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What does it mean to define an amalgamation of symptoms as a “psychiatric disorder?” Are psychiatric disorders an extreme variation of normative human behavior? Is human behavior simply an output phenotype of some neurologic chemical processes that become disordered in mental illness? Can depression be localized in the brain and subsequently turned on or off? If depression were to be localized in the brain, would it be an excess of a neurotransmitter, the depletion of a receptor, a malfunctioning neuron, an overactive connectome, poorly processed genetic material, or something as yet undefined? Those questions always have been present in our minds and influenced our understanding of patients, but a recent development in psychiatry raises questions about one of the few things we were historically confident about.
A part of our foundational understanding of depression was that it is not sadness, per se. One can be sad for any amount of time. It is not uncommon to feel sad for any variety of reasons, such as watching an adorable 60-second commercial for dog food.1 Those fleeting moments of sadness can even be empowering; they remind us about the things we care about and would be sad to miss.
Sadness in oneself can demonstrate the experience of empathic sadness for others. On the contrary, depression appears to have little apparent purpose, and instead results in a maladaptive way of coping that is all-consuming and often very damaging. Depression is not a mood but a state of being, something that is not defined by how one feels but who one is or has become because of the disorder. So it comes as somewhat of a surprise when we heard that ketamine could alleviate depression in minutes.2,3 As described by a ketamine expert, symptoms are relieved in “no less than an hour.”4 The surprise is not so much that a treatment would work but that improvement could be defined in such a short time frame.
Psychiatry has debated the definition of depression for its entire existence. There are many ways to tackle the concept of depression. A lot of the debate has been about the causes of depression. One example of the continued evolution of our understanding of depression is our prior categorization of depression as “exogenous” or “endogenous.”5 Exogenous depression was described as happening in the context of social stressors and as best treated with therapy. Endogenous depression was a supposedly truer form of depression as a disorder and was more biologically based. Patients suffering from endogenous depression were thought to have chemical abnormalities in the brain that could be alleviated by tricyclic antidepressants and subsequently SSRIs. Like many prior debates about depression, this one appears to be little discussed nowadays. A review of the use of the term “endogenous depression” in books shows an onset in the 1930s, a peak in the 1980s, and a rapid decline since.6
More recently, psychiatrists have defined depression using the DSM-5 criteria. Depression is thought to be the presence of at least five out of nine symptoms listed in the manual for a period of 2 weeks that cause significant distress or impairment.7 The DSM attempts to address criticism by providing information on its limitations and best use, and encourages clinical interpretation of symptoms. The DSM does not portray itself as a gold standard but rather as a tool for treatment planning and effective communication between peers. Furthermore, the National Institute on Mental Health is promoting an alternative understanding of depression using its own Research Domain Criteria, which attempt to provide a more objective understanding of the disorder based on biological rather than subjective correlates.
The growing literature on ketamine partly hinges on the belief that depression is something that can be redefined and changed at any moment. Many trials ask patients whether their depression remains in remission in the subsequent hours, days, and weeks following administration of the drug. However, one wonders if that is even possible. If a patient’s depression is alleviated in an hour, was it really clinical depression? Is it truly in remission? Contrary to our previous understanding, is depression, in reality, a switch that can be turned off by an infusion of an N-methyl-D-aspartate (NMDA)–receptor antagonist? Without minimizing the suffering of patients seeking ketamine or the relief provided to patients who benefit from the treatment, we simply are pointing out that the definition of depression did not account for this reported phenomenon of relatively instantaneous relief. The seemingly miraculous effects of ketamine suggest a new paradigm where any intervention – whether chemical, social, or psychological – could turn off the devastating effects of depression in an instant.
After all, the most widely used scale of depression, the nine-item Patient Health Questionnaire (PHQ-9) asks patients, “Over the last 2 weeks, how often have you been bothered by any of the following problems?” The highest answer one can give is “Nearly every day.” Are we incorrect to think that if one were suicidal every minute of the past 2 weeks, one would still score, nearly every day, even if one’s symptoms were relieved for the past hour? Thus, a maximum score of 27 would remain a 27 no matter what happened in the past hour.
We do realize that we are being overly literal. Ketamine makes some people feel better quickly, and researchers try to capture that effect by asking patients about their symptoms within short intervals. Furthermore, one has to start somewhere. After the infusion is a reasonable time to ask patients how they feel. We are also cognizant that many ketamine researchers do more long-term follow-ups and/or have recommended longer-term studies. Nonetheless,
Expanding our definition of depression to encompass experiences with short time frames may have unintended consequences. As living circumstances rarely change in minutes, the emphasis on rapid recovery makes the patients more in control of their reported experiences and thus their diagnoses. One cannot assess a patient’s impairment or disability from minute to minute. One is left with emphasizing the patient’s subjective symptoms and deemphasizing their relationships, goals, and daily functioning. How could one measure eating habits, hygiene, or participation in hobbies every hour? Another consequence of this reduced time frame is the expansion of a diagnosis that no longer requires the presence of symptoms for 2 weeks. Considering the already vast number of people diagnosed with depression,9,10 this small change may further expand the number diagnosed with a mood disorder. Perhaps to many practitioners and patients these arguments seem obtuse and fastidious, but there is a core failure in modern psychiatry to clearly differentiate the human condition from mental illness. Said failure has vast implications for psychiatric epidemiology, the sociological understanding of psychic suffering and suicide, as well as the overprescribing of psychotropic medications.
Ketamine is an exciting prospect to many psychiatrists who feel like we have had little advancement and few novel treatments in a long time; advertised breakthroughs in the treatment of depression since fluoxetine have not been particularly impressive. Furthermore, the concerns about potential ketamine abuse are not theoretical but a very real problem in some parts of the world.11,12 The concerns about abuse are worsened considering recent evidence that suggests that ketamine’s effect may be driven by its opiate rather than NMDA effects.13 While some have discussed those concerns, we think that the field also needs to address the fact that the debate about ketamine is also changing our definition of depression.
References
1. https://www.youtube.com/watch?v=MpcUN6XvGmk.
2. J Clin Psychiatry. 2016 Jun;77(6):e719-25.
3. Emerg (Tehran). 2014 Winter;2(1):36-9.
4. “Is esketamine the game-changer for depression we want?” Rolling Stone. 2019 Mar 11.
5. Psychol Med. 1971;1(3):191-6.
6. https://books.google.com/ngrams.
7. Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). American Psychiatric Association, 2013.
8. Am J Psychiatry. 2014 Apr;171(4):395-7.
9. “Many people taking antidepressants discover they cannot quit.” New York Times. 2018 Apr 7.
10. “Antidepressants show greatest increase in number of prescription items dispensed.” National Health Service. 2015 Jul 5.
11. “The ketamine connection.” BBC News. 2015 Jul 10.
12. Front Psychiatry. 2018 Jul 17. doi: 10.33389/fpsyt.2018.00313.
13. Am J Psychiatry. 2018 Dec 1;175(2):1205-15.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. Among his writings is Coercion and the critical psychiatrist, chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Cham, Switzerland: Springer Nature Switzerland, 2019, pp. 155-77). Dr. Lehman is an associate professor of psychiatry at UCSD. He is codirector of all Acute and Intensive Psychiatric Treatment at the VA Medical Center in San Diego, where he practices clinical psychiatry. He also is the course director for the UCSD third-year medical student psychiatry clerkship.
*This article was updated 3/25/2019.
What does it mean to define an amalgamation of symptoms as a “psychiatric disorder?” Are psychiatric disorders an extreme variation of normative human behavior? Is human behavior simply an output phenotype of some neurologic chemical processes that become disordered in mental illness? Can depression be localized in the brain and subsequently turned on or off? If depression were to be localized in the brain, would it be an excess of a neurotransmitter, the depletion of a receptor, a malfunctioning neuron, an overactive connectome, poorly processed genetic material, or something as yet undefined? Those questions always have been present in our minds and influenced our understanding of patients, but a recent development in psychiatry raises questions about one of the few things we were historically confident about.
A part of our foundational understanding of depression was that it is not sadness, per se. One can be sad for any amount of time. It is not uncommon to feel sad for any variety of reasons, such as watching an adorable 60-second commercial for dog food.1 Those fleeting moments of sadness can even be empowering; they remind us about the things we care about and would be sad to miss.
Sadness in oneself can demonstrate the experience of empathic sadness for others. On the contrary, depression appears to have little apparent purpose, and instead results in a maladaptive way of coping that is all-consuming and often very damaging. Depression is not a mood but a state of being, something that is not defined by how one feels but who one is or has become because of the disorder. So it comes as somewhat of a surprise when we heard that ketamine could alleviate depression in minutes.2,3 As described by a ketamine expert, symptoms are relieved in “no less than an hour.”4 The surprise is not so much that a treatment would work but that improvement could be defined in such a short time frame.
Psychiatry has debated the definition of depression for its entire existence. There are many ways to tackle the concept of depression. A lot of the debate has been about the causes of depression. One example of the continued evolution of our understanding of depression is our prior categorization of depression as “exogenous” or “endogenous.”5 Exogenous depression was described as happening in the context of social stressors and as best treated with therapy. Endogenous depression was a supposedly truer form of depression as a disorder and was more biologically based. Patients suffering from endogenous depression were thought to have chemical abnormalities in the brain that could be alleviated by tricyclic antidepressants and subsequently SSRIs. Like many prior debates about depression, this one appears to be little discussed nowadays. A review of the use of the term “endogenous depression” in books shows an onset in the 1930s, a peak in the 1980s, and a rapid decline since.6
More recently, psychiatrists have defined depression using the DSM-5 criteria. Depression is thought to be the presence of at least five out of nine symptoms listed in the manual for a period of 2 weeks that cause significant distress or impairment.7 The DSM attempts to address criticism by providing information on its limitations and best use, and encourages clinical interpretation of symptoms. The DSM does not portray itself as a gold standard but rather as a tool for treatment planning and effective communication between peers. Furthermore, the National Institute on Mental Health is promoting an alternative understanding of depression using its own Research Domain Criteria, which attempt to provide a more objective understanding of the disorder based on biological rather than subjective correlates.
The growing literature on ketamine partly hinges on the belief that depression is something that can be redefined and changed at any moment. Many trials ask patients whether their depression remains in remission in the subsequent hours, days, and weeks following administration of the drug. However, one wonders if that is even possible. If a patient’s depression is alleviated in an hour, was it really clinical depression? Is it truly in remission? Contrary to our previous understanding, is depression, in reality, a switch that can be turned off by an infusion of an N-methyl-D-aspartate (NMDA)–receptor antagonist? Without minimizing the suffering of patients seeking ketamine or the relief provided to patients who benefit from the treatment, we simply are pointing out that the definition of depression did not account for this reported phenomenon of relatively instantaneous relief. The seemingly miraculous effects of ketamine suggest a new paradigm where any intervention – whether chemical, social, or psychological – could turn off the devastating effects of depression in an instant.
After all, the most widely used scale of depression, the nine-item Patient Health Questionnaire (PHQ-9) asks patients, “Over the last 2 weeks, how often have you been bothered by any of the following problems?” The highest answer one can give is “Nearly every day.” Are we incorrect to think that if one were suicidal every minute of the past 2 weeks, one would still score, nearly every day, even if one’s symptoms were relieved for the past hour? Thus, a maximum score of 27 would remain a 27 no matter what happened in the past hour.
We do realize that we are being overly literal. Ketamine makes some people feel better quickly, and researchers try to capture that effect by asking patients about their symptoms within short intervals. Furthermore, one has to start somewhere. After the infusion is a reasonable time to ask patients how they feel. We are also cognizant that many ketamine researchers do more long-term follow-ups and/or have recommended longer-term studies. Nonetheless,
Expanding our definition of depression to encompass experiences with short time frames may have unintended consequences. As living circumstances rarely change in minutes, the emphasis on rapid recovery makes the patients more in control of their reported experiences and thus their diagnoses. One cannot assess a patient’s impairment or disability from minute to minute. One is left with emphasizing the patient’s subjective symptoms and deemphasizing their relationships, goals, and daily functioning. How could one measure eating habits, hygiene, or participation in hobbies every hour? Another consequence of this reduced time frame is the expansion of a diagnosis that no longer requires the presence of symptoms for 2 weeks. Considering the already vast number of people diagnosed with depression,9,10 this small change may further expand the number diagnosed with a mood disorder. Perhaps to many practitioners and patients these arguments seem obtuse and fastidious, but there is a core failure in modern psychiatry to clearly differentiate the human condition from mental illness. Said failure has vast implications for psychiatric epidemiology, the sociological understanding of psychic suffering and suicide, as well as the overprescribing of psychotropic medications.
Ketamine is an exciting prospect to many psychiatrists who feel like we have had little advancement and few novel treatments in a long time; advertised breakthroughs in the treatment of depression since fluoxetine have not been particularly impressive. Furthermore, the concerns about potential ketamine abuse are not theoretical but a very real problem in some parts of the world.11,12 The concerns about abuse are worsened considering recent evidence that suggests that ketamine’s effect may be driven by its opiate rather than NMDA effects.13 While some have discussed those concerns, we think that the field also needs to address the fact that the debate about ketamine is also changing our definition of depression.
References
1. https://www.youtube.com/watch?v=MpcUN6XvGmk.
2. J Clin Psychiatry. 2016 Jun;77(6):e719-25.
3. Emerg (Tehran). 2014 Winter;2(1):36-9.
4. “Is esketamine the game-changer for depression we want?” Rolling Stone. 2019 Mar 11.
5. Psychol Med. 1971;1(3):191-6.
6. https://books.google.com/ngrams.
7. Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). American Psychiatric Association, 2013.
8. Am J Psychiatry. 2014 Apr;171(4):395-7.
9. “Many people taking antidepressants discover they cannot quit.” New York Times. 2018 Apr 7.
10. “Antidepressants show greatest increase in number of prescription items dispensed.” National Health Service. 2015 Jul 5.
11. “The ketamine connection.” BBC News. 2015 Jul 10.
12. Front Psychiatry. 2018 Jul 17. doi: 10.33389/fpsyt.2018.00313.
13. Am J Psychiatry. 2018 Dec 1;175(2):1205-15.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. Among his writings is Coercion and the critical psychiatrist, chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Cham, Switzerland: Springer Nature Switzerland, 2019, pp. 155-77). Dr. Lehman is an associate professor of psychiatry at UCSD. He is codirector of all Acute and Intensive Psychiatric Treatment at the VA Medical Center in San Diego, where he practices clinical psychiatry. He also is the course director for the UCSD third-year medical student psychiatry clerkship.
*This article was updated 3/25/2019.
What does it mean to define an amalgamation of symptoms as a “psychiatric disorder?” Are psychiatric disorders an extreme variation of normative human behavior? Is human behavior simply an output phenotype of some neurologic chemical processes that become disordered in mental illness? Can depression be localized in the brain and subsequently turned on or off? If depression were to be localized in the brain, would it be an excess of a neurotransmitter, the depletion of a receptor, a malfunctioning neuron, an overactive connectome, poorly processed genetic material, or something as yet undefined? Those questions always have been present in our minds and influenced our understanding of patients, but a recent development in psychiatry raises questions about one of the few things we were historically confident about.
A part of our foundational understanding of depression was that it is not sadness, per se. One can be sad for any amount of time. It is not uncommon to feel sad for any variety of reasons, such as watching an adorable 60-second commercial for dog food.1 Those fleeting moments of sadness can even be empowering; they remind us about the things we care about and would be sad to miss.
Sadness in oneself can demonstrate the experience of empathic sadness for others. On the contrary, depression appears to have little apparent purpose, and instead results in a maladaptive way of coping that is all-consuming and often very damaging. Depression is not a mood but a state of being, something that is not defined by how one feels but who one is or has become because of the disorder. So it comes as somewhat of a surprise when we heard that ketamine could alleviate depression in minutes.2,3 As described by a ketamine expert, symptoms are relieved in “no less than an hour.”4 The surprise is not so much that a treatment would work but that improvement could be defined in such a short time frame.
Psychiatry has debated the definition of depression for its entire existence. There are many ways to tackle the concept of depression. A lot of the debate has been about the causes of depression. One example of the continued evolution of our understanding of depression is our prior categorization of depression as “exogenous” or “endogenous.”5 Exogenous depression was described as happening in the context of social stressors and as best treated with therapy. Endogenous depression was a supposedly truer form of depression as a disorder and was more biologically based. Patients suffering from endogenous depression were thought to have chemical abnormalities in the brain that could be alleviated by tricyclic antidepressants and subsequently SSRIs. Like many prior debates about depression, this one appears to be little discussed nowadays. A review of the use of the term “endogenous depression” in books shows an onset in the 1930s, a peak in the 1980s, and a rapid decline since.6
More recently, psychiatrists have defined depression using the DSM-5 criteria. Depression is thought to be the presence of at least five out of nine symptoms listed in the manual for a period of 2 weeks that cause significant distress or impairment.7 The DSM attempts to address criticism by providing information on its limitations and best use, and encourages clinical interpretation of symptoms. The DSM does not portray itself as a gold standard but rather as a tool for treatment planning and effective communication between peers. Furthermore, the National Institute on Mental Health is promoting an alternative understanding of depression using its own Research Domain Criteria, which attempt to provide a more objective understanding of the disorder based on biological rather than subjective correlates.
The growing literature on ketamine partly hinges on the belief that depression is something that can be redefined and changed at any moment. Many trials ask patients whether their depression remains in remission in the subsequent hours, days, and weeks following administration of the drug. However, one wonders if that is even possible. If a patient’s depression is alleviated in an hour, was it really clinical depression? Is it truly in remission? Contrary to our previous understanding, is depression, in reality, a switch that can be turned off by an infusion of an N-methyl-D-aspartate (NMDA)–receptor antagonist? Without minimizing the suffering of patients seeking ketamine or the relief provided to patients who benefit from the treatment, we simply are pointing out that the definition of depression did not account for this reported phenomenon of relatively instantaneous relief. The seemingly miraculous effects of ketamine suggest a new paradigm where any intervention – whether chemical, social, or psychological – could turn off the devastating effects of depression in an instant.
After all, the most widely used scale of depression, the nine-item Patient Health Questionnaire (PHQ-9) asks patients, “Over the last 2 weeks, how often have you been bothered by any of the following problems?” The highest answer one can give is “Nearly every day.” Are we incorrect to think that if one were suicidal every minute of the past 2 weeks, one would still score, nearly every day, even if one’s symptoms were relieved for the past hour? Thus, a maximum score of 27 would remain a 27 no matter what happened in the past hour.
We do realize that we are being overly literal. Ketamine makes some people feel better quickly, and researchers try to capture that effect by asking patients about their symptoms within short intervals. Furthermore, one has to start somewhere. After the infusion is a reasonable time to ask patients how they feel. We are also cognizant that many ketamine researchers do more long-term follow-ups and/or have recommended longer-term studies. Nonetheless,
Expanding our definition of depression to encompass experiences with short time frames may have unintended consequences. As living circumstances rarely change in minutes, the emphasis on rapid recovery makes the patients more in control of their reported experiences and thus their diagnoses. One cannot assess a patient’s impairment or disability from minute to minute. One is left with emphasizing the patient’s subjective symptoms and deemphasizing their relationships, goals, and daily functioning. How could one measure eating habits, hygiene, or participation in hobbies every hour? Another consequence of this reduced time frame is the expansion of a diagnosis that no longer requires the presence of symptoms for 2 weeks. Considering the already vast number of people diagnosed with depression,9,10 this small change may further expand the number diagnosed with a mood disorder. Perhaps to many practitioners and patients these arguments seem obtuse and fastidious, but there is a core failure in modern psychiatry to clearly differentiate the human condition from mental illness. Said failure has vast implications for psychiatric epidemiology, the sociological understanding of psychic suffering and suicide, as well as the overprescribing of psychotropic medications.
Ketamine is an exciting prospect to many psychiatrists who feel like we have had little advancement and few novel treatments in a long time; advertised breakthroughs in the treatment of depression since fluoxetine have not been particularly impressive. Furthermore, the concerns about potential ketamine abuse are not theoretical but a very real problem in some parts of the world.11,12 The concerns about abuse are worsened considering recent evidence that suggests that ketamine’s effect may be driven by its opiate rather than NMDA effects.13 While some have discussed those concerns, we think that the field also needs to address the fact that the debate about ketamine is also changing our definition of depression.
References
1. https://www.youtube.com/watch?v=MpcUN6XvGmk.
2. J Clin Psychiatry. 2016 Jun;77(6):e719-25.
3. Emerg (Tehran). 2014 Winter;2(1):36-9.
4. “Is esketamine the game-changer for depression we want?” Rolling Stone. 2019 Mar 11.
5. Psychol Med. 1971;1(3):191-6.
6. https://books.google.com/ngrams.
7. Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). American Psychiatric Association, 2013.
8. Am J Psychiatry. 2014 Apr;171(4):395-7.
9. “Many people taking antidepressants discover they cannot quit.” New York Times. 2018 Apr 7.
10. “Antidepressants show greatest increase in number of prescription items dispensed.” National Health Service. 2015 Jul 5.
11. “The ketamine connection.” BBC News. 2015 Jul 10.
12. Front Psychiatry. 2018 Jul 17. doi: 10.33389/fpsyt.2018.00313.
13. Am J Psychiatry. 2018 Dec 1;175(2):1205-15.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. Among his writings is Coercion and the critical psychiatrist, chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Cham, Switzerland: Springer Nature Switzerland, 2019, pp. 155-77). Dr. Lehman is an associate professor of psychiatry at UCSD. He is codirector of all Acute and Intensive Psychiatric Treatment at the VA Medical Center in San Diego, where he practices clinical psychiatry. He also is the course director for the UCSD third-year medical student psychiatry clerkship.
*This article was updated 3/25/2019.