for more than a decade, perhaps to keep a bed filled. Over the past half-century, this one decision has resulted in 1 million preventable suicides¹² and half a million senseless murders by paranoid individuals, including many rampage shootings.¹³

More than two-thirds of homeless individuals suffer from an untreated mental condition.¹⁴ The vast majority of them will refuse all offers of treatment because they also have anosognosia, a brain-based disorder causing denial of illness.¹⁵ By referring to these individuals as “homeless,” we are also lowering real estate values for a square block around where they happen to be camped out. That cost has never been calculated, but it is another real consequence of this devastating Supreme Court decision.¹⁶

Detractors and mental health rights activists may argue that individual rights cannot be infringed. In that case, those same detractors and mental health rights activists must take responsibility for the thousands of lives and billions of dollars in economic damage caused by their refusal to allow an effective solution to the suicide epidemic to be implemented. Enforced outpatient treatment by the U.S. Air Force dropped its suicide rate by 60%. As an unintended benefit, the murder rate dropped by 50%.¹⁷

Through the adoption of well-established, indisputably effective approaches, suicide and its horrible and painful costs can be ended. It is high time we did so.

Dr. Behar is a psychiatrist in Lower Merion, Pa. He graduated from Hahnemann Medical College, Philadelphia, in 1975, and has had postgraduate training at SUNY Stony Brook, University of Iowa, the National Institute of Mental Health, and Columbia University. His practice focuses on difficult, treatment-resistant cases.

References

1. U.S. Centers for Disease Control and Prevention. Suicide Prevention. 2020.

2. Luoma JB et al. Contact with mental health and primary care providers before suicide: A review of the evidence. Am J Psychiatry. 2002 Jun 1. doi: 10.1176/appi.ajp.159.6.909.

3. World Health Organization. Suicide. 2021 Jun 17.

4. National Institute of Corrections. Correctional suicide prevention: Policies and procedures. 1995.

5. Hufford MR. Alcohol and suicidal behavior. Clin Psychol Rev. 2001 Jul;21(5):797-811.

6. Stanley B and Brown GK. Safety planning intervention: A brief intervention to mitigate suicide risk. Cogn Behav Pract. 2012 May;19(2):256-64.

7. Ibid.

8. Brown GK and Jager-Hyman S. Evidence-based psychotherapies for suicide prevention: Future directions. Am J Prev Med. 2014 Sep;47(3 Suppl 2):S186-94.

9. Isometsä ET. Psychological autopsy studies – A review. Eur Psychiatry. 2001 Nov;16(7):379-85.

10. Van Orden KA et al. The interpersonal theory of suicide. Psychol Rev. 2010 Apr; 117(2):575-600.

11. O’Connor v. Donaldson, 422 U.S. 563 (1975).

12. Calculated based on annual suicide statistics from the CDC and the time elapsed since the Supreme Court decision in O’Connor v. Donaldson.

13. Metzl JM and MacLeish KT. Mental illness, mass shootings, and the politics of American firearms. Am J Public Health. 2015 Feb;105(2):240-9.

14. Fazel S et al. The prevalence of mental disorders among the homeless in western countries: Systematic review and meta-regression analysis. PLoS Med. 2008 Dec 2;5(12):e225.

15. Amador XF and David AS. (eds.) Insight and psychosis: Awareness of illness in schizophrenia and related disorders (2nd ed.). Oxford Univ Press. 2004.

16. Calculated based on the potential impact of homelessness on property values and the relationship between untreated mental illness and homelessness.

17. Armed Forces Health Surveillance Branch. Surveillance snapshot: Manner and cause of death, active component, U.S. Armed Forces, 1998-2015. Medical Surveillance Monthly Report. 2016 Apr;23(4):19.

A few weeks ago we went to Phoenix Theater’s production of “A Chorus Line.” As with all their shows, it was excellent.

The penultimate scene is where one of the auditioning dancers suffers a career-ending injury, forcing the others to consider what they’d do if they couldn’t dance anymore, and facing the fact that sooner or later it will happen to all of them.

Let’s flip it onto us: What if tomorrow you couldn’t practice medicine anymore? To keep it from getting too depressing, let’s say it was because of paperwork. Your medical license expired and you weren’t warned in advance, and because of some legal glitch you can’t ever renew it now.

It’s a good question. I mean, I’ve wanted to be doctor as long as I can remember. (Actually I wanted to be Batman, then a scientist, then a doctor. Though I’d still rather be Batman. I’m even the same age as he was in The Dark Knight Returns.)

For all the paperwork and insurance fights and aggravations the job brings, I still love doing it. I get up on weekday mornings and feel good about going to the office. I generally feel good about what I’ve done to help people (or at least did my best to try) at the end of the day.

During my first year of residency (30 years ago) I remember telling my parents that, if even if I were phenomenally wealthy, I’d still do this job for free. Well, I’m not phenomenally wealthy, but I still enjoy the job.

If I couldn’t do it anymore, I’d be pretty sad. I mean, it’s not like I couldn’t find something else – consulting, research, writing, joining my daughter at her bakery – but I doubt I’d like it as much. Even if money weren’t an issue, there’s only so many jigsaw puzzles to do and books to read.

What about you?

Realistically, most of us won’t do this for the rest of our lives. Our expiration date may be longer than that of a professional dancer, but we still have one. Even if the mind stays sharp, sooner or later we all reach a point where it’s time to move on and leave the field in the capable hands of the next generation, just as a prior group of physicians left it to us. As the line in the song states, “the gift was ours to borrow.” And yes, I still see being able to do this for a living as a privilege and gift. But inevitably we all have to pass it on to the next ones, as will they someday.

But I’ll miss it. An oncologist I know was retired for a few months before he signed up for a nonmedical volunteer job at his old hospital, helping people find the rooms and departments they need to go to. He’s happy with it.

Being a doctor, and the desire to help others, becomes so ingrained into our personalities, and is such a central part of who we are, that it’s hard to walk away from it.

But when you do, you need to do your best to do it without regret. After all, you got to do something that many only dream of. Helping others and (I hope) having a job you enjoy.

I have dancers, and retired dancers, in my practice. The retired ones still miss it, but very few of them leave. They do volunteer teaching at community theaters, or just keep dancing on their own in groups of like-minded friends, as best they can. While medicine has made us one of the longer-lived mammals, it doesn’t stop the years.

When it’s time to walk away and point to tomorrow, do it without regrets, and remember that, even with the sweetness and the sorrow, it was what you did for love.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

A few weeks ago we went to Phoenix Theater’s production of “A Chorus Line.” As with all their shows, it was excellent.

The penultimate scene is where one of the auditioning dancers suffers a career-ending injury, forcing the others to consider what they’d do if they couldn’t dance anymore, and facing the fact that sooner or later it will happen to all of them.

Let’s flip it onto us: What if tomorrow you couldn’t practice medicine anymore? To keep it from getting too depressing, let’s say it was because of paperwork. Your medical license expired and you weren’t warned in advance, and because of some legal glitch you can’t ever renew it now.

It’s a good question. I mean, I’ve wanted to be doctor as long as I can remember. (Actually I wanted to be Batman, then a scientist, then a doctor. Though I’d still rather be Batman. I’m even the same age as he was in The Dark Knight Returns.)

For all the paperwork and insurance fights and aggravations the job brings, I still love doing it. I get up on weekday mornings and feel good about going to the office. I generally feel good about what I’ve done to help people (or at least did my best to try) at the end of the day.

During my first year of residency (30 years ago) I remember telling my parents that, if even if I were phenomenally wealthy, I’d still do this job for free. Well, I’m not phenomenally wealthy, but I still enjoy the job.

If I couldn’t do it anymore, I’d be pretty sad. I mean, it’s not like I couldn’t find something else – consulting, research, writing, joining my daughter at her bakery – but I doubt I’d like it as much. Even if money weren’t an issue, there’s only so many jigsaw puzzles to do and books to read.

What about you?

Realistically, most of us won’t do this for the rest of our lives. Our expiration date may be longer than that of a professional dancer, but we still have one. Even if the mind stays sharp, sooner or later we all reach a point where it’s time to move on and leave the field in the capable hands of the next generation, just as a prior group of physicians left it to us. As the line in the song states, “the gift was ours to borrow.” And yes, I still see being able to do this for a living as a privilege and gift. But inevitably we all have to pass it on to the next ones, as will they someday.

But I’ll miss it. An oncologist I know was retired for a few months before he signed up for a nonmedical volunteer job at his old hospital, helping people find the rooms and departments they need to go to. He’s happy with it.

Being a doctor, and the desire to help others, becomes so ingrained into our personalities, and is such a central part of who we are, that it’s hard to walk away from it.

But when you do, you need to do your best to do it without regret. After all, you got to do something that many only dream of. Helping others and (I hope) having a job you enjoy.

I have dancers, and retired dancers, in my practice. The retired ones still miss it, but very few of them leave. They do volunteer teaching at community theaters, or just keep dancing on their own in groups of like-minded friends, as best they can. While medicine has made us one of the longer-lived mammals, it doesn’t stop the years.

When it’s time to walk away and point to tomorrow, do it without regrets, and remember that, even with the sweetness and the sorrow, it was what you did for love.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

A few weeks ago we went to Phoenix Theater’s production of “A Chorus Line.” As with all their shows, it was excellent.

The penultimate scene is where one of the auditioning dancers suffers a career-ending injury, forcing the others to consider what they’d do if they couldn’t dance anymore, and facing the fact that sooner or later it will happen to all of them.

Let’s flip it onto us: What if tomorrow you couldn’t practice medicine anymore? To keep it from getting too depressing, let’s say it was because of paperwork. Your medical license expired and you weren’t warned in advance, and because of some legal glitch you can’t ever renew it now.

It’s a good question. I mean, I’ve wanted to be doctor as long as I can remember. (Actually I wanted to be Batman, then a scientist, then a doctor. Though I’d still rather be Batman. I’m even the same age as he was in The Dark Knight Returns.)

For all the paperwork and insurance fights and aggravations the job brings, I still love doing it. I get up on weekday mornings and feel good about going to the office. I generally feel good about what I’ve done to help people (or at least did my best to try) at the end of the day.

During my first year of residency (30 years ago) I remember telling my parents that, if even if I were phenomenally wealthy, I’d still do this job for free. Well, I’m not phenomenally wealthy, but I still enjoy the job.

If I couldn’t do it anymore, I’d be pretty sad. I mean, it’s not like I couldn’t find something else – consulting, research, writing, joining my daughter at her bakery – but I doubt I’d like it as much. Even if money weren’t an issue, there’s only so many jigsaw puzzles to do and books to read.

What about you?

Realistically, most of us won’t do this for the rest of our lives. Our expiration date may be longer than that of a professional dancer, but we still have one. Even if the mind stays sharp, sooner or later we all reach a point where it’s time to move on and leave the field in the capable hands of the next generation, just as a prior group of physicians left it to us. As the line in the song states, “the gift was ours to borrow.” And yes, I still see being able to do this for a living as a privilege and gift. But inevitably we all have to pass it on to the next ones, as will they someday.

But I’ll miss it. An oncologist I know was retired for a few months before he signed up for a nonmedical volunteer job at his old hospital, helping people find the rooms and departments they need to go to. He’s happy with it.

Being a doctor, and the desire to help others, becomes so ingrained into our personalities, and is such a central part of who we are, that it’s hard to walk away from it.

But when you do, you need to do your best to do it without regret. After all, you got to do something that many only dream of. Helping others and (I hope) having a job you enjoy.

I have dancers, and retired dancers, in my practice. The retired ones still miss it, but very few of them leave. They do volunteer teaching at community theaters, or just keep dancing on their own in groups of like-minded friends, as best they can. While medicine has made us one of the longer-lived mammals, it doesn’t stop the years.

When it’s time to walk away and point to tomorrow, do it without regrets, and remember that, even with the sweetness and the sorrow, it was what you did for love.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

This transcript has been edited for clarity.

I’m Dr. Neil Skolnik. Today we are going to talk about the 2023 American College of Cardiology Expert Consensus Decision Pathway on Management of Heart Failure With Preserved Ejection Fraction (HFpEF). The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.

We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.  

I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.

When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).

Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.

For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic  peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.

Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.

Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.

To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.

Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.

After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.

Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.

In summary:

• Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
• Initially evaluate with an NT-proBNP level and an echocardiogram.
• First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.

This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.

Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.

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

This transcript has been edited for clarity.

I’m Dr. Neil Skolnik. Today we are going to talk about the 2023 American College of Cardiology Expert Consensus Decision Pathway on Management of Heart Failure With Preserved Ejection Fraction (HFpEF). The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.

We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.  

I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.

When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).

Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.

For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic  peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.

Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.

Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.

To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.

Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.

After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.

Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.

In summary:

• Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
• Initially evaluate with an NT-proBNP level and an echocardiogram.
• First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.

This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.

Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.

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

This transcript has been edited for clarity.

I’m Dr. Neil Skolnik. Today we are going to talk about the 2023 American College of Cardiology Expert Consensus Decision Pathway on Management of Heart Failure With Preserved Ejection Fraction (HFpEF). The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.

We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.  

I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.

When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).

Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.

For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic  peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.

Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.

Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.

To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.

Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.

After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.

Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.

In summary:

• Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
• Initially evaluate with an NT-proBNP level and an echocardiogram.
• First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.

This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.

Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.

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

For health professionals, the thought that our parents and grandparents don’t have sex – or didn’t – might be comforting.

The reality is that, for a significant proportion of our older patients, sex has no use-by date. Humans are sexual beings throughout their lives, yet the culture has concealed that fact.

According to Rome, the purpose of sex is to make children. According to Hollywood, sex is only for the young, the healthy, and the beautiful. For the medical profession, sex consists mainly of risks or dysfunctions.

The results of these biases? Many middle-aged people fear their later sexual life. And medical professionals rarely ask about sexuality. That failing can be harmful. Sexuality and intimacy are essential elements for quality of life, with clear physical, emotional, and relational benefits.

Let’s look at the data when researchers dared to ask seniors about their sexuality.

We start with the 2015 U.K. national research on sexuality. The study found a link between age and a decline in various aspects of sexual activity – but not a zeroing-out. For example, among men aged 70-79, 59% reported having had sex in the past year, with 19% having intercourse at least twice a month and 18% masturbating at least that often. Above age 80, those numbers dropped to 39%, 6%, and 5%, respectively. The reason behind the declines? A combination of taboo, fear of disease, use of medications or other interventions that disrupt sexual function or cause disfigurement, and a little bit of age itself.

What about women? Among women ages 70-79, 39% said they’d had sex in the past year, with 6% having intercourse at least twice per month and 5% masturbating two times or more monthly. Above age 80, those numbers were 10%, 4.5%, and 1%, respectively. Driving the falloff in women were the same factors as for men, plus the sad reality that many heterosexual women become widowed because their older male partners die earlier.

The male-female difference also reflects lower levels of testosterone in women. And, because women say they value intimacy more than performance, we have two explanations for their lower frequency of masturbation. After all, a lot of intimacy occurs without either intercourse or masturbation.

Surprising and relevant is the amount of distress – or rather, their relative lack thereof – older patients report because of sexual problems. At age 18-44, 11% of U.S. women indicated sexual distress; at age 45-64, the figure was 15%; and at age 65 and up, 9%.

For clinicians, those figures should prompt us to look more closely at alternative forms of sexual expression – those not involving intercourse or masturbation – in the aged, a field physicians typically do not consider.

Although dyspareunia or erectile problems affect many in long-standing relationships, neither is a reason to abstain from sexual pleasure. Indeed, in many couples, oral sex will replace vaginal intercourse, and if urinary, fecal, or flatal incontinence intrude, couples often waive oral sex in favor of more cuddling, kissing, digital stimulation, and other forms of sexual pleasure.
 

What about the expiry date for sex?

Fascinating research from Nils Beckman, PhD, and colleagues found that the sex drive persists even as people (and men in particular) reach their 100th year. Dr. Beckman’s group interviewed 269 Swedish seniors, all without dementia, at age 97. Sexual desire was affirmed by 27% of men and 5% of women in the survey. Among the men, 32% said they still had sexual thoughts, compared with 18% of women. Meanwhile, 26% of the men and 15% of the women said they missed sexual activity.

What should clinicians do with this information? First, we could start talking about sex with our older patients. According to the 97-year-old Swedes, most want us to! More than 8 in 10 of both women and men in the survey expressed positive views about questions on sexuality. And please don’t be scared to address the subject in the single senior. They, too, can have a sexual or relationship issue and are happy when we raise the subject. They’re not scared to talk about masturbation, either.

When caring for those with chronic diseases, cancer, in the course of physical rehabilitation, and even in the last phase of life, the clinical experience indicates that our patients are happy when we address sexuality and intimacy. Doing so can open the door to the admission of a problem and a corresponding solution, a lubricant or a PDE5 inhibitor.

But sometimes the solution is the conversation itself: Roughly 25% of patients are sufficiently helped simply by talking about sex. Addressing the importance of sexual pleasure is nearly always valuable.

Here are a few ice-breakers I find helpful:

• Did taking this medication change aspects of sexuality? If so, does that bother you?
• Knowing that continuing intimacy is healthy, do you mind if I address that subject?
• We know that aspects of sexuality and intimacy are healthy. Without a partner, some people become sexually isolated. Would you like to talk about that?’

If addressing sexuality has benefits, what about sex itself?

We are gradually learning more about the many short-, intermediate-, and long-term health benefits of solo and joint sexual activity. Short-term benefits include muscle relaxation, pain relief (even, perhaps ironically, for headaches), and better sleep – all pretty valuable for older adults. Examples of intermediate-term benefits include stress relief and less depression. Research from the United States has found that hugging can reduce the concentrations of proinflammatory cytokines, and kissing positively influences cholesterol levels.

Finally, while the long-term benefits of sex might be less relevant for seniors, they do exist.

Among them are delayed onset of dementia and a substantial reduction in cardiovascular and cerebrovascular problems in men. More sex has been linked to longevity, with men benefiting a bit more than women from going through the entire process, including an orgasm, whereas women appear to gain from having a “satisfying” sex life, which does not always require an orgasm.

Let us not forget that these benefits apply to both patients and clinicians alike. Addressing intimacy and sexuality can ease eventual sexual concerns and potentially create a stronger clinician-patient relationship.

Dr. Gianotten, MD is emeritus senior lecturer in medical sexology, Erasmus University Medical Centre, Rotterdam, the Netherlands. He reported no conflicts of interest.

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

For health professionals, the thought that our parents and grandparents don’t have sex – or didn’t – might be comforting.

The reality is that, for a significant proportion of our older patients, sex has no use-by date. Humans are sexual beings throughout their lives, yet the culture has concealed that fact.

According to Rome, the purpose of sex is to make children. According to Hollywood, sex is only for the young, the healthy, and the beautiful. For the medical profession, sex consists mainly of risks or dysfunctions.

The results of these biases? Many middle-aged people fear their later sexual life. And medical professionals rarely ask about sexuality. That failing can be harmful. Sexuality and intimacy are essential elements for quality of life, with clear physical, emotional, and relational benefits.

Let’s look at the data when researchers dared to ask seniors about their sexuality.

We start with the 2015 U.K. national research on sexuality. The study found a link between age and a decline in various aspects of sexual activity – but not a zeroing-out. For example, among men aged 70-79, 59% reported having had sex in the past year, with 19% having intercourse at least twice a month and 18% masturbating at least that often. Above age 80, those numbers dropped to 39%, 6%, and 5%, respectively. The reason behind the declines? A combination of taboo, fear of disease, use of medications or other interventions that disrupt sexual function or cause disfigurement, and a little bit of age itself.

What about women? Among women ages 70-79, 39% said they’d had sex in the past year, with 6% having intercourse at least twice per month and 5% masturbating two times or more monthly. Above age 80, those numbers were 10%, 4.5%, and 1%, respectively. Driving the falloff in women were the same factors as for men, plus the sad reality that many heterosexual women become widowed because their older male partners die earlier.

The male-female difference also reflects lower levels of testosterone in women. And, because women say they value intimacy more than performance, we have two explanations for their lower frequency of masturbation. After all, a lot of intimacy occurs without either intercourse or masturbation.

Surprising and relevant is the amount of distress – or rather, their relative lack thereof – older patients report because of sexual problems. At age 18-44, 11% of U.S. women indicated sexual distress; at age 45-64, the figure was 15%; and at age 65 and up, 9%.

For clinicians, those figures should prompt us to look more closely at alternative forms of sexual expression – those not involving intercourse or masturbation – in the aged, a field physicians typically do not consider.

Although dyspareunia or erectile problems affect many in long-standing relationships, neither is a reason to abstain from sexual pleasure. Indeed, in many couples, oral sex will replace vaginal intercourse, and if urinary, fecal, or flatal incontinence intrude, couples often waive oral sex in favor of more cuddling, kissing, digital stimulation, and other forms of sexual pleasure.
 

What about the expiry date for sex?

Fascinating research from Nils Beckman, PhD, and colleagues found that the sex drive persists even as people (and men in particular) reach their 100th year. Dr. Beckman’s group interviewed 269 Swedish seniors, all without dementia, at age 97. Sexual desire was affirmed by 27% of men and 5% of women in the survey. Among the men, 32% said they still had sexual thoughts, compared with 18% of women. Meanwhile, 26% of the men and 15% of the women said they missed sexual activity.

What should clinicians do with this information? First, we could start talking about sex with our older patients. According to the 97-year-old Swedes, most want us to! More than 8 in 10 of both women and men in the survey expressed positive views about questions on sexuality. And please don’t be scared to address the subject in the single senior. They, too, can have a sexual or relationship issue and are happy when we raise the subject. They’re not scared to talk about masturbation, either.

When caring for those with chronic diseases, cancer, in the course of physical rehabilitation, and even in the last phase of life, the clinical experience indicates that our patients are happy when we address sexuality and intimacy. Doing so can open the door to the admission of a problem and a corresponding solution, a lubricant or a PDE5 inhibitor.

But sometimes the solution is the conversation itself: Roughly 25% of patients are sufficiently helped simply by talking about sex. Addressing the importance of sexual pleasure is nearly always valuable.

Here are a few ice-breakers I find helpful:

• Did taking this medication change aspects of sexuality? If so, does that bother you?
• Knowing that continuing intimacy is healthy, do you mind if I address that subject?
• We know that aspects of sexuality and intimacy are healthy. Without a partner, some people become sexually isolated. Would you like to talk about that?’

If addressing sexuality has benefits, what about sex itself?

We are gradually learning more about the many short-, intermediate-, and long-term health benefits of solo and joint sexual activity. Short-term benefits include muscle relaxation, pain relief (even, perhaps ironically, for headaches), and better sleep – all pretty valuable for older adults. Examples of intermediate-term benefits include stress relief and less depression. Research from the United States has found that hugging can reduce the concentrations of proinflammatory cytokines, and kissing positively influences cholesterol levels.

Finally, while the long-term benefits of sex might be less relevant for seniors, they do exist.

Among them are delayed onset of dementia and a substantial reduction in cardiovascular and cerebrovascular problems in men. More sex has been linked to longevity, with men benefiting a bit more than women from going through the entire process, including an orgasm, whereas women appear to gain from having a “satisfying” sex life, which does not always require an orgasm.

Let us not forget that these benefits apply to both patients and clinicians alike. Addressing intimacy and sexuality can ease eventual sexual concerns and potentially create a stronger clinician-patient relationship.

Dr. Gianotten, MD is emeritus senior lecturer in medical sexology, Erasmus University Medical Centre, Rotterdam, the Netherlands. He reported no conflicts of interest.

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

For health professionals, the thought that our parents and grandparents don’t have sex – or didn’t – might be comforting.

The reality is that, for a significant proportion of our older patients, sex has no use-by date. Humans are sexual beings throughout their lives, yet the culture has concealed that fact.

According to Rome, the purpose of sex is to make children. According to Hollywood, sex is only for the young, the healthy, and the beautiful. For the medical profession, sex consists mainly of risks or dysfunctions.

The results of these biases? Many middle-aged people fear their later sexual life. And medical professionals rarely ask about sexuality. That failing can be harmful. Sexuality and intimacy are essential elements for quality of life, with clear physical, emotional, and relational benefits.

Let’s look at the data when researchers dared to ask seniors about their sexuality.

We start with the 2015 U.K. national research on sexuality. The study found a link between age and a decline in various aspects of sexual activity – but not a zeroing-out. For example, among men aged 70-79, 59% reported having had sex in the past year, with 19% having intercourse at least twice a month and 18% masturbating at least that often. Above age 80, those numbers dropped to 39%, 6%, and 5%, respectively. The reason behind the declines? A combination of taboo, fear of disease, use of medications or other interventions that disrupt sexual function or cause disfigurement, and a little bit of age itself.

What about women? Among women ages 70-79, 39% said they’d had sex in the past year, with 6% having intercourse at least twice per month and 5% masturbating two times or more monthly. Above age 80, those numbers were 10%, 4.5%, and 1%, respectively. Driving the falloff in women were the same factors as for men, plus the sad reality that many heterosexual women become widowed because their older male partners die earlier.

The male-female difference also reflects lower levels of testosterone in women. And, because women say they value intimacy more than performance, we have two explanations for their lower frequency of masturbation. After all, a lot of intimacy occurs without either intercourse or masturbation.

Surprising and relevant is the amount of distress – or rather, their relative lack thereof – older patients report because of sexual problems. At age 18-44, 11% of U.S. women indicated sexual distress; at age 45-64, the figure was 15%; and at age 65 and up, 9%.

For clinicians, those figures should prompt us to look more closely at alternative forms of sexual expression – those not involving intercourse or masturbation – in the aged, a field physicians typically do not consider.

Although dyspareunia or erectile problems affect many in long-standing relationships, neither is a reason to abstain from sexual pleasure. Indeed, in many couples, oral sex will replace vaginal intercourse, and if urinary, fecal, or flatal incontinence intrude, couples often waive oral sex in favor of more cuddling, kissing, digital stimulation, and other forms of sexual pleasure.
 

What about the expiry date for sex?

Fascinating research from Nils Beckman, PhD, and colleagues found that the sex drive persists even as people (and men in particular) reach their 100th year. Dr. Beckman’s group interviewed 269 Swedish seniors, all without dementia, at age 97. Sexual desire was affirmed by 27% of men and 5% of women in the survey. Among the men, 32% said they still had sexual thoughts, compared with 18% of women. Meanwhile, 26% of the men and 15% of the women said they missed sexual activity.

What should clinicians do with this information? First, we could start talking about sex with our older patients. According to the 97-year-old Swedes, most want us to! More than 8 in 10 of both women and men in the survey expressed positive views about questions on sexuality. And please don’t be scared to address the subject in the single senior. They, too, can have a sexual or relationship issue and are happy when we raise the subject. They’re not scared to talk about masturbation, either.

When caring for those with chronic diseases, cancer, in the course of physical rehabilitation, and even in the last phase of life, the clinical experience indicates that our patients are happy when we address sexuality and intimacy. Doing so can open the door to the admission of a problem and a corresponding solution, a lubricant or a PDE5 inhibitor.

But sometimes the solution is the conversation itself: Roughly 25% of patients are sufficiently helped simply by talking about sex. Addressing the importance of sexual pleasure is nearly always valuable.

Here are a few ice-breakers I find helpful:

• Did taking this medication change aspects of sexuality? If so, does that bother you?
• Knowing that continuing intimacy is healthy, do you mind if I address that subject?
• We know that aspects of sexuality and intimacy are healthy. Without a partner, some people become sexually isolated. Would you like to talk about that?’

If addressing sexuality has benefits, what about sex itself?

We are gradually learning more about the many short-, intermediate-, and long-term health benefits of solo and joint sexual activity. Short-term benefits include muscle relaxation, pain relief (even, perhaps ironically, for headaches), and better sleep – all pretty valuable for older adults. Examples of intermediate-term benefits include stress relief and less depression. Research from the United States has found that hugging can reduce the concentrations of proinflammatory cytokines, and kissing positively influences cholesterol levels.

Finally, while the long-term benefits of sex might be less relevant for seniors, they do exist.

Among them are delayed onset of dementia and a substantial reduction in cardiovascular and cerebrovascular problems in men. More sex has been linked to longevity, with men benefiting a bit more than women from going through the entire process, including an orgasm, whereas women appear to gain from having a “satisfying” sex life, which does not always require an orgasm.

Let us not forget that these benefits apply to both patients and clinicians alike. Addressing intimacy and sexuality can ease eventual sexual concerns and potentially create a stronger clinician-patient relationship.

Dr. Gianotten, MD is emeritus senior lecturer in medical sexology, Erasmus University Medical Centre, Rotterdam, the Netherlands. He reported no conflicts of interest.

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

We are living in an era of increasing sensitivity to our diversity and the ways we interact, but also an era of growing resistance to change and accommodation. As clinicians, we hope to be among the sensitive and the progressive, open to improving our views and interactions. And as part of our respect for those we treat, we seek to speak clearly with them about our assessment of what is disrupting their lives and about their options.

Using the right words is crucial in that work. Well-chosen words can be heard and understood. Poorly chosen words can be confusing or off-putting; they may miscommunicate or be offensive. Maintaining the quality of clinician-patient communication requires special care, because one party is expert and the other may not be, and because only one party is identified as ill. Careful choice of words is also important among colleagues, who may not always mean the same things when using the same words.

Dr. Cohen

In psychiatry, consumer knowledge and access are growing. There are effective standard treatments and promising new ones. But our terminology is often antique and obscure. This is so despite a recognition that some terms we use may communicate poorly and some are deprecating.

A notable example is “schizophrenia.” Originally referring to cognitive phenomena that were not adequately coherent with reality or one another, it has gone through periods of describing most psychosis to particular subsets of psychoses. Debates persist on specific criteria for key symptoms and typical course. Even two clinicians trained in the same site may not agree on the defining criteria, and the public, mostly informed by books, movies, and newspapers, is even more confused, often believing schizophrenia is multiple-personality disorder. In addition, the press and public often associate schizophrenia with violent behavior and uniformly bad outcomes, and for those reasons, a diagnosis is not only frightening but also stigmatizing.¹

Many papers have presented the case for retiring “schizophrenia.”² And practical efforts to rename schizophrenia have been made. These efforts have occurred in countries in which English is not the primary language.³ In Japan, schizophrenia was replaced by “integration disorder.” In Hong Kong, “disorder of thought and perception” was implemented. Korea chose “attunement disorder.” A recent large survey of stakeholders, including clinicians, researchers, and consumers in the United States, explored alternatives in English.⁴ Terms receiving approval included: “psychosis spectrum syndrome,” “altered perception syndrome,” and “neuro-emotional integration disorder.”

Despite these recommendations, the standard manuals of diagnosis, the ICD and DSM, have maintained the century-old term “schizophrenia” in their most recent editions, released in 2022. Aside from the inertia commonly associated with long-standing practices, it has been noted that many of the alternatives suggested or, in some places, implemented, are complex, somewhat vague, or too inclusive to distinguish different clinical presentations requiring different treatment approaches. They might not be compelling for use or optimal to guide caregiving.

Perhaps more concerning than “schizophrenia” are terms used to describe personality disorders.⁵ “Personality disorder” itself is problematic, implying a core and possibly unalterable fault in an individual. And among the personality disorders, words for the related group of disorders called “Cluster B” in the DSM raise issues. This includes the terms narcissistic, antisocial, histrionic, and borderline in DSM-5-TR. The first three terms are clearly pejorative. The last is unclear: What is the border between? Originally, it was bordering on psychosis, but as explained in DSM and ICD, borderline disorder is much more closely related to other personality disorders.

Notably, the “Cluster B” disorders run together in families, but men are more likely to be called antisocial and women borderline, even though the overlap in signs and symptoms is profound, suggesting marginally different manifestations of the same condition. The ICD has made changes to address the problems associated with some of these terms. ICD proposes personality “difficulty” to replace personality “disorder”; a modest change but less offensive. And it proposes seeing all, or at least most, personality disorders as being related to one another. Most share features of disturbances in sense-of-self and relationships with others. As descriptors, ICD kept “borderline pattern,” but replaced “antisocial” with “dissocial,” in an effort to be accurate but less demeaning. Other descriptors it proposes are negative affectivity, detachment, disinhibition, and anankastia, the last referring to compulsions.

These are notable advances. Can the field find even better terms to communicate hard to hear information, with words that are less problematic? In search of options, we surveyed clinicians at academic centers about the terms they preferred to avoid and the ones they prefer to use in talking with patients.⁶ Their practices may be informative.

Briefly summarized, these clinicians preferred not to use “schizophrenia” and very few used “antisocial,” “histrionic,” or “narcissistic.” Most avoided using “borderline” as well. Instead, they recommended discussing specific symptoms and manifestations of illness or dysfunctional behavior and relationships with their patients. They employed terms including “psychosis,” “hallucination,” “delusion,” “thinking disorder,” and “mood disorder.” They explained these terms, as needed, and found that patients understood them.

For Cluster B personality disorders, they spoke of personality traits and styles and specifically about “conduct,” “rule breaking,” “coping,” “self-focus,” “emotionality,” and “reactivity.” Those choices are not perfect, of course. Medical terms are often not standard words used in a conversational way. But the words chosen by these clinicians are generally straightforward and may communicate in a clear and acceptable fashion. It is also notable that the terms match how the clinicians assess and treat their patients, as observed in a separate study of their practices.⁷ That is, the clinicians advised that they look for and suggest treatments for the specific symptoms they see that most disrupt an individual’s life, such as delusions or mood instability. They are not much guided by diagnoses, like schizophrenia or borderline disorder. That makes the chosen terms not only less confusing or off-putting but also more practical.

Changing terminology in any field is difficult. We are trained to use standard terms. Clearly, however, many clinicians avoid some terms and use alternatives in their work. Asked why, they responded that they did so precisely to communicate more effectively and more respectfully. That is key to their treatment goals. Perhaps others will consider these choices useful in their work. And perhaps both the DSM and the ICD will not only continue to consider but will decide to implement alternatives for problematic terms in the years ahead, as they discuss their next revisions.

Dr. Cohen is director of the Program for Neuropsychiatric Research at McLean Hospital, Belmont, Mass., and Robertson-Steele Professor of Psychiatry at Harvard Medical School, Boston.

References

1. Lasalvia A et al. Renaming schizophrenia? A survey among psychiatrists, mental health service users and family members in Italy. Schizophr Res. 2021;228:502-9.

2. Gülöksüz S et al. Renaming schizophrenia: 5 x 5. Epidemiol Psychiatr Sci. 2019;28(3):254-7.

3. Sartorius N et al. Name change for schizophrenia. Schizophr Bull. 2014;40(2):255-8.

4. Mesholam-Gately RI et al. Are we ready for a name change for schizophrenia? A survey of multiple stakeholders. Schizophr Res. 2021;238:152-60.

5. Mulder R. The evolving nosology of personality disorder and its clinical utility. World Psychiatry. 2021 Oct;20(3):361-2.

6. Cohen BM et al. Diagnostic terms psychiatrists prefer to use for common psychotic and personality disorders. J Psychiatr Res. 2022 Sep 5;155:226-31.

7. Cohen BM, et al. Use of DSM-5 diagnoses vs. other clinical information by US academic-affiliated psychiatrists in assessing and treating psychotic disorders. World Psychiatry. 2021 Oct;20(3):447-8.

We are living in an era of increasing sensitivity to our diversity and the ways we interact, but also an era of growing resistance to change and accommodation. As clinicians, we hope to be among the sensitive and the progressive, open to improving our views and interactions. And as part of our respect for those we treat, we seek to speak clearly with them about our assessment of what is disrupting their lives and about their options.

Using the right words is crucial in that work. Well-chosen words can be heard and understood. Poorly chosen words can be confusing or off-putting; they may miscommunicate or be offensive. Maintaining the quality of clinician-patient communication requires special care, because one party is expert and the other may not be, and because only one party is identified as ill. Careful choice of words is also important among colleagues, who may not always mean the same things when using the same words.

Dr. Cohen

In psychiatry, consumer knowledge and access are growing. There are effective standard treatments and promising new ones. But our terminology is often antique and obscure. This is so despite a recognition that some terms we use may communicate poorly and some are deprecating.

A notable example is “schizophrenia.” Originally referring to cognitive phenomena that were not adequately coherent with reality or one another, it has gone through periods of describing most psychosis to particular subsets of psychoses. Debates persist on specific criteria for key symptoms and typical course. Even two clinicians trained in the same site may not agree on the defining criteria, and the public, mostly informed by books, movies, and newspapers, is even more confused, often believing schizophrenia is multiple-personality disorder. In addition, the press and public often associate schizophrenia with violent behavior and uniformly bad outcomes, and for those reasons, a diagnosis is not only frightening but also stigmatizing.¹

Many papers have presented the case for retiring “schizophrenia.”² And practical efforts to rename schizophrenia have been made. These efforts have occurred in countries in which English is not the primary language.³ In Japan, schizophrenia was replaced by “integration disorder.” In Hong Kong, “disorder of thought and perception” was implemented. Korea chose “attunement disorder.” A recent large survey of stakeholders, including clinicians, researchers, and consumers in the United States, explored alternatives in English.⁴ Terms receiving approval included: “psychosis spectrum syndrome,” “altered perception syndrome,” and “neuro-emotional integration disorder.”

Despite these recommendations, the standard manuals of diagnosis, the ICD and DSM, have maintained the century-old term “schizophrenia” in their most recent editions, released in 2022. Aside from the inertia commonly associated with long-standing practices, it has been noted that many of the alternatives suggested or, in some places, implemented, are complex, somewhat vague, or too inclusive to distinguish different clinical presentations requiring different treatment approaches. They might not be compelling for use or optimal to guide caregiving.

Perhaps more concerning than “schizophrenia” are terms used to describe personality disorders.⁵ “Personality disorder” itself is problematic, implying a core and possibly unalterable fault in an individual. And among the personality disorders, words for the related group of disorders called “Cluster B” in the DSM raise issues. This includes the terms narcissistic, antisocial, histrionic, and borderline in DSM-5-TR. The first three terms are clearly pejorative. The last is unclear: What is the border between? Originally, it was bordering on psychosis, but as explained in DSM and ICD, borderline disorder is much more closely related to other personality disorders.

Notably, the “Cluster B” disorders run together in families, but men are more likely to be called antisocial and women borderline, even though the overlap in signs and symptoms is profound, suggesting marginally different manifestations of the same condition. The ICD has made changes to address the problems associated with some of these terms. ICD proposes personality “difficulty” to replace personality “disorder”; a modest change but less offensive. And it proposes seeing all, or at least most, personality disorders as being related to one another. Most share features of disturbances in sense-of-self and relationships with others. As descriptors, ICD kept “borderline pattern,” but replaced “antisocial” with “dissocial,” in an effort to be accurate but less demeaning. Other descriptors it proposes are negative affectivity, detachment, disinhibition, and anankastia, the last referring to compulsions.

These are notable advances. Can the field find even better terms to communicate hard to hear information, with words that are less problematic? In search of options, we surveyed clinicians at academic centers about the terms they preferred to avoid and the ones they prefer to use in talking with patients.⁶ Their practices may be informative.

Briefly summarized, these clinicians preferred not to use “schizophrenia” and very few used “antisocial,” “histrionic,” or “narcissistic.” Most avoided using “borderline” as well. Instead, they recommended discussing specific symptoms and manifestations of illness or dysfunctional behavior and relationships with their patients. They employed terms including “psychosis,” “hallucination,” “delusion,” “thinking disorder,” and “mood disorder.” They explained these terms, as needed, and found that patients understood them.

For Cluster B personality disorders, they spoke of personality traits and styles and specifically about “conduct,” “rule breaking,” “coping,” “self-focus,” “emotionality,” and “reactivity.” Those choices are not perfect, of course. Medical terms are often not standard words used in a conversational way. But the words chosen by these clinicians are generally straightforward and may communicate in a clear and acceptable fashion. It is also notable that the terms match how the clinicians assess and treat their patients, as observed in a separate study of their practices.⁷ That is, the clinicians advised that they look for and suggest treatments for the specific symptoms they see that most disrupt an individual’s life, such as delusions or mood instability. They are not much guided by diagnoses, like schizophrenia or borderline disorder. That makes the chosen terms not only less confusing or off-putting but also more practical.

Changing terminology in any field is difficult. We are trained to use standard terms. Clearly, however, many clinicians avoid some terms and use alternatives in their work. Asked why, they responded that they did so precisely to communicate more effectively and more respectfully. That is key to their treatment goals. Perhaps others will consider these choices useful in their work. And perhaps both the DSM and the ICD will not only continue to consider but will decide to implement alternatives for problematic terms in the years ahead, as they discuss their next revisions.

Dr. Cohen is director of the Program for Neuropsychiatric Research at McLean Hospital, Belmont, Mass., and Robertson-Steele Professor of Psychiatry at Harvard Medical School, Boston.

References

1. Lasalvia A et al. Renaming schizophrenia? A survey among psychiatrists, mental health service users and family members in Italy. Schizophr Res. 2021;228:502-9.

2. Gülöksüz S et al. Renaming schizophrenia: 5 x 5. Epidemiol Psychiatr Sci. 2019;28(3):254-7.

3. Sartorius N et al. Name change for schizophrenia. Schizophr Bull. 2014;40(2):255-8.

4. Mesholam-Gately RI et al. Are we ready for a name change for schizophrenia? A survey of multiple stakeholders. Schizophr Res. 2021;238:152-60.

5. Mulder R. The evolving nosology of personality disorder and its clinical utility. World Psychiatry. 2021 Oct;20(3):361-2.

6. Cohen BM et al. Diagnostic terms psychiatrists prefer to use for common psychotic and personality disorders. J Psychiatr Res. 2022 Sep 5;155:226-31.

7. Cohen BM, et al. Use of DSM-5 diagnoses vs. other clinical information by US academic-affiliated psychiatrists in assessing and treating psychotic disorders. World Psychiatry. 2021 Oct;20(3):447-8.

We are living in an era of increasing sensitivity to our diversity and the ways we interact, but also an era of growing resistance to change and accommodation. As clinicians, we hope to be among the sensitive and the progressive, open to improving our views and interactions. And as part of our respect for those we treat, we seek to speak clearly with them about our assessment of what is disrupting their lives and about their options.

Using the right words is crucial in that work. Well-chosen words can be heard and understood. Poorly chosen words can be confusing or off-putting; they may miscommunicate or be offensive. Maintaining the quality of clinician-patient communication requires special care, because one party is expert and the other may not be, and because only one party is identified as ill. Careful choice of words is also important among colleagues, who may not always mean the same things when using the same words.

Dr. Cohen

In psychiatry, consumer knowledge and access are growing. There are effective standard treatments and promising new ones. But our terminology is often antique and obscure. This is so despite a recognition that some terms we use may communicate poorly and some are deprecating.

A notable example is “schizophrenia.” Originally referring to cognitive phenomena that were not adequately coherent with reality or one another, it has gone through periods of describing most psychosis to particular subsets of psychoses. Debates persist on specific criteria for key symptoms and typical course. Even two clinicians trained in the same site may not agree on the defining criteria, and the public, mostly informed by books, movies, and newspapers, is even more confused, often believing schizophrenia is multiple-personality disorder. In addition, the press and public often associate schizophrenia with violent behavior and uniformly bad outcomes, and for those reasons, a diagnosis is not only frightening but also stigmatizing.¹

Many papers have presented the case for retiring “schizophrenia.”² And practical efforts to rename schizophrenia have been made. These efforts have occurred in countries in which English is not the primary language.³ In Japan, schizophrenia was replaced by “integration disorder.” In Hong Kong, “disorder of thought and perception” was implemented. Korea chose “attunement disorder.” A recent large survey of stakeholders, including clinicians, researchers, and consumers in the United States, explored alternatives in English.⁴ Terms receiving approval included: “psychosis spectrum syndrome,” “altered perception syndrome,” and “neuro-emotional integration disorder.”

Despite these recommendations, the standard manuals of diagnosis, the ICD and DSM, have maintained the century-old term “schizophrenia” in their most recent editions, released in 2022. Aside from the inertia commonly associated with long-standing practices, it has been noted that many of the alternatives suggested or, in some places, implemented, are complex, somewhat vague, or too inclusive to distinguish different clinical presentations requiring different treatment approaches. They might not be compelling for use or optimal to guide caregiving.

Perhaps more concerning than “schizophrenia” are terms used to describe personality disorders.⁵ “Personality disorder” itself is problematic, implying a core and possibly unalterable fault in an individual. And among the personality disorders, words for the related group of disorders called “Cluster B” in the DSM raise issues. This includes the terms narcissistic, antisocial, histrionic, and borderline in DSM-5-TR. The first three terms are clearly pejorative. The last is unclear: What is the border between? Originally, it was bordering on psychosis, but as explained in DSM and ICD, borderline disorder is much more closely related to other personality disorders.

Notably, the “Cluster B” disorders run together in families, but men are more likely to be called antisocial and women borderline, even though the overlap in signs and symptoms is profound, suggesting marginally different manifestations of the same condition. The ICD has made changes to address the problems associated with some of these terms. ICD proposes personality “difficulty” to replace personality “disorder”; a modest change but less offensive. And it proposes seeing all, or at least most, personality disorders as being related to one another. Most share features of disturbances in sense-of-self and relationships with others. As descriptors, ICD kept “borderline pattern,” but replaced “antisocial” with “dissocial,” in an effort to be accurate but less demeaning. Other descriptors it proposes are negative affectivity, detachment, disinhibition, and anankastia, the last referring to compulsions.

These are notable advances. Can the field find even better terms to communicate hard to hear information, with words that are less problematic? In search of options, we surveyed clinicians at academic centers about the terms they preferred to avoid and the ones they prefer to use in talking with patients.⁶ Their practices may be informative.

Briefly summarized, these clinicians preferred not to use “schizophrenia” and very few used “antisocial,” “histrionic,” or “narcissistic.” Most avoided using “borderline” as well. Instead, they recommended discussing specific symptoms and manifestations of illness or dysfunctional behavior and relationships with their patients. They employed terms including “psychosis,” “hallucination,” “delusion,” “thinking disorder,” and “mood disorder.” They explained these terms, as needed, and found that patients understood them.

For Cluster B personality disorders, they spoke of personality traits and styles and specifically about “conduct,” “rule breaking,” “coping,” “self-focus,” “emotionality,” and “reactivity.” Those choices are not perfect, of course. Medical terms are often not standard words used in a conversational way. But the words chosen by these clinicians are generally straightforward and may communicate in a clear and acceptable fashion. It is also notable that the terms match how the clinicians assess and treat their patients, as observed in a separate study of their practices.⁷ That is, the clinicians advised that they look for and suggest treatments for the specific symptoms they see that most disrupt an individual’s life, such as delusions or mood instability. They are not much guided by diagnoses, like schizophrenia or borderline disorder. That makes the chosen terms not only less confusing or off-putting but also more practical.

Changing terminology in any field is difficult. We are trained to use standard terms. Clearly, however, many clinicians avoid some terms and use alternatives in their work. Asked why, they responded that they did so precisely to communicate more effectively and more respectfully. That is key to their treatment goals. Perhaps others will consider these choices useful in their work. And perhaps both the DSM and the ICD will not only continue to consider but will decide to implement alternatives for problematic terms in the years ahead, as they discuss their next revisions.

Dr. Cohen is director of the Program for Neuropsychiatric Research at McLean Hospital, Belmont, Mass., and Robertson-Steele Professor of Psychiatry at Harvard Medical School, Boston.

References

1. Lasalvia A et al. Renaming schizophrenia? A survey among psychiatrists, mental health service users and family members in Italy. Schizophr Res. 2021;228:502-9.

2. Gülöksüz S et al. Renaming schizophrenia: 5 x 5. Epidemiol Psychiatr Sci. 2019;28(3):254-7.

3. Sartorius N et al. Name change for schizophrenia. Schizophr Bull. 2014;40(2):255-8.

4. Mesholam-Gately RI et al. Are we ready for a name change for schizophrenia? A survey of multiple stakeholders. Schizophr Res. 2021;238:152-60.

5. Mulder R. The evolving nosology of personality disorder and its clinical utility. World Psychiatry. 2021 Oct;20(3):361-2.

6. Cohen BM et al. Diagnostic terms psychiatrists prefer to use for common psychotic and personality disorders. J Psychiatr Res. 2022 Sep 5;155:226-31.

7. Cohen BM, et al. Use of DSM-5 diagnoses vs. other clinical information by US academic-affiliated psychiatrists in assessing and treating psychotic disorders. World Psychiatry. 2021 Oct;20(3):447-8.

This transcript has been edited for clarity.

Andrew N. Wilner, MD: I’m your host, Dr. Andrew Wilner, reporting virtually from the 2023 American Academy of Neurology meeting in Boston. It’s my pleasure today to speak with Dr. Shae Datta, codirector of the NYU Langone Concussion Center.

She’s also a clinical assistant professor of neurology at NYU School of Medicine. Dr. Datta is chair of the AAN Sports Neurology Section, and she’s leading a panel on concussion at this year’s meeting. She’s going to give us an update. Welcome, Dr. Datta.

Shae Datta, MD: Thank you so much, Andrew. I really love the fact that I’m here speaking to you about all of the new, exciting developments in the field.

Dr. Wilner: Before we get too deep, tell us how you got interested in this topic.

Dr. Datta: I initially thought, when I was in training as a resident, that I wanted to do something like neurocritical care or EEG. It also puzzled me why these seemingly smaller head injuries that didn’t end up in the hospital or ICU were bounced from neurology headache clinic to neuro-ophthalmology headache clinic to neurovestibular headache clinic, and nobody seemed to be able to put together the dots about why they’re having so many different issues — but at the same time, nobody could help them.

At that time, this field was very new. I was on a plane to Paris to a neurocritical care conference as a resident, and I saw the movie Concussion with Will Smith.

It featured one of my current mentors who taught at the fellowship that I graduated from, and it was a fascinating field. I just started looking deeply into it, and I saw that there was a new training fellowship for sports neurology and concussion management, and this is basically why we’re here today.
 

New concussion consensus guidelines coming

Dr. Wilner: I think this field has really exploded. It used to be that you banged your head, you did a CT scan – remember, I trained about 45 years ago – and if there was nothing on the CT scan, you were done. If you had headaches, you took Tylenol until they went away.

Now, we do MRI, and we realized that it’s really a syndrome. I understand that there are going to be some formal guidelines that have been put together. Is that correct?

Dr. Datta: That’s correct. The 6th International Consensus Conference on Concussion in Sport, in Amsterdam, where I attended and presented a poster, was really a meeting of all the best minds – clinicians and researchers in brain injury – to form a consensus on the newest guidelines that are going to direct our treatment going forward.

Dr. Wilner: I’m going to ask you a trick question because the last time I looked it up I did not get a satisfying answer. What is a concussion?

Dr. Datta: That’s a very good question, and everyone always asks. A concussion is an external force that is emitted upon the head or the neck, or the body, in general, that may cause temporary loss of function. It’s a functional problem.

We don’t see much on CT. We can do MRI. We can do SPECT or we can do these very fancy images, sometimes, of high-velocity head injuries and see small microhemorrhages.

Often, we don’t see anything, but still the patient is loopy. They can’t see straight. They are double-visioned. They have vertigo. Why is that happening? On the cellular level, we have an energy deficit in the sodium-potassium-ATPase pump of the neurons themselves.

Dr. Wilner: Suppose you do see diffuse axonal injury; does that take it out of concussion, or can you have a concussion with visible injury?

Dr. Datta: I think you can have overlap in the symptoms. The diffuse axonal injury would put it into a higher grade of head injury as opposed to a mild traumatic brain injury. Definitely, we would need to work together with our trauma doctors to ensure that patients are not on blood thinners or anything until they heal well enough. Obviously, I would pick them up as an outpatient and follow them until we resolve or rehab them as best as possible.

Concussion assessment tools

Dr. Wilner: There are many sports out there where concussions are fairly frequent, like American football and hockey, for example. Are there any statements in the new guidelines?

Dr. Datta: There are no statements for or against a particular sport because that would really make too much of a bold statement about cause and effect. There is a cause and effect in long-term, repetitive exposure, I would say, in terms of someone being able to play or sustain injury.

Right now, at least at the concussion conference I went to and in the upcoming consensus statement, they will not comment on a specific sport. Obviously, we know that the higher-impact sports are a little more dangerous.

Let’s be honest. At the high school, middle school, or even younger level, some kids are not necessarily the most athletic, right? They play because their friends are playing. If they’re repeatedly getting injured, it’s time for an astute clinician, or a coach, and a whole team to assess them to see if maybe this person is just going to continue to get hurt if they’re not taken out of the game and perhaps they should go to a lower-impact sport.

Dr. Wilner: In schools, often there’s a big size and weight difference. There are 14-year-olds who are 6 fett 2 inches and 200 pounds, and there are 14-year-olds who are 5 feet 2 inches and 110 pounds. Obviously, they’re mismatched on the football field.

You mentioned coaches. Is there anything in the guidelines about training coaches?

Dr. Datta: Specifically, there was nothing in the guidelines about that. There’s a tool for coaches at every level to use, which is called the Sports Concussion Assessment Tool, or SCAT, which is going to be updated to the SCAT6. At the NCAA level, they must receive annual training on concussion management and be given an NCAA concussion handout for coaches.

Obviously, there are more rigorous protocols for national-level coaching. As it stands now, it is not mandatory, but they are given tools to assess someone once they’ve gotten a hit to take them out of the game.

Dr. Wilner: I’ve been following the concussion research through the years. They did some neuropsychological testing on athletes who’ve had this many concussions or that many concussions, and they would find deficits here or subtle deficits there, but they had no baseline.

Then, there was a movement to start testing athletes before the season starts so that they could do a repeat test after concussion and see if there is any difference. Is that something we’re recommending?

Dr. Datta: Most of the time, NCAA-level – certainly where I trained – and national-level sports do testing, but it’s not everywhere. Prior guidelines have indicated that preseason testing is not required. That is largely because there has been no standardized neuropsychological testing established.

There are computerized testing options where the validity and reliability are questionable. Also, let’s say it’s a college student; they didn’t sleep all night and then they took this computer test. They would probably do worse than they would if they had received a head hit.

Just to be on the safe side, most places that have collegiate-level sports that are at a high level do preseason testing. If I were to speak personally, aside from the guidelines, I would say that it’s been helpful for me to look at the before and after, in general, overall, to make a decision about my treatment protocol.

Dr. Wilner: Let’s talk about the patient. You have a 20-year-old guy. He’s playing football. There’s a big play. Bonk, he gets hit on the head. He’s on the ground. He’s dazed, staggers a little bit, gets up, and you ask how he is feeling. He says he’s fine and then he wobbles off to the sideline. What do you do with that kid?

Dr. Datta: Obviously, the first thing is to remove him from the play environment to a quiet space. Second, either an athletic trainer or a coach would administer basic screening neurologic tests, such as “where are you, what’s today’s date, what is your name?” and other orientation questions.

They’ll also go through the SCAT – that’ll be SCAT6 starting in July – the SCAT5 symptom questionnaire to see what symptoms they have. Often, they’re using sideline testing software.

There are two things that can be used on a card to test eye movements, to see if they’re slower. They come out of NYU, coincidentally – the Memory Image Completion (MIC) and the Mobile Universal Lexicon Evaluation System (MULES) – and are used to determine whether eye movements are slower. That way, you can tell whether someone is, compared with before they got their head hit, slower than before.

Based on this composite information, usually the teammates and the head people on the team will know if a player looks different.

They need to be taken out, obviously, if there is nausea or vomiting, any neurologic signs and symptoms, or a neck injury that needs to be stabilized. ABCs first, right? If there’s any vomiting or seizures, they should be taken to the ER right away.

The first thing is to take them out, then do a sideline assessment. Third, see if they need to immediately go to the ED versus follow-up outpatient with me within a day or two.

Dr. Wilner: I think it’s the subtle injuries that are the tough ones. Back to our 20-year-old. He says: “Oh, I’m fine. I want to go back in the game.” Everybody can tell he’s not quite right, even though he passed all the tests. What do you do then?

Dr. Datta: You have to make a judgment call for the safety of the player. They always want to go back, right? This is also an issue when they’re competing for college scholarships and things of that nature. Sometimes they’re sandbagging, where they memorize the answers.

Everything’s on the Internet nowadays, right? We have to make a judgment call as members of the healthcare community and the sports community to keep that player safe.

Just keep them out. Don’t bring them back in the game. Keep them out for a reasonable amount of time. There’s a test called the Buffalo Concussion Treadmill Test; Dr. John Leddy from University of Buffalo has developed a way for us to put athletes through a screening protocol.

This can be part of their vestibular and ocular rehabilitation, where if they don’t have symptoms when we bring their heart rate to certain levels, then we can slowly clear them for return to play as long as they’re nonsymptomatic.

Dr. Wilner: I spoke with your colleague, Dr. Riggins, who is also on your panel, and we were talking about when they can go back. She said they can go back when they don’t have any symptoms. No more headache, no more dizziness, no more lightheadedness, no more trouble concentrating or with memory – all those things have gone away.

Sometimes these symptoms are stubborn. If you have, say, 100 patients like our 20-year-old who got bonked on the head, has some headaches, and doesn’t feel quite right, what usually happens? How many are back to play the next day, the next week, or the next month? How many are out for the season? How does that play out?

Dr. Datta: It depends on a couple of different factors. One, have they had previous head injuries? Two, do they have preexisting symptoms or signs, or diagnoses like migraines, which are likely to get worse after a head injury? Anything that’s preexisting, like a mood disorder, anxiety, depression, or trouble sleeping, is going to get worse.

If they were compensating for untreated ADD or borderline personality or bipolar, I’ve seen many people who’ve developed them. These are not the norm, but I’m saying that you have to be very careful.

Getting back to the question, you treat them. Reasonably, if they’re healthy and they don’t have preexisting signs and symptoms, I would say more than half are back in about 2 weeks.. I would say 60%-70%. It all depends. If they have preexisting issues, then it’s going to take much longer.
 

From SCAT to SCOAT

Dr. Wilner: This has been very informative. Before we wrap up, tell us what to expect from these guidelines in July. How are they really going to help?

Dr. Datta: The consensus statement is going to come out with something called a SCOAT, which stands for Sport Concussion Office Assessment Tool. We’ve been using the SCAT, which was meant for more sideline assessment because that’s all we had, and it’s worked perfectly well.

This will be better because we often see them within 24-48 hours, when the symptoms are sometimes a little bit better.

We also will see the sport and concussion group come up with added athlete perspectives, ethics discussion, power-sport athlete considerations, and development of this new SCOAT.

Dr. Wilner: Dr. Datta, this is very exciting. I look forward to reading these guidelines in July. I want to thank you for your hard work. I also look forward to talking to you at next year’s meeting. Thank you very much for giving us this update.

Dr. Datta: No problem. It’s my pleasure.

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

This transcript has been edited for clarity.

Andrew N. Wilner, MD: I’m your host, Dr. Andrew Wilner, reporting virtually from the 2023 American Academy of Neurology meeting in Boston. It’s my pleasure today to speak with Dr. Shae Datta, codirector of the NYU Langone Concussion Center.

She’s also a clinical assistant professor of neurology at NYU School of Medicine. Dr. Datta is chair of the AAN Sports Neurology Section, and she’s leading a panel on concussion at this year’s meeting. She’s going to give us an update. Welcome, Dr. Datta.

Shae Datta, MD: Thank you so much, Andrew. I really love the fact that I’m here speaking to you about all of the new, exciting developments in the field.

Dr. Wilner: Before we get too deep, tell us how you got interested in this topic.

Dr. Datta: I initially thought, when I was in training as a resident, that I wanted to do something like neurocritical care or EEG. It also puzzled me why these seemingly smaller head injuries that didn’t end up in the hospital or ICU were bounced from neurology headache clinic to neuro-ophthalmology headache clinic to neurovestibular headache clinic, and nobody seemed to be able to put together the dots about why they’re having so many different issues — but at the same time, nobody could help them.

At that time, this field was very new. I was on a plane to Paris to a neurocritical care conference as a resident, and I saw the movie Concussion with Will Smith.

It featured one of my current mentors who taught at the fellowship that I graduated from, and it was a fascinating field. I just started looking deeply into it, and I saw that there was a new training fellowship for sports neurology and concussion management, and this is basically why we’re here today.
 

New concussion consensus guidelines coming

Dr. Wilner: I think this field has really exploded. It used to be that you banged your head, you did a CT scan – remember, I trained about 45 years ago – and if there was nothing on the CT scan, you were done. If you had headaches, you took Tylenol until they went away.

Now, we do MRI, and we realized that it’s really a syndrome. I understand that there are going to be some formal guidelines that have been put together. Is that correct?

Dr. Datta: That’s correct. The 6th International Consensus Conference on Concussion in Sport, in Amsterdam, where I attended and presented a poster, was really a meeting of all the best minds – clinicians and researchers in brain injury – to form a consensus on the newest guidelines that are going to direct our treatment going forward.

Dr. Wilner: I’m going to ask you a trick question because the last time I looked it up I did not get a satisfying answer. What is a concussion?

Dr. Datta: That’s a very good question, and everyone always asks. A concussion is an external force that is emitted upon the head or the neck, or the body, in general, that may cause temporary loss of function. It’s a functional problem.

We don’t see much on CT. We can do MRI. We can do SPECT or we can do these very fancy images, sometimes, of high-velocity head injuries and see small microhemorrhages.

Often, we don’t see anything, but still the patient is loopy. They can’t see straight. They are double-visioned. They have vertigo. Why is that happening? On the cellular level, we have an energy deficit in the sodium-potassium-ATPase pump of the neurons themselves.

Dr. Wilner: Suppose you do see diffuse axonal injury; does that take it out of concussion, or can you have a concussion with visible injury?

Dr. Datta: I think you can have overlap in the symptoms. The diffuse axonal injury would put it into a higher grade of head injury as opposed to a mild traumatic brain injury. Definitely, we would need to work together with our trauma doctors to ensure that patients are not on blood thinners or anything until they heal well enough. Obviously, I would pick them up as an outpatient and follow them until we resolve or rehab them as best as possible.

Concussion assessment tools

Dr. Wilner: There are many sports out there where concussions are fairly frequent, like American football and hockey, for example. Are there any statements in the new guidelines?

Dr. Datta: There are no statements for or against a particular sport because that would really make too much of a bold statement about cause and effect. There is a cause and effect in long-term, repetitive exposure, I would say, in terms of someone being able to play or sustain injury.

Right now, at least at the concussion conference I went to and in the upcoming consensus statement, they will not comment on a specific sport. Obviously, we know that the higher-impact sports are a little more dangerous.

Let’s be honest. At the high school, middle school, or even younger level, some kids are not necessarily the most athletic, right? They play because their friends are playing. If they’re repeatedly getting injured, it’s time for an astute clinician, or a coach, and a whole team to assess them to see if maybe this person is just going to continue to get hurt if they’re not taken out of the game and perhaps they should go to a lower-impact sport.

Dr. Wilner: In schools, often there’s a big size and weight difference. There are 14-year-olds who are 6 fett 2 inches and 200 pounds, and there are 14-year-olds who are 5 feet 2 inches and 110 pounds. Obviously, they’re mismatched on the football field.

You mentioned coaches. Is there anything in the guidelines about training coaches?

Dr. Datta: Specifically, there was nothing in the guidelines about that. There’s a tool for coaches at every level to use, which is called the Sports Concussion Assessment Tool, or SCAT, which is going to be updated to the SCAT6. At the NCAA level, they must receive annual training on concussion management and be given an NCAA concussion handout for coaches.

Obviously, there are more rigorous protocols for national-level coaching. As it stands now, it is not mandatory, but they are given tools to assess someone once they’ve gotten a hit to take them out of the game.

Dr. Wilner: I’ve been following the concussion research through the years. They did some neuropsychological testing on athletes who’ve had this many concussions or that many concussions, and they would find deficits here or subtle deficits there, but they had no baseline.

Then, there was a movement to start testing athletes before the season starts so that they could do a repeat test after concussion and see if there is any difference. Is that something we’re recommending?

Dr. Datta: Most of the time, NCAA-level – certainly where I trained – and national-level sports do testing, but it’s not everywhere. Prior guidelines have indicated that preseason testing is not required. That is largely because there has been no standardized neuropsychological testing established.

There are computerized testing options where the validity and reliability are questionable. Also, let’s say it’s a college student; they didn’t sleep all night and then they took this computer test. They would probably do worse than they would if they had received a head hit.

Just to be on the safe side, most places that have collegiate-level sports that are at a high level do preseason testing. If I were to speak personally, aside from the guidelines, I would say that it’s been helpful for me to look at the before and after, in general, overall, to make a decision about my treatment protocol.

Dr. Wilner: Let’s talk about the patient. You have a 20-year-old guy. He’s playing football. There’s a big play. Bonk, he gets hit on the head. He’s on the ground. He’s dazed, staggers a little bit, gets up, and you ask how he is feeling. He says he’s fine and then he wobbles off to the sideline. What do you do with that kid?

Dr. Datta: Obviously, the first thing is to remove him from the play environment to a quiet space. Second, either an athletic trainer or a coach would administer basic screening neurologic tests, such as “where are you, what’s today’s date, what is your name?” and other orientation questions.

They’ll also go through the SCAT – that’ll be SCAT6 starting in July – the SCAT5 symptom questionnaire to see what symptoms they have. Often, they’re using sideline testing software.

There are two things that can be used on a card to test eye movements, to see if they’re slower. They come out of NYU, coincidentally – the Memory Image Completion (MIC) and the Mobile Universal Lexicon Evaluation System (MULES) – and are used to determine whether eye movements are slower. That way, you can tell whether someone is, compared with before they got their head hit, slower than before.

Based on this composite information, usually the teammates and the head people on the team will know if a player looks different.

They need to be taken out, obviously, if there is nausea or vomiting, any neurologic signs and symptoms, or a neck injury that needs to be stabilized. ABCs first, right? If there’s any vomiting or seizures, they should be taken to the ER right away.

The first thing is to take them out, then do a sideline assessment. Third, see if they need to immediately go to the ED versus follow-up outpatient with me within a day or two.

Dr. Wilner: I think it’s the subtle injuries that are the tough ones. Back to our 20-year-old. He says: “Oh, I’m fine. I want to go back in the game.” Everybody can tell he’s not quite right, even though he passed all the tests. What do you do then?

Dr. Datta: You have to make a judgment call for the safety of the player. They always want to go back, right? This is also an issue when they’re competing for college scholarships and things of that nature. Sometimes they’re sandbagging, where they memorize the answers.

Everything’s on the Internet nowadays, right? We have to make a judgment call as members of the healthcare community and the sports community to keep that player safe.

Just keep them out. Don’t bring them back in the game. Keep them out for a reasonable amount of time. There’s a test called the Buffalo Concussion Treadmill Test; Dr. John Leddy from University of Buffalo has developed a way for us to put athletes through a screening protocol.

This can be part of their vestibular and ocular rehabilitation, where if they don’t have symptoms when we bring their heart rate to certain levels, then we can slowly clear them for return to play as long as they’re nonsymptomatic.

Dr. Wilner: I spoke with your colleague, Dr. Riggins, who is also on your panel, and we were talking about when they can go back. She said they can go back when they don’t have any symptoms. No more headache, no more dizziness, no more lightheadedness, no more trouble concentrating or with memory – all those things have gone away.

Sometimes these symptoms are stubborn. If you have, say, 100 patients like our 20-year-old who got bonked on the head, has some headaches, and doesn’t feel quite right, what usually happens? How many are back to play the next day, the next week, or the next month? How many are out for the season? How does that play out?

Dr. Datta: It depends on a couple of different factors. One, have they had previous head injuries? Two, do they have preexisting symptoms or signs, or diagnoses like migraines, which are likely to get worse after a head injury? Anything that’s preexisting, like a mood disorder, anxiety, depression, or trouble sleeping, is going to get worse.

If they were compensating for untreated ADD or borderline personality or bipolar, I’ve seen many people who’ve developed them. These are not the norm, but I’m saying that you have to be very careful.

Getting back to the question, you treat them. Reasonably, if they’re healthy and they don’t have preexisting signs and symptoms, I would say more than half are back in about 2 weeks.. I would say 60%-70%. It all depends. If they have preexisting issues, then it’s going to take much longer.
 

From SCAT to SCOAT

Dr. Wilner: This has been very informative. Before we wrap up, tell us what to expect from these guidelines in July. How are they really going to help?

Dr. Datta: The consensus statement is going to come out with something called a SCOAT, which stands for Sport Concussion Office Assessment Tool. We’ve been using the SCAT, which was meant for more sideline assessment because that’s all we had, and it’s worked perfectly well.

This will be better because we often see them within 24-48 hours, when the symptoms are sometimes a little bit better.

We also will see the sport and concussion group come up with added athlete perspectives, ethics discussion, power-sport athlete considerations, and development of this new SCOAT.

Dr. Wilner: Dr. Datta, this is very exciting. I look forward to reading these guidelines in July. I want to thank you for your hard work. I also look forward to talking to you at next year’s meeting. Thank you very much for giving us this update.

Dr. Datta: No problem. It’s my pleasure.

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

This transcript has been edited for clarity.

Andrew N. Wilner, MD: I’m your host, Dr. Andrew Wilner, reporting virtually from the 2023 American Academy of Neurology meeting in Boston. It’s my pleasure today to speak with Dr. Shae Datta, codirector of the NYU Langone Concussion Center.

She’s also a clinical assistant professor of neurology at NYU School of Medicine. Dr. Datta is chair of the AAN Sports Neurology Section, and she’s leading a panel on concussion at this year’s meeting. She’s going to give us an update. Welcome, Dr. Datta.

Shae Datta, MD: Thank you so much, Andrew. I really love the fact that I’m here speaking to you about all of the new, exciting developments in the field.

Dr. Wilner: Before we get too deep, tell us how you got interested in this topic.

Dr. Datta: I initially thought, when I was in training as a resident, that I wanted to do something like neurocritical care or EEG. It also puzzled me why these seemingly smaller head injuries that didn’t end up in the hospital or ICU were bounced from neurology headache clinic to neuro-ophthalmology headache clinic to neurovestibular headache clinic, and nobody seemed to be able to put together the dots about why they’re having so many different issues — but at the same time, nobody could help them.

At that time, this field was very new. I was on a plane to Paris to a neurocritical care conference as a resident, and I saw the movie Concussion with Will Smith.

It featured one of my current mentors who taught at the fellowship that I graduated from, and it was a fascinating field. I just started looking deeply into it, and I saw that there was a new training fellowship for sports neurology and concussion management, and this is basically why we’re here today.
 

New concussion consensus guidelines coming

Dr. Wilner: I think this field has really exploded. It used to be that you banged your head, you did a CT scan – remember, I trained about 45 years ago – and if there was nothing on the CT scan, you were done. If you had headaches, you took Tylenol until they went away.

Now, we do MRI, and we realized that it’s really a syndrome. I understand that there are going to be some formal guidelines that have been put together. Is that correct?

Dr. Datta: That’s correct. The 6th International Consensus Conference on Concussion in Sport, in Amsterdam, where I attended and presented a poster, was really a meeting of all the best minds – clinicians and researchers in brain injury – to form a consensus on the newest guidelines that are going to direct our treatment going forward.

Dr. Wilner: I’m going to ask you a trick question because the last time I looked it up I did not get a satisfying answer. What is a concussion?

Dr. Datta: That’s a very good question, and everyone always asks. A concussion is an external force that is emitted upon the head or the neck, or the body, in general, that may cause temporary loss of function. It’s a functional problem.

We don’t see much on CT. We can do MRI. We can do SPECT or we can do these very fancy images, sometimes, of high-velocity head injuries and see small microhemorrhages.

Often, we don’t see anything, but still the patient is loopy. They can’t see straight. They are double-visioned. They have vertigo. Why is that happening? On the cellular level, we have an energy deficit in the sodium-potassium-ATPase pump of the neurons themselves.

Dr. Wilner: Suppose you do see diffuse axonal injury; does that take it out of concussion, or can you have a concussion with visible injury?

Dr. Datta: I think you can have overlap in the symptoms. The diffuse axonal injury would put it into a higher grade of head injury as opposed to a mild traumatic brain injury. Definitely, we would need to work together with our trauma doctors to ensure that patients are not on blood thinners or anything until they heal well enough. Obviously, I would pick them up as an outpatient and follow them until we resolve or rehab them as best as possible.

Concussion assessment tools

Dr. Wilner: There are many sports out there where concussions are fairly frequent, like American football and hockey, for example. Are there any statements in the new guidelines?

Dr. Datta: There are no statements for or against a particular sport because that would really make too much of a bold statement about cause and effect. There is a cause and effect in long-term, repetitive exposure, I would say, in terms of someone being able to play or sustain injury.

Right now, at least at the concussion conference I went to and in the upcoming consensus statement, they will not comment on a specific sport. Obviously, we know that the higher-impact sports are a little more dangerous.

Let’s be honest. At the high school, middle school, or even younger level, some kids are not necessarily the most athletic, right? They play because their friends are playing. If they’re repeatedly getting injured, it’s time for an astute clinician, or a coach, and a whole team to assess them to see if maybe this person is just going to continue to get hurt if they’re not taken out of the game and perhaps they should go to a lower-impact sport.

Dr. Wilner: In schools, often there’s a big size and weight difference. There are 14-year-olds who are 6 fett 2 inches and 200 pounds, and there are 14-year-olds who are 5 feet 2 inches and 110 pounds. Obviously, they’re mismatched on the football field.

You mentioned coaches. Is there anything in the guidelines about training coaches?

Dr. Datta: Specifically, there was nothing in the guidelines about that. There’s a tool for coaches at every level to use, which is called the Sports Concussion Assessment Tool, or SCAT, which is going to be updated to the SCAT6. At the NCAA level, they must receive annual training on concussion management and be given an NCAA concussion handout for coaches.

Obviously, there are more rigorous protocols for national-level coaching. As it stands now, it is not mandatory, but they are given tools to assess someone once they’ve gotten a hit to take them out of the game.

Dr. Wilner: I’ve been following the concussion research through the years. They did some neuropsychological testing on athletes who’ve had this many concussions or that many concussions, and they would find deficits here or subtle deficits there, but they had no baseline.

Then, there was a movement to start testing athletes before the season starts so that they could do a repeat test after concussion and see if there is any difference. Is that something we’re recommending?

Dr. Datta: Most of the time, NCAA-level – certainly where I trained – and national-level sports do testing, but it’s not everywhere. Prior guidelines have indicated that preseason testing is not required. That is largely because there has been no standardized neuropsychological testing established.

There are computerized testing options where the validity and reliability are questionable. Also, let’s say it’s a college student; they didn’t sleep all night and then they took this computer test. They would probably do worse than they would if they had received a head hit.

Just to be on the safe side, most places that have collegiate-level sports that are at a high level do preseason testing. If I were to speak personally, aside from the guidelines, I would say that it’s been helpful for me to look at the before and after, in general, overall, to make a decision about my treatment protocol.

Dr. Wilner: Let’s talk about the patient. You have a 20-year-old guy. He’s playing football. There’s a big play. Bonk, he gets hit on the head. He’s on the ground. He’s dazed, staggers a little bit, gets up, and you ask how he is feeling. He says he’s fine and then he wobbles off to the sideline. What do you do with that kid?

Dr. Datta: Obviously, the first thing is to remove him from the play environment to a quiet space. Second, either an athletic trainer or a coach would administer basic screening neurologic tests, such as “where are you, what’s today’s date, what is your name?” and other orientation questions.

They’ll also go through the SCAT – that’ll be SCAT6 starting in July – the SCAT5 symptom questionnaire to see what symptoms they have. Often, they’re using sideline testing software.

There are two things that can be used on a card to test eye movements, to see if they’re slower. They come out of NYU, coincidentally – the Memory Image Completion (MIC) and the Mobile Universal Lexicon Evaluation System (MULES) – and are used to determine whether eye movements are slower. That way, you can tell whether someone is, compared with before they got their head hit, slower than before.

Based on this composite information, usually the teammates and the head people on the team will know if a player looks different.

They need to be taken out, obviously, if there is nausea or vomiting, any neurologic signs and symptoms, or a neck injury that needs to be stabilized. ABCs first, right? If there’s any vomiting or seizures, they should be taken to the ER right away.

The first thing is to take them out, then do a sideline assessment. Third, see if they need to immediately go to the ED versus follow-up outpatient with me within a day or two.

Dr. Wilner: I think it’s the subtle injuries that are the tough ones. Back to our 20-year-old. He says: “Oh, I’m fine. I want to go back in the game.” Everybody can tell he’s not quite right, even though he passed all the tests. What do you do then?

Dr. Datta: You have to make a judgment call for the safety of the player. They always want to go back, right? This is also an issue when they’re competing for college scholarships and things of that nature. Sometimes they’re sandbagging, where they memorize the answers.

Everything’s on the Internet nowadays, right? We have to make a judgment call as members of the healthcare community and the sports community to keep that player safe.

Just keep them out. Don’t bring them back in the game. Keep them out for a reasonable amount of time. There’s a test called the Buffalo Concussion Treadmill Test; Dr. John Leddy from University of Buffalo has developed a way for us to put athletes through a screening protocol.

This can be part of their vestibular and ocular rehabilitation, where if they don’t have symptoms when we bring their heart rate to certain levels, then we can slowly clear them for return to play as long as they’re nonsymptomatic.

Dr. Wilner: I spoke with your colleague, Dr. Riggins, who is also on your panel, and we were talking about when they can go back. She said they can go back when they don’t have any symptoms. No more headache, no more dizziness, no more lightheadedness, no more trouble concentrating or with memory – all those things have gone away.

Sometimes these symptoms are stubborn. If you have, say, 100 patients like our 20-year-old who got bonked on the head, has some headaches, and doesn’t feel quite right, what usually happens? How many are back to play the next day, the next week, or the next month? How many are out for the season? How does that play out?

Dr. Datta: It depends on a couple of different factors. One, have they had previous head injuries? Two, do they have preexisting symptoms or signs, or diagnoses like migraines, which are likely to get worse after a head injury? Anything that’s preexisting, like a mood disorder, anxiety, depression, or trouble sleeping, is going to get worse.

If they were compensating for untreated ADD or borderline personality or bipolar, I’ve seen many people who’ve developed them. These are not the norm, but I’m saying that you have to be very careful.

Getting back to the question, you treat them. Reasonably, if they’re healthy and they don’t have preexisting signs and symptoms, I would say more than half are back in about 2 weeks.. I would say 60%-70%. It all depends. If they have preexisting issues, then it’s going to take much longer.
 

From SCAT to SCOAT

Dr. Wilner: This has been very informative. Before we wrap up, tell us what to expect from these guidelines in July. How are they really going to help?

Dr. Datta: The consensus statement is going to come out with something called a SCOAT, which stands for Sport Concussion Office Assessment Tool. We’ve been using the SCAT, which was meant for more sideline assessment because that’s all we had, and it’s worked perfectly well.

This will be better because we often see them within 24-48 hours, when the symptoms are sometimes a little bit better.

We also will see the sport and concussion group come up with added athlete perspectives, ethics discussion, power-sport athlete considerations, and development of this new SCOAT.

Dr. Wilner: Dr. Datta, this is very exciting. I look forward to reading these guidelines in July. I want to thank you for your hard work. I also look forward to talking to you at next year’s meeting. Thank you very much for giving us this update.

Dr. Datta: No problem. It’s my pleasure.

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

Tuesdays and Fridays are tough. Not so much because of clinic, but rather because of the 32 minutes before clinic that I’m on the Peloton bike. They are the mornings I dedicate to training VO_2max. 

Training VO_2max, or maximal oxygen consumption, is simple. Spin for a leisurely, easy-breathing, 4 minutes, then for 4 minutes push yourself until you see the light of heaven and wish for death to come. Then relax for 4 minutes again. Repeat this cycle four to six times. Done justly, you will dread Tuesdays and Fridays too. The punishing cycle of a 4-minute push, then 4-minute recovery is, however, an excellent way to improve cardiovascular fitness. And no, I’m not training for the Boston Marathon, so why am I working so hard? Because I’m training for marathon clinic days for the next 20 years.

Now more than ever, I feel we have to be physically fit to deal with a physicians’ day’s work. By the time the last patient leaves, I’m beat. From the first bell, patients are packed in, our in boxes are overflowing with messages, pathology results are piling up. It’s exhausting. The root cause is too much work, yes, but I believe being physically fit could help. 

I was talking to an 86-year-old patient about this very topic recently. He was short, with a well-manicured goatee and shiny head. He stuck his arm out to shake my hand. “Glad we’re back to handshakes again, doc.” His grip was that of a 30-year-old. “Buff” you’d likely describe him: He is noticeably muscular, not a skinny old man. He’s an old Navy Master Chief who started a business in wholesale flowers, which distributes all over the United States. And he’s still working full time. Impressed, I asked his secret for such vigor. PT, he replied. 

PT, or physical training, is a foundational element of the Navy. Every sailor starts his or her day with morning PT before carrying out their duties. Some 30 years later, this guy is still getting after it. He does push-ups, sit-ups, and pull-ups nearly every morning. Morning PT is what he attributes to his success not only in health, but also business. As he sees it, he has the business savvy and experience of an old guy and the energy and stamina of a college kid. A good combination for a successful life.

I’ve always been pretty fit. Lately, I’ve been trying to take it to the next level, to not just be “physically active,” but rather “high-performance fit.” There are plenty of sources for instruction; how to stay young and healthy isn’t a new idea after all. I mean, Herodotus wrote of finding the Fountain of Youth in the 5th century BCE. A couple thousand years later, it’s still on trend. One of my favorite sages giving health span advice is Peter Attia, MD. I’ve been a fan since I met him at TEDMED in 2013 and I marvel at the astounding body of work he has created since. A Johns Hopkins–trained surgeon, he has spent his career reviewing the scientific literature about longevity and sharing it as actionable content. His book, “Outlive: The Science and Art of Longevity” (New York: Penguin Random House, 2023) is a nice summary of his work. I recommend it. 

Right now I’m switching between type 2 muscle fiber work (lots of jumping like my 2-year-old) and cardiovascular training including the aforementioned VO_2max work. I cannot say that my patient inbox is any cleaner, or that I’m faster in the office, but I’m not flagging by the end of the day anymore. Master Chief challenged me to match his 10 pull-ups before he returns for his follow up visit. I’ll gladly give up Peloton sprints to work on that.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.

Tuesdays and Fridays are tough. Not so much because of clinic, but rather because of the 32 minutes before clinic that I’m on the Peloton bike. They are the mornings I dedicate to training VO_2max. 

Training VO_2max, or maximal oxygen consumption, is simple. Spin for a leisurely, easy-breathing, 4 minutes, then for 4 minutes push yourself until you see the light of heaven and wish for death to come. Then relax for 4 minutes again. Repeat this cycle four to six times. Done justly, you will dread Tuesdays and Fridays too. The punishing cycle of a 4-minute push, then 4-minute recovery is, however, an excellent way to improve cardiovascular fitness. And no, I’m not training for the Boston Marathon, so why am I working so hard? Because I’m training for marathon clinic days for the next 20 years.

Now more than ever, I feel we have to be physically fit to deal with a physicians’ day’s work. By the time the last patient leaves, I’m beat. From the first bell, patients are packed in, our in boxes are overflowing with messages, pathology results are piling up. It’s exhausting. The root cause is too much work, yes, but I believe being physically fit could help. 

I was talking to an 86-year-old patient about this very topic recently. He was short, with a well-manicured goatee and shiny head. He stuck his arm out to shake my hand. “Glad we’re back to handshakes again, doc.” His grip was that of a 30-year-old. “Buff” you’d likely describe him: He is noticeably muscular, not a skinny old man. He’s an old Navy Master Chief who started a business in wholesale flowers, which distributes all over the United States. And he’s still working full time. Impressed, I asked his secret for such vigor. PT, he replied. 

PT, or physical training, is a foundational element of the Navy. Every sailor starts his or her day with morning PT before carrying out their duties. Some 30 years later, this guy is still getting after it. He does push-ups, sit-ups, and pull-ups nearly every morning. Morning PT is what he attributes to his success not only in health, but also business. As he sees it, he has the business savvy and experience of an old guy and the energy and stamina of a college kid. A good combination for a successful life.

I’ve always been pretty fit. Lately, I’ve been trying to take it to the next level, to not just be “physically active,” but rather “high-performance fit.” There are plenty of sources for instruction; how to stay young and healthy isn’t a new idea after all. I mean, Herodotus wrote of finding the Fountain of Youth in the 5th century BCE. A couple thousand years later, it’s still on trend. One of my favorite sages giving health span advice is Peter Attia, MD. I’ve been a fan since I met him at TEDMED in 2013 and I marvel at the astounding body of work he has created since. A Johns Hopkins–trained surgeon, he has spent his career reviewing the scientific literature about longevity and sharing it as actionable content. His book, “Outlive: The Science and Art of Longevity” (New York: Penguin Random House, 2023) is a nice summary of his work. I recommend it. 

Right now I’m switching between type 2 muscle fiber work (lots of jumping like my 2-year-old) and cardiovascular training including the aforementioned VO_2max work. I cannot say that my patient inbox is any cleaner, or that I’m faster in the office, but I’m not flagging by the end of the day anymore. Master Chief challenged me to match his 10 pull-ups before he returns for his follow up visit. I’ll gladly give up Peloton sprints to work on that.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.

Tuesdays and Fridays are tough. Not so much because of clinic, but rather because of the 32 minutes before clinic that I’m on the Peloton bike. They are the mornings I dedicate to training VO_2max. 

Training VO_2max, or maximal oxygen consumption, is simple. Spin for a leisurely, easy-breathing, 4 minutes, then for 4 minutes push yourself until you see the light of heaven and wish for death to come. Then relax for 4 minutes again. Repeat this cycle four to six times. Done justly, you will dread Tuesdays and Fridays too. The punishing cycle of a 4-minute push, then 4-minute recovery is, however, an excellent way to improve cardiovascular fitness. And no, I’m not training for the Boston Marathon, so why am I working so hard? Because I’m training for marathon clinic days for the next 20 years.

Now more than ever, I feel we have to be physically fit to deal with a physicians’ day’s work. By the time the last patient leaves, I’m beat. From the first bell, patients are packed in, our in boxes are overflowing with messages, pathology results are piling up. It’s exhausting. The root cause is too much work, yes, but I believe being physically fit could help. 

I was talking to an 86-year-old patient about this very topic recently. He was short, with a well-manicured goatee and shiny head. He stuck his arm out to shake my hand. “Glad we’re back to handshakes again, doc.” His grip was that of a 30-year-old. “Buff” you’d likely describe him: He is noticeably muscular, not a skinny old man. He’s an old Navy Master Chief who started a business in wholesale flowers, which distributes all over the United States. And he’s still working full time. Impressed, I asked his secret for such vigor. PT, he replied. 

PT, or physical training, is a foundational element of the Navy. Every sailor starts his or her day with morning PT before carrying out their duties. Some 30 years later, this guy is still getting after it. He does push-ups, sit-ups, and pull-ups nearly every morning. Morning PT is what he attributes to his success not only in health, but also business. As he sees it, he has the business savvy and experience of an old guy and the energy and stamina of a college kid. A good combination for a successful life.

I’ve always been pretty fit. Lately, I’ve been trying to take it to the next level, to not just be “physically active,” but rather “high-performance fit.” There are plenty of sources for instruction; how to stay young and healthy isn’t a new idea after all. I mean, Herodotus wrote of finding the Fountain of Youth in the 5th century BCE. A couple thousand years later, it’s still on trend. One of my favorite sages giving health span advice is Peter Attia, MD. I’ve been a fan since I met him at TEDMED in 2013 and I marvel at the astounding body of work he has created since. A Johns Hopkins–trained surgeon, he has spent his career reviewing the scientific literature about longevity and sharing it as actionable content. His book, “Outlive: The Science and Art of Longevity” (New York: Penguin Random House, 2023) is a nice summary of his work. I recommend it. 

Right now I’m switching between type 2 muscle fiber work (lots of jumping like my 2-year-old) and cardiovascular training including the aforementioned VO_2max work. I cannot say that my patient inbox is any cleaner, or that I’m faster in the office, but I’m not flagging by the end of the day anymore. Master Chief challenged me to match his 10 pull-ups before he returns for his follow up visit. I’ll gladly give up Peloton sprints to work on that.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.

Last month, I described a 28-year-old patient with a history of injection drug use who presented with pain in his left forearm. His history showed that, within the past 2 years, he’d been seen for cutaneous infections multiple times as an outpatient and in the emergency department. His records indicated that he was diagnosed with a penicillin allergy as a child when he developed a rash after receiving amoxicillin. I believed the next course of action should be to test for a penicillin allergy with an oral amoxicillin challenge.
 

Thank you for your excellent questions regarding this case. Great to hear the enthusiasm for testing for penicillin allergy!

One question focused on the course of action in the case of a mild or moderate IgE-mediated reaction after a single dose test with amoxicillin. Treatment for these reactions should include an antihistamine. I would reserve intravenous antihistamines for more severe cases, which also require treatment with a course of corticosteroids. However, the risk for a moderate to severe reaction to amoxicillin on retesting is quite low.

Clinicians need to exercise caution in the use of systemic corticosteroids. These drugs can be lifesaving, but even short courses of corticosteroids are associated with potentially serious adverse events. In a review of adverse events associated with short-course systemic corticosteroids among children, the rate of vomiting was 5.4%; behavioral change, 4.7%; and sleep disturbance, 4.3%. One child died after contracting herpes zoster, more than one-third of children developed elevated blood pressure, and 81.1% had evidence of suppression of the hypothalamic-pituitary-adrenal axis.

Among adults, short courses of systemic corticosteroids are associated with acute increases in the risks for gastrointestinal bleeding and hypertension. Cumulative exposure to short courses of corticosteroids over time results in higher risks for obesity, type 2 diabetes, and osteoporosis.

Another question prompted by this young man’s case focused on the durability of IgE reactions against penicillin. The IgE response to penicillin does indeed wane over time; 80% of patients with a previous true penicillin allergy can tolerate the antibiotic after 10 years. Thus, about 95% of patients with a remote history of penicillin allergy are tolerant of penicillin, and testing can be performed using the algorithm described.

Clinicians should avoid applying current guidelines for the evaluation of patients with penicillin allergy to other common drug allergies. The overall prevalence of sulfonamide allergy is 3%-8%, and the vast majority of these reactions follow treatment with trimethoprim-sulfamethoxazole. Sulfa allergy is even more common among persons living with HIV infection. The natural history of sulfa allergy is not as well established as penicillin allergy. Allergy testing is encouraged in these cases. Graded oral challenge testing is best reserved for patients who are unlikely to have a true sulfa allergy based on their history.

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

Last month, I described a 28-year-old patient with a history of injection drug use who presented with pain in his left forearm. His history showed that, within the past 2 years, he’d been seen for cutaneous infections multiple times as an outpatient and in the emergency department. His records indicated that he was diagnosed with a penicillin allergy as a child when he developed a rash after receiving amoxicillin. I believed the next course of action should be to test for a penicillin allergy with an oral amoxicillin challenge.
 

Thank you for your excellent questions regarding this case. Great to hear the enthusiasm for testing for penicillin allergy!

One question focused on the course of action in the case of a mild or moderate IgE-mediated reaction after a single dose test with amoxicillin. Treatment for these reactions should include an antihistamine. I would reserve intravenous antihistamines for more severe cases, which also require treatment with a course of corticosteroids. However, the risk for a moderate to severe reaction to amoxicillin on retesting is quite low.

Clinicians need to exercise caution in the use of systemic corticosteroids. These drugs can be lifesaving, but even short courses of corticosteroids are associated with potentially serious adverse events. In a review of adverse events associated with short-course systemic corticosteroids among children, the rate of vomiting was 5.4%; behavioral change, 4.7%; and sleep disturbance, 4.3%. One child died after contracting herpes zoster, more than one-third of children developed elevated blood pressure, and 81.1% had evidence of suppression of the hypothalamic-pituitary-adrenal axis.

Among adults, short courses of systemic corticosteroids are associated with acute increases in the risks for gastrointestinal bleeding and hypertension. Cumulative exposure to short courses of corticosteroids over time results in higher risks for obesity, type 2 diabetes, and osteoporosis.

Another question prompted by this young man’s case focused on the durability of IgE reactions against penicillin. The IgE response to penicillin does indeed wane over time; 80% of patients with a previous true penicillin allergy can tolerate the antibiotic after 10 years. Thus, about 95% of patients with a remote history of penicillin allergy are tolerant of penicillin, and testing can be performed using the algorithm described.

Clinicians should avoid applying current guidelines for the evaluation of patients with penicillin allergy to other common drug allergies. The overall prevalence of sulfonamide allergy is 3%-8%, and the vast majority of these reactions follow treatment with trimethoprim-sulfamethoxazole. Sulfa allergy is even more common among persons living with HIV infection. The natural history of sulfa allergy is not as well established as penicillin allergy. Allergy testing is encouraged in these cases. Graded oral challenge testing is best reserved for patients who are unlikely to have a true sulfa allergy based on their history.

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

Last month, I described a 28-year-old patient with a history of injection drug use who presented with pain in his left forearm. His history showed that, within the past 2 years, he’d been seen for cutaneous infections multiple times as an outpatient and in the emergency department. His records indicated that he was diagnosed with a penicillin allergy as a child when he developed a rash after receiving amoxicillin. I believed the next course of action should be to test for a penicillin allergy with an oral amoxicillin challenge.
 

Thank you for your excellent questions regarding this case. Great to hear the enthusiasm for testing for penicillin allergy!

One question focused on the course of action in the case of a mild or moderate IgE-mediated reaction after a single dose test with amoxicillin. Treatment for these reactions should include an antihistamine. I would reserve intravenous antihistamines for more severe cases, which also require treatment with a course of corticosteroids. However, the risk for a moderate to severe reaction to amoxicillin on retesting is quite low.

Clinicians need to exercise caution in the use of systemic corticosteroids. These drugs can be lifesaving, but even short courses of corticosteroids are associated with potentially serious adverse events. In a review of adverse events associated with short-course systemic corticosteroids among children, the rate of vomiting was 5.4%; behavioral change, 4.7%; and sleep disturbance, 4.3%. One child died after contracting herpes zoster, more than one-third of children developed elevated blood pressure, and 81.1% had evidence of suppression of the hypothalamic-pituitary-adrenal axis.

Among adults, short courses of systemic corticosteroids are associated with acute increases in the risks for gastrointestinal bleeding and hypertension. Cumulative exposure to short courses of corticosteroids over time results in higher risks for obesity, type 2 diabetes, and osteoporosis.

Another question prompted by this young man’s case focused on the durability of IgE reactions against penicillin. The IgE response to penicillin does indeed wane over time; 80% of patients with a previous true penicillin allergy can tolerate the antibiotic after 10 years. Thus, about 95% of patients with a remote history of penicillin allergy are tolerant of penicillin, and testing can be performed using the algorithm described.

Clinicians should avoid applying current guidelines for the evaluation of patients with penicillin allergy to other common drug allergies. The overall prevalence of sulfonamide allergy is 3%-8%, and the vast majority of these reactions follow treatment with trimethoprim-sulfamethoxazole. Sulfa allergy is even more common among persons living with HIV infection. The natural history of sulfa allergy is not as well established as penicillin allergy. Allergy testing is encouraged in these cases. Graded oral challenge testing is best reserved for patients who are unlikely to have a true sulfa allergy based on their history.

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

“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

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

“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

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

“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

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