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Bored? Change the world or read a book
A weekend, for most of us in solo practice, doesn’t really signify time off from work. It just means we’re not seeing patients at the office.
There’s always business stuff to do (like payroll and paying bills), legal cases to review, the never-ending forms for a million things, and all the other stuff there never seems to be enough time to do on weekdays.
So this weekend I started attacking the pile after dinner on Friday and found myself done by Saturday afternoon. Which is rare, usually I spend the better part of a weekend at my desk.
And then, unexpectedly faced with an empty desk, I found myself wondering what to do.
Boredom is one of the odder human conditions. Certainly, there are more ways to waste time now than there ever have been. TV, Netflix, phone games, TikTok, books, just to name a few.
But do we always have to be entertained? Many great scientists have said that world-changing ideas have come to them when they weren’t working, such as while showering or riding to work. Leo Szilard was crossing a London street in 1933 when he suddenly saw how a nuclear chain reaction would be self-sustaining once initiated. (Fortunately, he wasn’t hit by a car in the process.)
But I’m not Szilard. So I rationalized a reason not to exercise and sat on the couch with a book.
The remarkable human brain doesn’t shut down easily. With nothing else to do, most other mammals tend to doze off. But not us. It’s always on, trying to think of the next goal, the next move, the next whatever.
Having nothing to do sounds like a great idea, until you have nothing to do. It may be fine for a few days, but after a while you realize there’s only so long you can stare at the waves or mountains before your mind turns back to “what’s next.”
This isn’t a bad thing. Being bored is probably constructive. Without realizing it we use it to form new ideas and start new plans.
Maybe this is why we’re here. The mind that keeps working is a powerful tool, driving us forward in all walks of life. Perhaps it’s this feature that pushed the development of intelligence further and led us to form civilizations.
Perhaps it’s the real reason we keep moving forward.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
A weekend, for most of us in solo practice, doesn’t really signify time off from work. It just means we’re not seeing patients at the office.
There’s always business stuff to do (like payroll and paying bills), legal cases to review, the never-ending forms for a million things, and all the other stuff there never seems to be enough time to do on weekdays.
So this weekend I started attacking the pile after dinner on Friday and found myself done by Saturday afternoon. Which is rare, usually I spend the better part of a weekend at my desk.
And then, unexpectedly faced with an empty desk, I found myself wondering what to do.
Boredom is one of the odder human conditions. Certainly, there are more ways to waste time now than there ever have been. TV, Netflix, phone games, TikTok, books, just to name a few.
But do we always have to be entertained? Many great scientists have said that world-changing ideas have come to them when they weren’t working, such as while showering or riding to work. Leo Szilard was crossing a London street in 1933 when he suddenly saw how a nuclear chain reaction would be self-sustaining once initiated. (Fortunately, he wasn’t hit by a car in the process.)
But I’m not Szilard. So I rationalized a reason not to exercise and sat on the couch with a book.
The remarkable human brain doesn’t shut down easily. With nothing else to do, most other mammals tend to doze off. But not us. It’s always on, trying to think of the next goal, the next move, the next whatever.
Having nothing to do sounds like a great idea, until you have nothing to do. It may be fine for a few days, but after a while you realize there’s only so long you can stare at the waves or mountains before your mind turns back to “what’s next.”
This isn’t a bad thing. Being bored is probably constructive. Without realizing it we use it to form new ideas and start new plans.
Maybe this is why we’re here. The mind that keeps working is a powerful tool, driving us forward in all walks of life. Perhaps it’s this feature that pushed the development of intelligence further and led us to form civilizations.
Perhaps it’s the real reason we keep moving forward.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
A weekend, for most of us in solo practice, doesn’t really signify time off from work. It just means we’re not seeing patients at the office.
There’s always business stuff to do (like payroll and paying bills), legal cases to review, the never-ending forms for a million things, and all the other stuff there never seems to be enough time to do on weekdays.
So this weekend I started attacking the pile after dinner on Friday and found myself done by Saturday afternoon. Which is rare, usually I spend the better part of a weekend at my desk.
And then, unexpectedly faced with an empty desk, I found myself wondering what to do.
Boredom is one of the odder human conditions. Certainly, there are more ways to waste time now than there ever have been. TV, Netflix, phone games, TikTok, books, just to name a few.
But do we always have to be entertained? Many great scientists have said that world-changing ideas have come to them when they weren’t working, such as while showering or riding to work. Leo Szilard was crossing a London street in 1933 when he suddenly saw how a nuclear chain reaction would be self-sustaining once initiated. (Fortunately, he wasn’t hit by a car in the process.)
But I’m not Szilard. So I rationalized a reason not to exercise and sat on the couch with a book.
The remarkable human brain doesn’t shut down easily. With nothing else to do, most other mammals tend to doze off. But not us. It’s always on, trying to think of the next goal, the next move, the next whatever.
Having nothing to do sounds like a great idea, until you have nothing to do. It may be fine for a few days, but after a while you realize there’s only so long you can stare at the waves or mountains before your mind turns back to “what’s next.”
This isn’t a bad thing. Being bored is probably constructive. Without realizing it we use it to form new ideas and start new plans.
Maybe this is why we’re here. The mind that keeps working is a powerful tool, driving us forward in all walks of life. Perhaps it’s this feature that pushed the development of intelligence further and led us to form civilizations.
Perhaps it’s the real reason we keep moving forward.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
Book Review: Quality improvement in mental health care
Sunil Khushalani and Antonio DePaolo,
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare”
(London: Routledge, Taylor & Francis, 2022)
Since the publication of our book, “Lean Behavioral Health: The Kings County Hospital Story” (Oxford, England: Oxford University Press, 2014) almost a decade ago, “Transforming Mental Healthcare” is the first major book published about the use of a system for quality improvement across the health care continuum. That it has taken this long is probably surprising to those of us who have spent careers on trying to improve what is universally described as a system that is “broken” and in need of a major overhaul.
Every news cycle that reports mass violence typically spends a good bit of time talking about the failures of the mental health care system. One important lesson I learned when taking over the beleaguered Kings County (N.Y.) psychiatry service in 2009 (a department that has made extraordinary improvements over the years and is now exclaimed by the U.S. Department of Justice as “a model program”), is that the employees on the front line are often erroneously blamed for such failures.
The failure is systemic and usually starts at the top of the table of organization, not at the bottom. Dr. Khushalani and Dr. DePaolo have produced an excellent volume that should be purchased by every mental health care CEO and given “with thanks” to the local leaders overseeing the direct care of some of our nation’s most vulnerable patient populations.
The first part of “Transforming Mental Healthcare” provides an excellent overview of the current state of our mental health care system and its too numerous to name problems. This section could be a primer for all our legislators so their eyes can be opened to the failures on the ground that require their help in correcting. Many of the “failures” of our mental health care are societal failures – lack of affordable housing, access to care, reimbursement for care, gun access, etc. – and cannot be “fixed” by providers of care. Such problems are societal problems that call for societal and governmental solutions, and not only at the local level but from coast to coast.
The remainder of this easy to read and follow text provides many rich resources for the deliverers of mental health care. (e.g., plan-do-act, standard work, and A3 thinking).
The closing section focuses on leadership and culture – often overlooked to the detriment of any organization that doesn’t pay close attention to supporting both. Culture is cultivated and nourished by the organization’s leaders. Culture empowers staff to become problem solvers and agents of improvement. Empowered staff support and enrich their culture. Together a workplace that brings out the best of all its people is created, and burnout is held at bay.
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare” is a welcome and essential addition to the current morass, which is our mental health care delivery system, an oasis in the desert from which perhaps the lotus flower can emerge.
Dr. Merlino is emeritus professor of psychiatry, SUNY Downstate College of Medicine, Rhinebeck, N.Y., and formerly director of psychiatry at Kings County Hospital Center, Brooklyn, NY. He is the coauthor of “Lean Behavioral Health: The Kings County Hospital Story.” .
Sunil Khushalani and Antonio DePaolo,
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare”
(London: Routledge, Taylor & Francis, 2022)
Since the publication of our book, “Lean Behavioral Health: The Kings County Hospital Story” (Oxford, England: Oxford University Press, 2014) almost a decade ago, “Transforming Mental Healthcare” is the first major book published about the use of a system for quality improvement across the health care continuum. That it has taken this long is probably surprising to those of us who have spent careers on trying to improve what is universally described as a system that is “broken” and in need of a major overhaul.
Every news cycle that reports mass violence typically spends a good bit of time talking about the failures of the mental health care system. One important lesson I learned when taking over the beleaguered Kings County (N.Y.) psychiatry service in 2009 (a department that has made extraordinary improvements over the years and is now exclaimed by the U.S. Department of Justice as “a model program”), is that the employees on the front line are often erroneously blamed for such failures.
The failure is systemic and usually starts at the top of the table of organization, not at the bottom. Dr. Khushalani and Dr. DePaolo have produced an excellent volume that should be purchased by every mental health care CEO and given “with thanks” to the local leaders overseeing the direct care of some of our nation’s most vulnerable patient populations.
The first part of “Transforming Mental Healthcare” provides an excellent overview of the current state of our mental health care system and its too numerous to name problems. This section could be a primer for all our legislators so their eyes can be opened to the failures on the ground that require their help in correcting. Many of the “failures” of our mental health care are societal failures – lack of affordable housing, access to care, reimbursement for care, gun access, etc. – and cannot be “fixed” by providers of care. Such problems are societal problems that call for societal and governmental solutions, and not only at the local level but from coast to coast.
The remainder of this easy to read and follow text provides many rich resources for the deliverers of mental health care. (e.g., plan-do-act, standard work, and A3 thinking).
The closing section focuses on leadership and culture – often overlooked to the detriment of any organization that doesn’t pay close attention to supporting both. Culture is cultivated and nourished by the organization’s leaders. Culture empowers staff to become problem solvers and agents of improvement. Empowered staff support and enrich their culture. Together a workplace that brings out the best of all its people is created, and burnout is held at bay.
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare” is a welcome and essential addition to the current morass, which is our mental health care delivery system, an oasis in the desert from which perhaps the lotus flower can emerge.
Dr. Merlino is emeritus professor of psychiatry, SUNY Downstate College of Medicine, Rhinebeck, N.Y., and formerly director of psychiatry at Kings County Hospital Center, Brooklyn, NY. He is the coauthor of “Lean Behavioral Health: The Kings County Hospital Story.” .
Sunil Khushalani and Antonio DePaolo,
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare”
(London: Routledge, Taylor & Francis, 2022)
Since the publication of our book, “Lean Behavioral Health: The Kings County Hospital Story” (Oxford, England: Oxford University Press, 2014) almost a decade ago, “Transforming Mental Healthcare” is the first major book published about the use of a system for quality improvement across the health care continuum. That it has taken this long is probably surprising to those of us who have spent careers on trying to improve what is universally described as a system that is “broken” and in need of a major overhaul.
Every news cycle that reports mass violence typically spends a good bit of time talking about the failures of the mental health care system. One important lesson I learned when taking over the beleaguered Kings County (N.Y.) psychiatry service in 2009 (a department that has made extraordinary improvements over the years and is now exclaimed by the U.S. Department of Justice as “a model program”), is that the employees on the front line are often erroneously blamed for such failures.
The failure is systemic and usually starts at the top of the table of organization, not at the bottom. Dr. Khushalani and Dr. DePaolo have produced an excellent volume that should be purchased by every mental health care CEO and given “with thanks” to the local leaders overseeing the direct care of some of our nation’s most vulnerable patient populations.
The first part of “Transforming Mental Healthcare” provides an excellent overview of the current state of our mental health care system and its too numerous to name problems. This section could be a primer for all our legislators so their eyes can be opened to the failures on the ground that require their help in correcting. Many of the “failures” of our mental health care are societal failures – lack of affordable housing, access to care, reimbursement for care, gun access, etc. – and cannot be “fixed” by providers of care. Such problems are societal problems that call for societal and governmental solutions, and not only at the local level but from coast to coast.
The remainder of this easy to read and follow text provides many rich resources for the deliverers of mental health care. (e.g., plan-do-act, standard work, and A3 thinking).
The closing section focuses on leadership and culture – often overlooked to the detriment of any organization that doesn’t pay close attention to supporting both. Culture is cultivated and nourished by the organization’s leaders. Culture empowers staff to become problem solvers and agents of improvement. Empowered staff support and enrich their culture. Together a workplace that brings out the best of all its people is created, and burnout is held at bay.
“Transforming Mental Healthcare: Applying Performance Improvement Methods to Mental Healthcare” is a welcome and essential addition to the current morass, which is our mental health care delivery system, an oasis in the desert from which perhaps the lotus flower can emerge.
Dr. Merlino is emeritus professor of psychiatry, SUNY Downstate College of Medicine, Rhinebeck, N.Y., and formerly director of psychiatry at Kings County Hospital Center, Brooklyn, NY. He is the coauthor of “Lean Behavioral Health: The Kings County Hospital Story.” .
Adapting to Changes in Acne Management: Take One Step at a Time
After most dermatology residents graduate from their programs, they go out into practice and will often carry with them what they learned from their teachers, especially clinicians. Everyone else in their dermatology residency programs approaches disease management and the use of different therapies in the same way, right?
It does not take very long before these same dermatology residents realize that things are different in real-world clinical practice in many ways. Most clinicians develop a range of fairly predictable patterns in how they approach and treat common skin disorders such as acne, rosacea, psoriasis, atopic dermatitis/eczema, and seborrheic dermatitis. These patterns often include what testing is performed at baseline and at follow-up.
Recently, I have been giving thought to how clinicians—myself included—change their approaches to management of specific skin diseases over time, especially as new information and therapies emerge. Are we fast adopters, or are we slow adopters? How much evidence do we need to see before we consider adjusting our approach? Is the needle moving too fast or not fast enough?
I would like to use an example that relates to acne treatment, especially as this is one of the most common skin disorders encountered in outpatient dermatologic practice. Despite lack of US Food and Drug Administration (FDA) approval for use in acne, oral spironolactone commonly is used in females, especially adults, with acne vulgaris and has a long history as an acceptable approach in dermatology.1 Because spironolactone is a potassium-sparing diuretic, one question that commonly arises is: Do we monitor serum potassium levels at baseline and periodically during treatment with spironolactone? There has never been a definitive consensus on which approach to take. However, there has been evidence to suggest that such monitoring is not necessary in young healthy women due to a negligible risk for clinically relevant hyperkalemia.2,3
In fact, the suggestion that there is a very low risk for clinically significant hyperkalemia in healthy young women treated with spironolactone is accurate based on population-based studies. Nevertheless, the clinician is faced with confirming the patient is in fact healthy rather than assuming this is the case due to her “young” age. In addition, it is important to exclude potential drug-drug interactions that can increase the risk for hyperkalemia when coadministered with spironolactone and also to exclude an unknown underlying decrease in renal function.1 At the end of the day, I support the continued research that is being done to evaluate questions that can challenge the recycled dogma on how we manage patients, and I do not fault those who follow what they believe to be new cogent evidence. However, in the case of oral spironolactone use, I also could never fault a clinician for monitoring renal function and electrolytes including serum potassium levels in a female patient treated for acne, especially with a drug that has the known potential to cause hyperkalemia in certain clinical situations and is not FDA approved for the indication of acne (ie, the guidance that accompanies the level of investigation needed for such FDA approval is missing). The clinical judgment of the clinician who is responsible for the individual patient trumps the results from population-based studies completed thus far. Ultimately, it is the responsibility of that clinician to assure the safety of their patient in a manner that they are comfortable with.
It takes time to make changes in our approaches to patient management, and in the majority of cases, that is rightfully so. There are several potential limitations to how certain data are collected, and a reasonable verification of results over time is what tends to change behavior patterns. Ultimately, the common goal is to do what is in the best interest of our patients. No one can argue successfully against that.
- Kim GK, Del Rosso JQ. Oral spironolactone in post-teenage female patients with acne vulgaris: practical considerations for the clinician based on current data and clinical experience. J Clin Aesthet Dermatol. 2012;5:37-50.
- Plovanich M, Weng QY, Arash Mostaghimi A. Low usefulness of potassium monitoring among healthy young women taking spironolactone for acne. JAMA Dermatol. 2015;151:941-944.
- Barbieri JS, Margolis DJ, Mostaghimi A. Temporal trends and clinician variability in potassium monitoring of healthy young women treated for acne with spironolactone. JAMA Dermatol. 2021;157:296-300.
After most dermatology residents graduate from their programs, they go out into practice and will often carry with them what they learned from their teachers, especially clinicians. Everyone else in their dermatology residency programs approaches disease management and the use of different therapies in the same way, right?
It does not take very long before these same dermatology residents realize that things are different in real-world clinical practice in many ways. Most clinicians develop a range of fairly predictable patterns in how they approach and treat common skin disorders such as acne, rosacea, psoriasis, atopic dermatitis/eczema, and seborrheic dermatitis. These patterns often include what testing is performed at baseline and at follow-up.
Recently, I have been giving thought to how clinicians—myself included—change their approaches to management of specific skin diseases over time, especially as new information and therapies emerge. Are we fast adopters, or are we slow adopters? How much evidence do we need to see before we consider adjusting our approach? Is the needle moving too fast or not fast enough?
I would like to use an example that relates to acne treatment, especially as this is one of the most common skin disorders encountered in outpatient dermatologic practice. Despite lack of US Food and Drug Administration (FDA) approval for use in acne, oral spironolactone commonly is used in females, especially adults, with acne vulgaris and has a long history as an acceptable approach in dermatology.1 Because spironolactone is a potassium-sparing diuretic, one question that commonly arises is: Do we monitor serum potassium levels at baseline and periodically during treatment with spironolactone? There has never been a definitive consensus on which approach to take. However, there has been evidence to suggest that such monitoring is not necessary in young healthy women due to a negligible risk for clinically relevant hyperkalemia.2,3
In fact, the suggestion that there is a very low risk for clinically significant hyperkalemia in healthy young women treated with spironolactone is accurate based on population-based studies. Nevertheless, the clinician is faced with confirming the patient is in fact healthy rather than assuming this is the case due to her “young” age. In addition, it is important to exclude potential drug-drug interactions that can increase the risk for hyperkalemia when coadministered with spironolactone and also to exclude an unknown underlying decrease in renal function.1 At the end of the day, I support the continued research that is being done to evaluate questions that can challenge the recycled dogma on how we manage patients, and I do not fault those who follow what they believe to be new cogent evidence. However, in the case of oral spironolactone use, I also could never fault a clinician for monitoring renal function and electrolytes including serum potassium levels in a female patient treated for acne, especially with a drug that has the known potential to cause hyperkalemia in certain clinical situations and is not FDA approved for the indication of acne (ie, the guidance that accompanies the level of investigation needed for such FDA approval is missing). The clinical judgment of the clinician who is responsible for the individual patient trumps the results from population-based studies completed thus far. Ultimately, it is the responsibility of that clinician to assure the safety of their patient in a manner that they are comfortable with.
It takes time to make changes in our approaches to patient management, and in the majority of cases, that is rightfully so. There are several potential limitations to how certain data are collected, and a reasonable verification of results over time is what tends to change behavior patterns. Ultimately, the common goal is to do what is in the best interest of our patients. No one can argue successfully against that.
After most dermatology residents graduate from their programs, they go out into practice and will often carry with them what they learned from their teachers, especially clinicians. Everyone else in their dermatology residency programs approaches disease management and the use of different therapies in the same way, right?
It does not take very long before these same dermatology residents realize that things are different in real-world clinical practice in many ways. Most clinicians develop a range of fairly predictable patterns in how they approach and treat common skin disorders such as acne, rosacea, psoriasis, atopic dermatitis/eczema, and seborrheic dermatitis. These patterns often include what testing is performed at baseline and at follow-up.
Recently, I have been giving thought to how clinicians—myself included—change their approaches to management of specific skin diseases over time, especially as new information and therapies emerge. Are we fast adopters, or are we slow adopters? How much evidence do we need to see before we consider adjusting our approach? Is the needle moving too fast or not fast enough?
I would like to use an example that relates to acne treatment, especially as this is one of the most common skin disorders encountered in outpatient dermatologic practice. Despite lack of US Food and Drug Administration (FDA) approval for use in acne, oral spironolactone commonly is used in females, especially adults, with acne vulgaris and has a long history as an acceptable approach in dermatology.1 Because spironolactone is a potassium-sparing diuretic, one question that commonly arises is: Do we monitor serum potassium levels at baseline and periodically during treatment with spironolactone? There has never been a definitive consensus on which approach to take. However, there has been evidence to suggest that such monitoring is not necessary in young healthy women due to a negligible risk for clinically relevant hyperkalemia.2,3
In fact, the suggestion that there is a very low risk for clinically significant hyperkalemia in healthy young women treated with spironolactone is accurate based on population-based studies. Nevertheless, the clinician is faced with confirming the patient is in fact healthy rather than assuming this is the case due to her “young” age. In addition, it is important to exclude potential drug-drug interactions that can increase the risk for hyperkalemia when coadministered with spironolactone and also to exclude an unknown underlying decrease in renal function.1 At the end of the day, I support the continued research that is being done to evaluate questions that can challenge the recycled dogma on how we manage patients, and I do not fault those who follow what they believe to be new cogent evidence. However, in the case of oral spironolactone use, I also could never fault a clinician for monitoring renal function and electrolytes including serum potassium levels in a female patient treated for acne, especially with a drug that has the known potential to cause hyperkalemia in certain clinical situations and is not FDA approved for the indication of acne (ie, the guidance that accompanies the level of investigation needed for such FDA approval is missing). The clinical judgment of the clinician who is responsible for the individual patient trumps the results from population-based studies completed thus far. Ultimately, it is the responsibility of that clinician to assure the safety of their patient in a manner that they are comfortable with.
It takes time to make changes in our approaches to patient management, and in the majority of cases, that is rightfully so. There are several potential limitations to how certain data are collected, and a reasonable verification of results over time is what tends to change behavior patterns. Ultimately, the common goal is to do what is in the best interest of our patients. No one can argue successfully against that.
- Kim GK, Del Rosso JQ. Oral spironolactone in post-teenage female patients with acne vulgaris: practical considerations for the clinician based on current data and clinical experience. J Clin Aesthet Dermatol. 2012;5:37-50.
- Plovanich M, Weng QY, Arash Mostaghimi A. Low usefulness of potassium monitoring among healthy young women taking spironolactone for acne. JAMA Dermatol. 2015;151:941-944.
- Barbieri JS, Margolis DJ, Mostaghimi A. Temporal trends and clinician variability in potassium monitoring of healthy young women treated for acne with spironolactone. JAMA Dermatol. 2021;157:296-300.
- Kim GK, Del Rosso JQ. Oral spironolactone in post-teenage female patients with acne vulgaris: practical considerations for the clinician based on current data and clinical experience. J Clin Aesthet Dermatol. 2012;5:37-50.
- Plovanich M, Weng QY, Arash Mostaghimi A. Low usefulness of potassium monitoring among healthy young women taking spironolactone for acne. JAMA Dermatol. 2015;151:941-944.
- Barbieri JS, Margolis DJ, Mostaghimi A. Temporal trends and clinician variability in potassium monitoring of healthy young women treated for acne with spironolactone. JAMA Dermatol. 2021;157:296-300.
What is palliative care and what’s new in practicing this type of medicine?
The World Health Organization defines palliative care as “an approach that improves the quality of life of patients (adults and children) and their families who are facing problems associated with life-threatening illness. It prevents and relieves suffering through the early identification, correct assessment, and treatment of pain and other problems, whether physical, psychosocial or spiritual.”1
The common misperception is that palliative care is only for those at end of life or only in the advanced stages of their illness. However, palliative care is ideally most helpful following individuals from diagnosis through their illness trajectory. Another misperception is that palliative care and hospice are the same thing. Though all hospice is palliative care, all palliative care is not hospice. Both palliative care and hospice provide care for individuals facing a serious illness and focus on the same philosophy of care, but palliative care can be initiated at any stage of illness, even if the goal is to pursue curative and life-prolonging therapies/interventions.
In contrast, hospice is considered for those who are at the end of life and are usually not pursuing life-prolonging therapies or interventions, instead focusing on comfort, symptom management, and optimization of quality of life.
Though there is a growing need for palliative care, there is a shortage of specialist palliative care providers. Much of the palliative care needs can be met by all providers who can offer basic symptom management, identification surrounding goals of care and discussions of advance care planning, and understanding of illness/prognosis and treatment options, which is called primary palliative care.2 In fact, two-thirds of patients with a serious illness other than cancer prefer discussion of end-of-life care or advance care planning with their primary care providers.3
Referral to specialty palliative care should be considered when there are more complexities to symptom/pain management and goals of care/end of life, transition to hospice, or complex communication dynamics.4
Though specialty palliative care was shown to be more comprehensive, both primary palliative care and specialty palliative care have led to improvements in the quality of life in individuals living with serious illness.5 Early integration of palliative care into routine care has been shown to improve symptom burden, mood, quality of life, survival, and health care costs.6
Updates in alternative and complementary therapies to palliative care
There are several alternative and complementary therapies to palliative care, including cannabis and psychedelics. These therapies are becoming or may become a familiar part of medical therapies that are listed in a patient’s history as part of their medical regimen, especially as more states continue to legalize and/or decriminalize the use of these alternative therapies for recreational or medicinal use.
Both cannabis and psychedelics have a longstanding history of therapeutic and holistic use. Cannabis has been used to manage symptoms such as pain since the 16th and 17th century.7 In palliative care, more patients may turn to various forms of cannabis as a source of relief from symptoms and suffering as their focus shifts more to quality of life.
Even with the increasing popularity of the use of cannabis among seriously ill patients, there is still a lack of evidence of the benefits of medical cannabis use in palliative care, and there is a lack of standardization of type of cannabis used and state regulations regarding their use.7
A recent systematic review found that despite the reported positive treatment effects of cannabis in palliative care, the results of the studies were conflicting. This highlights the need for further high-quality research to determine whether cannabis products are an effective treatment in palliative care patients.8
One limitation to note is that the majority of the included studies focused on cannabis use in patients with cancer for cancer-related symptoms. Few studies included patients with other serious conditions.
Psychedelics
There is evidence that psychedelic assisted therapy (PAT) is a safe and effective treatment for individuals with refractory depression, posttraumatic stress disorder, and substance use disorder.9 Plus, there have been ample studies providing support that PAT improves symptoms such as refractory anxiety/depression, demoralization, and existential distress in seriously ill patients, thus improving their quality of life and overall well-being.9
Nine U.S. cities and the State of Oregon have decriminalized or legalized the psychedelic psilocybin, based on the medical benefits patients have experienced evidenced from using it.10
In light of the increasing interest in PAT, Dr. Ira Byock provided the following points on what “all clinicians should know as they enter this uncharted territory”:
- Psychedelics have been around for a long time.
- Psychedelic-assisted therapies’ therapeutic effects are experiential.
- There are a variety of terms for specific categories of psychedelic compounds.
- Some palliative care teams are already caring for patients who undergo psychedelic experiences.
- Use of psychedelics should be well-observed by a skilled clinician with expertise.
I am hoping this provides a general refresher on palliative care and an overview of updates to alternative and complementary therapies for patients living with serious illness.9
Dr. Kang is a geriatrician and palliative care provider at the University of Washington, Seattle in the division of geriatrics and gerontology. She has no conflicts related to the content of this piece.
References
1. World Health Organization. Palliative care. 2020 Aug 5..
2. Weissman DE and Meier DE. Identifying patients in need of a palliative care assessment in the hospital setting a consensus report from the center to advance palliative care. J Palliat Med. 2011;14(1):17-23.
3. Sherry D et al. Is primary care physician involvement associated with earlier advance care planning? A study of patients in an academic primary care setting. J Palliat Med. 2022;25(1):75-80.
4. Quill TE and Abernethy AP. Generalist plus specialist palliative care-creating a more sustainable model. N Engl J Med. 2013;368:1173-75.
5. Ernecoff NC et al. Comparing specialty and primary palliative care interventions: Analysis of a systematic review. J Palliat Med. 2020;23(3):389-96.
6. Temmel JS et al. Early palliative care for patients with metastatic non–small-cell lung cancer. N Engl J Med. 2011;363:733-42.
7. Kogan M and Sexton M. Medical cannabis: A new old tool for palliative care. J Altern Complement Med . 2020 Sep;26(9):776-8.
8. Doppen M et al. Cannabis in palliative care: A systematic review of the current evidence. J Pain Symptom Manage. 2022 Jun 12;S0885-3924(22)00760-6.
9. Byock I. Psychedelics for serious illness: Five things clinicians need to know. The Center to Advance Palliative Care. Psychedelics for Serious Illness, Palliative in Practice, Center to Advance Palliative Care (capc.org). June 13, 2022.
10. Marks M. A strategy for rescheduling psilocybin. Scientific American. Oct. 11, 2021.
The World Health Organization defines palliative care as “an approach that improves the quality of life of patients (adults and children) and their families who are facing problems associated with life-threatening illness. It prevents and relieves suffering through the early identification, correct assessment, and treatment of pain and other problems, whether physical, psychosocial or spiritual.”1
The common misperception is that palliative care is only for those at end of life or only in the advanced stages of their illness. However, palliative care is ideally most helpful following individuals from diagnosis through their illness trajectory. Another misperception is that palliative care and hospice are the same thing. Though all hospice is palliative care, all palliative care is not hospice. Both palliative care and hospice provide care for individuals facing a serious illness and focus on the same philosophy of care, but palliative care can be initiated at any stage of illness, even if the goal is to pursue curative and life-prolonging therapies/interventions.
In contrast, hospice is considered for those who are at the end of life and are usually not pursuing life-prolonging therapies or interventions, instead focusing on comfort, symptom management, and optimization of quality of life.
Though there is a growing need for palliative care, there is a shortage of specialist palliative care providers. Much of the palliative care needs can be met by all providers who can offer basic symptom management, identification surrounding goals of care and discussions of advance care planning, and understanding of illness/prognosis and treatment options, which is called primary palliative care.2 In fact, two-thirds of patients with a serious illness other than cancer prefer discussion of end-of-life care or advance care planning with their primary care providers.3
Referral to specialty palliative care should be considered when there are more complexities to symptom/pain management and goals of care/end of life, transition to hospice, or complex communication dynamics.4
Though specialty palliative care was shown to be more comprehensive, both primary palliative care and specialty palliative care have led to improvements in the quality of life in individuals living with serious illness.5 Early integration of palliative care into routine care has been shown to improve symptom burden, mood, quality of life, survival, and health care costs.6
Updates in alternative and complementary therapies to palliative care
There are several alternative and complementary therapies to palliative care, including cannabis and psychedelics. These therapies are becoming or may become a familiar part of medical therapies that are listed in a patient’s history as part of their medical regimen, especially as more states continue to legalize and/or decriminalize the use of these alternative therapies for recreational or medicinal use.
Both cannabis and psychedelics have a longstanding history of therapeutic and holistic use. Cannabis has been used to manage symptoms such as pain since the 16th and 17th century.7 In palliative care, more patients may turn to various forms of cannabis as a source of relief from symptoms and suffering as their focus shifts more to quality of life.
Even with the increasing popularity of the use of cannabis among seriously ill patients, there is still a lack of evidence of the benefits of medical cannabis use in palliative care, and there is a lack of standardization of type of cannabis used and state regulations regarding their use.7
A recent systematic review found that despite the reported positive treatment effects of cannabis in palliative care, the results of the studies were conflicting. This highlights the need for further high-quality research to determine whether cannabis products are an effective treatment in palliative care patients.8
One limitation to note is that the majority of the included studies focused on cannabis use in patients with cancer for cancer-related symptoms. Few studies included patients with other serious conditions.
Psychedelics
There is evidence that psychedelic assisted therapy (PAT) is a safe and effective treatment for individuals with refractory depression, posttraumatic stress disorder, and substance use disorder.9 Plus, there have been ample studies providing support that PAT improves symptoms such as refractory anxiety/depression, demoralization, and existential distress in seriously ill patients, thus improving their quality of life and overall well-being.9
Nine U.S. cities and the State of Oregon have decriminalized or legalized the psychedelic psilocybin, based on the medical benefits patients have experienced evidenced from using it.10
In light of the increasing interest in PAT, Dr. Ira Byock provided the following points on what “all clinicians should know as they enter this uncharted territory”:
- Psychedelics have been around for a long time.
- Psychedelic-assisted therapies’ therapeutic effects are experiential.
- There are a variety of terms for specific categories of psychedelic compounds.
- Some palliative care teams are already caring for patients who undergo psychedelic experiences.
- Use of psychedelics should be well-observed by a skilled clinician with expertise.
I am hoping this provides a general refresher on palliative care and an overview of updates to alternative and complementary therapies for patients living with serious illness.9
Dr. Kang is a geriatrician and palliative care provider at the University of Washington, Seattle in the division of geriatrics and gerontology. She has no conflicts related to the content of this piece.
References
1. World Health Organization. Palliative care. 2020 Aug 5..
2. Weissman DE and Meier DE. Identifying patients in need of a palliative care assessment in the hospital setting a consensus report from the center to advance palliative care. J Palliat Med. 2011;14(1):17-23.
3. Sherry D et al. Is primary care physician involvement associated with earlier advance care planning? A study of patients in an academic primary care setting. J Palliat Med. 2022;25(1):75-80.
4. Quill TE and Abernethy AP. Generalist plus specialist palliative care-creating a more sustainable model. N Engl J Med. 2013;368:1173-75.
5. Ernecoff NC et al. Comparing specialty and primary palliative care interventions: Analysis of a systematic review. J Palliat Med. 2020;23(3):389-96.
6. Temmel JS et al. Early palliative care for patients with metastatic non–small-cell lung cancer. N Engl J Med. 2011;363:733-42.
7. Kogan M and Sexton M. Medical cannabis: A new old tool for palliative care. J Altern Complement Med . 2020 Sep;26(9):776-8.
8. Doppen M et al. Cannabis in palliative care: A systematic review of the current evidence. J Pain Symptom Manage. 2022 Jun 12;S0885-3924(22)00760-6.
9. Byock I. Psychedelics for serious illness: Five things clinicians need to know. The Center to Advance Palliative Care. Psychedelics for Serious Illness, Palliative in Practice, Center to Advance Palliative Care (capc.org). June 13, 2022.
10. Marks M. A strategy for rescheduling psilocybin. Scientific American. Oct. 11, 2021.
The World Health Organization defines palliative care as “an approach that improves the quality of life of patients (adults and children) and their families who are facing problems associated with life-threatening illness. It prevents and relieves suffering through the early identification, correct assessment, and treatment of pain and other problems, whether physical, psychosocial or spiritual.”1
The common misperception is that palliative care is only for those at end of life or only in the advanced stages of their illness. However, palliative care is ideally most helpful following individuals from diagnosis through their illness trajectory. Another misperception is that palliative care and hospice are the same thing. Though all hospice is palliative care, all palliative care is not hospice. Both palliative care and hospice provide care for individuals facing a serious illness and focus on the same philosophy of care, but palliative care can be initiated at any stage of illness, even if the goal is to pursue curative and life-prolonging therapies/interventions.
In contrast, hospice is considered for those who are at the end of life and are usually not pursuing life-prolonging therapies or interventions, instead focusing on comfort, symptom management, and optimization of quality of life.
Though there is a growing need for palliative care, there is a shortage of specialist palliative care providers. Much of the palliative care needs can be met by all providers who can offer basic symptom management, identification surrounding goals of care and discussions of advance care planning, and understanding of illness/prognosis and treatment options, which is called primary palliative care.2 In fact, two-thirds of patients with a serious illness other than cancer prefer discussion of end-of-life care or advance care planning with their primary care providers.3
Referral to specialty palliative care should be considered when there are more complexities to symptom/pain management and goals of care/end of life, transition to hospice, or complex communication dynamics.4
Though specialty palliative care was shown to be more comprehensive, both primary palliative care and specialty palliative care have led to improvements in the quality of life in individuals living with serious illness.5 Early integration of palliative care into routine care has been shown to improve symptom burden, mood, quality of life, survival, and health care costs.6
Updates in alternative and complementary therapies to palliative care
There are several alternative and complementary therapies to palliative care, including cannabis and psychedelics. These therapies are becoming or may become a familiar part of medical therapies that are listed in a patient’s history as part of their medical regimen, especially as more states continue to legalize and/or decriminalize the use of these alternative therapies for recreational or medicinal use.
Both cannabis and psychedelics have a longstanding history of therapeutic and holistic use. Cannabis has been used to manage symptoms such as pain since the 16th and 17th century.7 In palliative care, more patients may turn to various forms of cannabis as a source of relief from symptoms and suffering as their focus shifts more to quality of life.
Even with the increasing popularity of the use of cannabis among seriously ill patients, there is still a lack of evidence of the benefits of medical cannabis use in palliative care, and there is a lack of standardization of type of cannabis used and state regulations regarding their use.7
A recent systematic review found that despite the reported positive treatment effects of cannabis in palliative care, the results of the studies were conflicting. This highlights the need for further high-quality research to determine whether cannabis products are an effective treatment in palliative care patients.8
One limitation to note is that the majority of the included studies focused on cannabis use in patients with cancer for cancer-related symptoms. Few studies included patients with other serious conditions.
Psychedelics
There is evidence that psychedelic assisted therapy (PAT) is a safe and effective treatment for individuals with refractory depression, posttraumatic stress disorder, and substance use disorder.9 Plus, there have been ample studies providing support that PAT improves symptoms such as refractory anxiety/depression, demoralization, and existential distress in seriously ill patients, thus improving their quality of life and overall well-being.9
Nine U.S. cities and the State of Oregon have decriminalized or legalized the psychedelic psilocybin, based on the medical benefits patients have experienced evidenced from using it.10
In light of the increasing interest in PAT, Dr. Ira Byock provided the following points on what “all clinicians should know as they enter this uncharted territory”:
- Psychedelics have been around for a long time.
- Psychedelic-assisted therapies’ therapeutic effects are experiential.
- There are a variety of terms for specific categories of psychedelic compounds.
- Some palliative care teams are already caring for patients who undergo psychedelic experiences.
- Use of psychedelics should be well-observed by a skilled clinician with expertise.
I am hoping this provides a general refresher on palliative care and an overview of updates to alternative and complementary therapies for patients living with serious illness.9
Dr. Kang is a geriatrician and palliative care provider at the University of Washington, Seattle in the division of geriatrics and gerontology. She has no conflicts related to the content of this piece.
References
1. World Health Organization. Palliative care. 2020 Aug 5..
2. Weissman DE and Meier DE. Identifying patients in need of a palliative care assessment in the hospital setting a consensus report from the center to advance palliative care. J Palliat Med. 2011;14(1):17-23.
3. Sherry D et al. Is primary care physician involvement associated with earlier advance care planning? A study of patients in an academic primary care setting. J Palliat Med. 2022;25(1):75-80.
4. Quill TE and Abernethy AP. Generalist plus specialist palliative care-creating a more sustainable model. N Engl J Med. 2013;368:1173-75.
5. Ernecoff NC et al. Comparing specialty and primary palliative care interventions: Analysis of a systematic review. J Palliat Med. 2020;23(3):389-96.
6. Temmel JS et al. Early palliative care for patients with metastatic non–small-cell lung cancer. N Engl J Med. 2011;363:733-42.
7. Kogan M and Sexton M. Medical cannabis: A new old tool for palliative care. J Altern Complement Med . 2020 Sep;26(9):776-8.
8. Doppen M et al. Cannabis in palliative care: A systematic review of the current evidence. J Pain Symptom Manage. 2022 Jun 12;S0885-3924(22)00760-6.
9. Byock I. Psychedelics for serious illness: Five things clinicians need to know. The Center to Advance Palliative Care. Psychedelics for Serious Illness, Palliative in Practice, Center to Advance Palliative Care (capc.org). June 13, 2022.
10. Marks M. A strategy for rescheduling psilocybin. Scientific American. Oct. 11, 2021.
Caring for the young elite athlete
Concerns about the potential harm resulting from overzealous training regimens and performance schedules for young elite athletes seems to come in cycles much like the Olympics. But, more recently, the media attention has become more intense fueled by the very visible psychological vulnerabilities of some young gymnasts, tennis players, and figure skaters. Accusations of physical and psychological abuse by team physicians and coaches continue to surface with troubling regularity.
A recent article in the Wall St. Journal explores a variety of initiatives aimed at redefining the relationship between youth sports and the physical and mental health of its elite athletes. (Louise Radnofsky, The Wall Street Journal, June 9, 2022).
An example of the new awareness is the recent invitation of Peter Donnelly, PhD, an emeritus professor at the University of Toronto and long-time advocate for regulatory protections for youth athletes, to deliver a paper at a global conference in South Africa devoted to the elimination of child labor. Referring to youth sports, Dr. Donnelly observes “What if McDonalds had the same accident rate? ... There would be huge commissions of inquiry, regulations, and policies.” He suggests that the United Nations Convention on the Rights of the Child might be a mechanism to address the problem.
Writing in the Marquette University Sports Law Review in 2015, Kristin Hoffman, a law student at the time, suggested that the federal Fair Labor Standards Act or state child labor laws could be used to restructure sports like gymnastics or figure skating with tarnished histories. California law prohibits child actors from working more than 5 hours a day on school days and 7 hours on nonschool days but says little about child athletes. On paper, the National Collegiate Athletic Association limits college athletes to 20 hours participation per week but teenagers on club teams are not limited and may sometimes practice 30 hours or more.
Regulation in any form is a tough sell in this country. Coaches, parents, and athletes caught up in the myth that more repetitions and more touches on the ball are always the ticket to success will argue that most elite athletes are self-motivated and don’t view the long hours as a hardship.
Exactly how many are self-driven and how many are being pushed by parents and coaches is unknown. Across the street from us lived a young girl who, despite not having the obvious physical gifts, was clearly committed to excel in sports. She begged her parents to set up lights to allow her to practice well into the evening. She went on to have a good college career as a player and a very successful career as a Division I coach. Now in retirement, she is very open about her mental health history that in large part explains her inner drive and her subsequent troubles.
We need to be realistic in our hope for regulating the current state of youth sports out of its current situation. State laws that put reasonable limits on the hourly commitment to sports much like the California child actor laws feel like a reasonable goal. However, as physicians for these young athletes we must take each child – and we must remind ourselves that they are still children – as an individual.
When faced with patients who are clearly on the elite sport pathway, our goal is to protect their health – both physical and mental. If they are having symptoms of overuse we need to help them find alternative activities that will rest their injuries but still allow them to satisfy their competitive zeal. However, we must be ever alert to the risk that what appears to be unusual self-motivation may be instead a warning that pathologic obsession and compulsion lurk below the surface.
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.
Concerns about the potential harm resulting from overzealous training regimens and performance schedules for young elite athletes seems to come in cycles much like the Olympics. But, more recently, the media attention has become more intense fueled by the very visible psychological vulnerabilities of some young gymnasts, tennis players, and figure skaters. Accusations of physical and psychological abuse by team physicians and coaches continue to surface with troubling regularity.
A recent article in the Wall St. Journal explores a variety of initiatives aimed at redefining the relationship between youth sports and the physical and mental health of its elite athletes. (Louise Radnofsky, The Wall Street Journal, June 9, 2022).
An example of the new awareness is the recent invitation of Peter Donnelly, PhD, an emeritus professor at the University of Toronto and long-time advocate for regulatory protections for youth athletes, to deliver a paper at a global conference in South Africa devoted to the elimination of child labor. Referring to youth sports, Dr. Donnelly observes “What if McDonalds had the same accident rate? ... There would be huge commissions of inquiry, regulations, and policies.” He suggests that the United Nations Convention on the Rights of the Child might be a mechanism to address the problem.
Writing in the Marquette University Sports Law Review in 2015, Kristin Hoffman, a law student at the time, suggested that the federal Fair Labor Standards Act or state child labor laws could be used to restructure sports like gymnastics or figure skating with tarnished histories. California law prohibits child actors from working more than 5 hours a day on school days and 7 hours on nonschool days but says little about child athletes. On paper, the National Collegiate Athletic Association limits college athletes to 20 hours participation per week but teenagers on club teams are not limited and may sometimes practice 30 hours or more.
Regulation in any form is a tough sell in this country. Coaches, parents, and athletes caught up in the myth that more repetitions and more touches on the ball are always the ticket to success will argue that most elite athletes are self-motivated and don’t view the long hours as a hardship.
Exactly how many are self-driven and how many are being pushed by parents and coaches is unknown. Across the street from us lived a young girl who, despite not having the obvious physical gifts, was clearly committed to excel in sports. She begged her parents to set up lights to allow her to practice well into the evening. She went on to have a good college career as a player and a very successful career as a Division I coach. Now in retirement, she is very open about her mental health history that in large part explains her inner drive and her subsequent troubles.
We need to be realistic in our hope for regulating the current state of youth sports out of its current situation. State laws that put reasonable limits on the hourly commitment to sports much like the California child actor laws feel like a reasonable goal. However, as physicians for these young athletes we must take each child – and we must remind ourselves that they are still children – as an individual.
When faced with patients who are clearly on the elite sport pathway, our goal is to protect their health – both physical and mental. If they are having symptoms of overuse we need to help them find alternative activities that will rest their injuries but still allow them to satisfy their competitive zeal. However, we must be ever alert to the risk that what appears to be unusual self-motivation may be instead a warning that pathologic obsession and compulsion lurk below the surface.
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.
Concerns about the potential harm resulting from overzealous training regimens and performance schedules for young elite athletes seems to come in cycles much like the Olympics. But, more recently, the media attention has become more intense fueled by the very visible psychological vulnerabilities of some young gymnasts, tennis players, and figure skaters. Accusations of physical and psychological abuse by team physicians and coaches continue to surface with troubling regularity.
A recent article in the Wall St. Journal explores a variety of initiatives aimed at redefining the relationship between youth sports and the physical and mental health of its elite athletes. (Louise Radnofsky, The Wall Street Journal, June 9, 2022).
An example of the new awareness is the recent invitation of Peter Donnelly, PhD, an emeritus professor at the University of Toronto and long-time advocate for regulatory protections for youth athletes, to deliver a paper at a global conference in South Africa devoted to the elimination of child labor. Referring to youth sports, Dr. Donnelly observes “What if McDonalds had the same accident rate? ... There would be huge commissions of inquiry, regulations, and policies.” He suggests that the United Nations Convention on the Rights of the Child might be a mechanism to address the problem.
Writing in the Marquette University Sports Law Review in 2015, Kristin Hoffman, a law student at the time, suggested that the federal Fair Labor Standards Act or state child labor laws could be used to restructure sports like gymnastics or figure skating with tarnished histories. California law prohibits child actors from working more than 5 hours a day on school days and 7 hours on nonschool days but says little about child athletes. On paper, the National Collegiate Athletic Association limits college athletes to 20 hours participation per week but teenagers on club teams are not limited and may sometimes practice 30 hours or more.
Regulation in any form is a tough sell in this country. Coaches, parents, and athletes caught up in the myth that more repetitions and more touches on the ball are always the ticket to success will argue that most elite athletes are self-motivated and don’t view the long hours as a hardship.
Exactly how many are self-driven and how many are being pushed by parents and coaches is unknown. Across the street from us lived a young girl who, despite not having the obvious physical gifts, was clearly committed to excel in sports. She begged her parents to set up lights to allow her to practice well into the evening. She went on to have a good college career as a player and a very successful career as a Division I coach. Now in retirement, she is very open about her mental health history that in large part explains her inner drive and her subsequent troubles.
We need to be realistic in our hope for regulating the current state of youth sports out of its current situation. State laws that put reasonable limits on the hourly commitment to sports much like the California child actor laws feel like a reasonable goal. However, as physicians for these young athletes we must take each child – and we must remind ourselves that they are still children – as an individual.
When faced with patients who are clearly on the elite sport pathway, our goal is to protect their health – both physical and mental. If they are having symptoms of overuse we need to help them find alternative activities that will rest their injuries but still allow them to satisfy their competitive zeal. However, we must be ever alert to the risk that what appears to be unusual self-motivation may be instead a warning that pathologic obsession and compulsion lurk below the surface.
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 mother’s double jeopardy
Jamestown, Colo., is a small mountain town several miles up through Lefthand Canyon out of Boulder, in the Rocky Mountains. The canyon roads are steep, winding, and narrow, and peopled by brightly clad cyclists struggling up the hill and flying down faster than the cars. The road through Jamestown is dusty in the summer with brightly colored oil barrels strategically placed in the middle of the single road through town. Slashed across their sides: “SLOW DOWN! Watch out for our feral children!”
Wild child or hothouse child? What is the best choice? Women bear the brunt of this deciding, whether they are working outside of the home, or stay-at-home caregivers, or both. Women know they will be blamed if they get it wrong.
Society has exacted a tall order on women who choose to have children. Patriarchal norms ask (White) women who choose both to work and have children, if they are really a “stay-at-home” mother who must work, or a “working” mother who prefers work over their children. The underlying attitude can be read as: “Are you someone who prioritizes paid work over caregiving, or are you someone who prioritizes caregiving over work?” You may be seen as a bad mother if you prioritize work over the welfare of your child. If you prioritize your child over your work, then you are not a reliable, dedicated worker. The working mother can’t win.
Woman’s central question is what kind of mother should I be? Mothers struggle with this question all their lives; when their child has difficulties, society’s question is what did you do wrong with your child? Mothers internalize the standard of the “good mother” and are aware of each minor transgression that depicts them as the “bad mother.” It is hard to escape the impossible perfectionistic standard of the good mother. But perhaps it has come time to push back on the moral imbalance.
Internalized sexism
As women move out of the home into the workplace, the societal pressures to maintain the status quo bear down on women, trying to keep them in their place.
Social pressures employ subtle “technologies of the self,” so that women – as any oppressed group – learn to internalize these technologies, and monitor themselves.1 This is now widely accepted as internalized sexism, whereby women feel that they are not good enough, do not have the right qualifications, and are “less” than the dominant group (men). This phenomenon is also recognized when racial and ethnic biases are assimilated unconsciously, as internalized racism. Should we also have internalized “momism”?
Women are caught between trying to claim their individualism as well as feeling the responsibility to be the self-denying mother. Everyone has an opinion about the place of women. Conservative activist Phyllis Schlafly considered “women’s lib” to be un-American, citing women in the military and the establishment of federal day care centers as actions of a communist state. A similar ideology helped form the antifeminist organization Concerned Women for America, which self-reports that it is the largest American public policy women’s organization. Formed in opposition to the National Organization for Women, CWA is focused on maintaining the traditional family, as understood by (White) evangelical Christians.
An example similar to CWA is the Council of Biblical Manhood and Womanhood. It was established to help evangelical Christian churches defend themselves against an accommodation of secular feminism and also against evangelical feminism (which pushes for more equality in the church). It promotes complementarianism – the idea that masculinity and femininity are ordained by God and that men and women are created to complement each other.
At the other extreme, the most radical of feminists believe in the need to create a women-only society where women would be free from the patriarchy. Less angry but decidedly weirder are the feminists called “FEMEN” who once staged a protest at the Vatican where topless women feigned intercourse with crucifixes, chanting slogans against the pope and religion.
Most women tread a path between extremes, a path which is difficult and lonely. Without a firm ideology, this path is strewn with doubts and pitfalls. Some career-oriented women who have delayed motherhood, knowing that they will soon be biologically past their peak and possibly also without a partner, wonder if they should become single mothers using sperm donation. For many women, the workplace does not offer much help with maternity leave or childcare. Even when maternity leave is available, there is a still a lack of understanding about what is needed.
“Think of it as caregiver bias. If you just extend maternity leave, what is implied is that you’re still expecting me to be the primary source of care for my child, when in fact my partner wants to share the load and will need support to do so as well,” said Pamela Culpepper, an expert in corporate diversity and inclusion.2
Intensive mothering
When the glamor of the workplace wears off and/or when the misogyny and the harassment become too much, women who have the financial stability may decide to return to the role of the stay-at-home mother. Perhaps, in the home, she can feel fulfilled. Yet, young American urban and suburban mothers now parent under a new name – “intensive mothering.”
Conducting in-depth interviews of 38 women of diverse backgrounds in the United States, Sharon Hays found women describing their 2- to 4-year-old children as innocent and priceless, and believing that they – the mothers – should be primarily responsible for rearing their children, using “child-rearing methods that are child centered, expert guided, emotionally absorbing, labor intensive, and financially expensive.”3 Ms. Hays clarified four beliefs that were common to all the women in the study: mothers are more suitable caregivers than fathers; mothering should be child centered; parenting consists of a set of skills that need to be learned; and parenting is labor-intensive but an emotionally fulfilling activity.
Hays wondered if this type of mothering developed as the last defense against “the impoverishment of social ties, communal obligations and unremunerated commitments.”3 She suggested that women succumbing to social pressures to return to the home is yet another example of how society is set up to benefit men, capitalism, political leaders, and those who try to maintain a “traditional” form of family life.3 Ms. Hays concluded that the practice of intensive mothering is a class-based practice of privileged white women, entangled with capitalism in that the buying of “essential” baby products is equated with good mothering. She found this ideology to be oppressive of all women, regardless of their social class, ethnic background, household composition, and financial situation. Ms. Hays noted that many women experience guilt for not matching up to these ideals.
In “Dead End Feminism,” Elisabeth Badinter asks if the upheaval in the role of women has caused so much uncertainty that it is easier for women to regress to a time when they were in the home and knew themselves as mothers. They ask if this has been reinforced by the movement to embrace all things natural, eschewing the falseness of chemicals and other things that threaten Mother Earth.4
There is no escaping the power of the mother: she will continue to symbolize all that is good and bad as the embodiment of the Mother Archetype. All of this is the background against which you will see the new mother in the family. She will not articulate her dilemma, that is your role as the family psychiatrist.
Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at alison.heru@ucdenver.edu.
References
1. Martin LH et al (eds.). Technologies of the Self: A Seminar with Michel Foucault. University of Massachusetts Press: Amherst, Mass.: University of Massachusetts Press, 2022.
2. How Pamela Culpepper Is Changing The Narrative Of Women In The Workplace. Huffpost. 2020 Mar 6. https://www.huffpost.com/entry/pamela-culpepper-diversity-inclusion-empowerment_n_5e56b6ffc5b62e9dc7dbc307.
3. Hays S. Cultural Contradictions of Motherhood. Yale University Press: New Haven, Conn.: Yale University Press, 1996.
4. Badinter E. (translated by Borossa J). Dead End Feminism. Malden, Mass.: Polity Press, 2006.
Jamestown, Colo., is a small mountain town several miles up through Lefthand Canyon out of Boulder, in the Rocky Mountains. The canyon roads are steep, winding, and narrow, and peopled by brightly clad cyclists struggling up the hill and flying down faster than the cars. The road through Jamestown is dusty in the summer with brightly colored oil barrels strategically placed in the middle of the single road through town. Slashed across their sides: “SLOW DOWN! Watch out for our feral children!”
Wild child or hothouse child? What is the best choice? Women bear the brunt of this deciding, whether they are working outside of the home, or stay-at-home caregivers, or both. Women know they will be blamed if they get it wrong.
Society has exacted a tall order on women who choose to have children. Patriarchal norms ask (White) women who choose both to work and have children, if they are really a “stay-at-home” mother who must work, or a “working” mother who prefers work over their children. The underlying attitude can be read as: “Are you someone who prioritizes paid work over caregiving, or are you someone who prioritizes caregiving over work?” You may be seen as a bad mother if you prioritize work over the welfare of your child. If you prioritize your child over your work, then you are not a reliable, dedicated worker. The working mother can’t win.
Woman’s central question is what kind of mother should I be? Mothers struggle with this question all their lives; when their child has difficulties, society’s question is what did you do wrong with your child? Mothers internalize the standard of the “good mother” and are aware of each minor transgression that depicts them as the “bad mother.” It is hard to escape the impossible perfectionistic standard of the good mother. But perhaps it has come time to push back on the moral imbalance.
Internalized sexism
As women move out of the home into the workplace, the societal pressures to maintain the status quo bear down on women, trying to keep them in their place.
Social pressures employ subtle “technologies of the self,” so that women – as any oppressed group – learn to internalize these technologies, and monitor themselves.1 This is now widely accepted as internalized sexism, whereby women feel that they are not good enough, do not have the right qualifications, and are “less” than the dominant group (men). This phenomenon is also recognized when racial and ethnic biases are assimilated unconsciously, as internalized racism. Should we also have internalized “momism”?
Women are caught between trying to claim their individualism as well as feeling the responsibility to be the self-denying mother. Everyone has an opinion about the place of women. Conservative activist Phyllis Schlafly considered “women’s lib” to be un-American, citing women in the military and the establishment of federal day care centers as actions of a communist state. A similar ideology helped form the antifeminist organization Concerned Women for America, which self-reports that it is the largest American public policy women’s organization. Formed in opposition to the National Organization for Women, CWA is focused on maintaining the traditional family, as understood by (White) evangelical Christians.
An example similar to CWA is the Council of Biblical Manhood and Womanhood. It was established to help evangelical Christian churches defend themselves against an accommodation of secular feminism and also against evangelical feminism (which pushes for more equality in the church). It promotes complementarianism – the idea that masculinity and femininity are ordained by God and that men and women are created to complement each other.
At the other extreme, the most radical of feminists believe in the need to create a women-only society where women would be free from the patriarchy. Less angry but decidedly weirder are the feminists called “FEMEN” who once staged a protest at the Vatican where topless women feigned intercourse with crucifixes, chanting slogans against the pope and religion.
Most women tread a path between extremes, a path which is difficult and lonely. Without a firm ideology, this path is strewn with doubts and pitfalls. Some career-oriented women who have delayed motherhood, knowing that they will soon be biologically past their peak and possibly also without a partner, wonder if they should become single mothers using sperm donation. For many women, the workplace does not offer much help with maternity leave or childcare. Even when maternity leave is available, there is a still a lack of understanding about what is needed.
“Think of it as caregiver bias. If you just extend maternity leave, what is implied is that you’re still expecting me to be the primary source of care for my child, when in fact my partner wants to share the load and will need support to do so as well,” said Pamela Culpepper, an expert in corporate diversity and inclusion.2
Intensive mothering
When the glamor of the workplace wears off and/or when the misogyny and the harassment become too much, women who have the financial stability may decide to return to the role of the stay-at-home mother. Perhaps, in the home, she can feel fulfilled. Yet, young American urban and suburban mothers now parent under a new name – “intensive mothering.”
Conducting in-depth interviews of 38 women of diverse backgrounds in the United States, Sharon Hays found women describing their 2- to 4-year-old children as innocent and priceless, and believing that they – the mothers – should be primarily responsible for rearing their children, using “child-rearing methods that are child centered, expert guided, emotionally absorbing, labor intensive, and financially expensive.”3 Ms. Hays clarified four beliefs that were common to all the women in the study: mothers are more suitable caregivers than fathers; mothering should be child centered; parenting consists of a set of skills that need to be learned; and parenting is labor-intensive but an emotionally fulfilling activity.
Hays wondered if this type of mothering developed as the last defense against “the impoverishment of social ties, communal obligations and unremunerated commitments.”3 She suggested that women succumbing to social pressures to return to the home is yet another example of how society is set up to benefit men, capitalism, political leaders, and those who try to maintain a “traditional” form of family life.3 Ms. Hays concluded that the practice of intensive mothering is a class-based practice of privileged white women, entangled with capitalism in that the buying of “essential” baby products is equated with good mothering. She found this ideology to be oppressive of all women, regardless of their social class, ethnic background, household composition, and financial situation. Ms. Hays noted that many women experience guilt for not matching up to these ideals.
In “Dead End Feminism,” Elisabeth Badinter asks if the upheaval in the role of women has caused so much uncertainty that it is easier for women to regress to a time when they were in the home and knew themselves as mothers. They ask if this has been reinforced by the movement to embrace all things natural, eschewing the falseness of chemicals and other things that threaten Mother Earth.4
There is no escaping the power of the mother: she will continue to symbolize all that is good and bad as the embodiment of the Mother Archetype. All of this is the background against which you will see the new mother in the family. She will not articulate her dilemma, that is your role as the family psychiatrist.
Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at alison.heru@ucdenver.edu.
References
1. Martin LH et al (eds.). Technologies of the Self: A Seminar with Michel Foucault. University of Massachusetts Press: Amherst, Mass.: University of Massachusetts Press, 2022.
2. How Pamela Culpepper Is Changing The Narrative Of Women In The Workplace. Huffpost. 2020 Mar 6. https://www.huffpost.com/entry/pamela-culpepper-diversity-inclusion-empowerment_n_5e56b6ffc5b62e9dc7dbc307.
3. Hays S. Cultural Contradictions of Motherhood. Yale University Press: New Haven, Conn.: Yale University Press, 1996.
4. Badinter E. (translated by Borossa J). Dead End Feminism. Malden, Mass.: Polity Press, 2006.
Jamestown, Colo., is a small mountain town several miles up through Lefthand Canyon out of Boulder, in the Rocky Mountains. The canyon roads are steep, winding, and narrow, and peopled by brightly clad cyclists struggling up the hill and flying down faster than the cars. The road through Jamestown is dusty in the summer with brightly colored oil barrels strategically placed in the middle of the single road through town. Slashed across their sides: “SLOW DOWN! Watch out for our feral children!”
Wild child or hothouse child? What is the best choice? Women bear the brunt of this deciding, whether they are working outside of the home, or stay-at-home caregivers, or both. Women know they will be blamed if they get it wrong.
Society has exacted a tall order on women who choose to have children. Patriarchal norms ask (White) women who choose both to work and have children, if they are really a “stay-at-home” mother who must work, or a “working” mother who prefers work over their children. The underlying attitude can be read as: “Are you someone who prioritizes paid work over caregiving, or are you someone who prioritizes caregiving over work?” You may be seen as a bad mother if you prioritize work over the welfare of your child. If you prioritize your child over your work, then you are not a reliable, dedicated worker. The working mother can’t win.
Woman’s central question is what kind of mother should I be? Mothers struggle with this question all their lives; when their child has difficulties, society’s question is what did you do wrong with your child? Mothers internalize the standard of the “good mother” and are aware of each minor transgression that depicts them as the “bad mother.” It is hard to escape the impossible perfectionistic standard of the good mother. But perhaps it has come time to push back on the moral imbalance.
Internalized sexism
As women move out of the home into the workplace, the societal pressures to maintain the status quo bear down on women, trying to keep them in their place.
Social pressures employ subtle “technologies of the self,” so that women – as any oppressed group – learn to internalize these technologies, and monitor themselves.1 This is now widely accepted as internalized sexism, whereby women feel that they are not good enough, do not have the right qualifications, and are “less” than the dominant group (men). This phenomenon is also recognized when racial and ethnic biases are assimilated unconsciously, as internalized racism. Should we also have internalized “momism”?
Women are caught between trying to claim their individualism as well as feeling the responsibility to be the self-denying mother. Everyone has an opinion about the place of women. Conservative activist Phyllis Schlafly considered “women’s lib” to be un-American, citing women in the military and the establishment of federal day care centers as actions of a communist state. A similar ideology helped form the antifeminist organization Concerned Women for America, which self-reports that it is the largest American public policy women’s organization. Formed in opposition to the National Organization for Women, CWA is focused on maintaining the traditional family, as understood by (White) evangelical Christians.
An example similar to CWA is the Council of Biblical Manhood and Womanhood. It was established to help evangelical Christian churches defend themselves against an accommodation of secular feminism and also against evangelical feminism (which pushes for more equality in the church). It promotes complementarianism – the idea that masculinity and femininity are ordained by God and that men and women are created to complement each other.
At the other extreme, the most radical of feminists believe in the need to create a women-only society where women would be free from the patriarchy. Less angry but decidedly weirder are the feminists called “FEMEN” who once staged a protest at the Vatican where topless women feigned intercourse with crucifixes, chanting slogans against the pope and religion.
Most women tread a path between extremes, a path which is difficult and lonely. Without a firm ideology, this path is strewn with doubts and pitfalls. Some career-oriented women who have delayed motherhood, knowing that they will soon be biologically past their peak and possibly also without a partner, wonder if they should become single mothers using sperm donation. For many women, the workplace does not offer much help with maternity leave or childcare. Even when maternity leave is available, there is a still a lack of understanding about what is needed.
“Think of it as caregiver bias. If you just extend maternity leave, what is implied is that you’re still expecting me to be the primary source of care for my child, when in fact my partner wants to share the load and will need support to do so as well,” said Pamela Culpepper, an expert in corporate diversity and inclusion.2
Intensive mothering
When the glamor of the workplace wears off and/or when the misogyny and the harassment become too much, women who have the financial stability may decide to return to the role of the stay-at-home mother. Perhaps, in the home, she can feel fulfilled. Yet, young American urban and suburban mothers now parent under a new name – “intensive mothering.”
Conducting in-depth interviews of 38 women of diverse backgrounds in the United States, Sharon Hays found women describing their 2- to 4-year-old children as innocent and priceless, and believing that they – the mothers – should be primarily responsible for rearing their children, using “child-rearing methods that are child centered, expert guided, emotionally absorbing, labor intensive, and financially expensive.”3 Ms. Hays clarified four beliefs that were common to all the women in the study: mothers are more suitable caregivers than fathers; mothering should be child centered; parenting consists of a set of skills that need to be learned; and parenting is labor-intensive but an emotionally fulfilling activity.
Hays wondered if this type of mothering developed as the last defense against “the impoverishment of social ties, communal obligations and unremunerated commitments.”3 She suggested that women succumbing to social pressures to return to the home is yet another example of how society is set up to benefit men, capitalism, political leaders, and those who try to maintain a “traditional” form of family life.3 Ms. Hays concluded that the practice of intensive mothering is a class-based practice of privileged white women, entangled with capitalism in that the buying of “essential” baby products is equated with good mothering. She found this ideology to be oppressive of all women, regardless of their social class, ethnic background, household composition, and financial situation. Ms. Hays noted that many women experience guilt for not matching up to these ideals.
In “Dead End Feminism,” Elisabeth Badinter asks if the upheaval in the role of women has caused so much uncertainty that it is easier for women to regress to a time when they were in the home and knew themselves as mothers. They ask if this has been reinforced by the movement to embrace all things natural, eschewing the falseness of chemicals and other things that threaten Mother Earth.4
There is no escaping the power of the mother: she will continue to symbolize all that is good and bad as the embodiment of the Mother Archetype. All of this is the background against which you will see the new mother in the family. She will not articulate her dilemma, that is your role as the family psychiatrist.
Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at alison.heru@ucdenver.edu.
References
1. Martin LH et al (eds.). Technologies of the Self: A Seminar with Michel Foucault. University of Massachusetts Press: Amherst, Mass.: University of Massachusetts Press, 2022.
2. How Pamela Culpepper Is Changing The Narrative Of Women In The Workplace. Huffpost. 2020 Mar 6. https://www.huffpost.com/entry/pamela-culpepper-diversity-inclusion-empowerment_n_5e56b6ffc5b62e9dc7dbc307.
3. Hays S. Cultural Contradictions of Motherhood. Yale University Press: New Haven, Conn.: Yale University Press, 1996.
4. Badinter E. (translated by Borossa J). Dead End Feminism. Malden, Mass.: Polity Press, 2006.
In the Heat of Anger: The Impact of Increasing Temperatures on Veteran and Military Mental Health
In June, an intense heatwave moved across the United States. According to the National Weather Service, about 50 million Americans were warned of excessively hot temperatures. In the Southwest, dozens of cities broke temperature records, and in New Mexico, my home state, terrible wildfires ravaged thousands of acres. Nor will the rest of the country be spared as the dome of heat is expected to move into the Midwest and even the Northeast before it is done.2 The ongoing COVID-19 pandemic and the heatwaves exacerbate each other.
The US Global Change Research Program studies the adverse effects of high temperatures on human health. High ambient heat is associated with cardiovascular, respiratory, renal, metabolic, vector- and food-borne illnesses, and malnutrition.3 Veterans, especially those who are older or homeless, are considered heat-vulnerable populations more susceptible to sunstroke, dehydration, and heat exhaustion. Last July, during record-breaking heat in many large cities, US Department of Veterans Affairs (VA) Secretary McDonough emphasized the availability of community and VA resources for veterans experiencing high temperatures, especially those who were homeless.4
The Veterans Health Administration (VHA) also reached out to service members who were deployed to the baking deserts of Iraq and Afghanistan, advising them that they may experience service-related heat stroke or exhaustion.5 Today’s military confronts many challenges in training troops in hot temperatures at home and in combat overseas.6 The 2019 report from the advocacy and research organization, the Union of Concerned Scientists (UCS) reported the need to ensure the preparedness of the fighting force and that increasing temperatures from climate change will make it harder to balance this mission with protecting the health of service members. The study estimated there were 17 heat-related deaths and a 60% jump in heat-related injuries in the previous decade. More worrisome, UCS predicted that if the temperature trend is not abated, by 2050, military bases will experience an additional month where the heat index will feel like it is 100 °F or more.7
In comparison, less attention has been focused on the adverse effects of high temperatures on mental health. Most of us recognize that too many hot days in the height of summer may cause fatigue, impatience, restlessness, and difficulty concentrating. A 2018 systematic review reported a strong association between high ambient temperature and suicide.8 Suicide has been among the highest public health priorities in the VHA and the military. There is also evidence of the correlation between emergency department (ED) visits for mental health conditions in non-VA hospitals and scorching days and sweltering nights. An analysis of data of > 3 million ED visits involving > 2 million insured patients revealed increased ED visits during periods of extreme heat for stress, substance use, somatoform, anxiety, mood, schizophrenia, schizotypal and delusional disorders, as well as self-harming behaviors. The association is likely even stronger in service members. The largest study ever conducted on the mental health of service members, the Army Study to Assess Risk and Resilience in Servicemembers (ARMY STARRS), found higher rates of mental health disorders than in the civilian population.9
What is the clinical science behind this long-established link between heat and mental health disorders? High temperatures disrupt sleep, interfere with memory and attention, and increase irritability and depression especially in persons with extant mental health disorders. Individuals with schizophrenia may have difficulty with temperature regulation, a problem antipsychotic and antidepressant medications may exacerbate. Extreme heat leads to extreme behavior, including domestic violence, chemical coping, and aggression. Individuals diagnosed with dementia may lack the mental wherewithal and economic resources to prepare for and respond to extreme heat, leading to higher morbidity and mortality.10,11 The so called heat hypothesis holds that extreme high temperatures increase hostile feelings and aggressive thoughts that trigger other directed violence.12
For many, summer is the most enjoyable time of year “when the livin’ is easy,” as the George Gershwin song claims. We can relax in air-conditioned homes or sit by a swimming pool, sipping iced tea. As federal practitioners, and even more as humans, we need to realize that our patients, those on active duty, veterans, and the underserved populations who are the mission of the US Commissioned Corps and the Indian Health Service, are not as fortunate. As temperatures climb, we must redouble our efforts to educate our patients about the dangers of extreme heat and advocate for policies and procedures in our respective federal agencies that will positively impact climate change.
During clinical encounters with patients with mental health conditions, we should be mindful of the potential increase in substance use, suicidal ideation, aggressive impulses, and medication adverse effects when temperatures are high. Most important, we must raise awareness and participate in public health initiatives to ensure that populations whose prior service, current duty, or health disparities place them at greater risk of harm from increasing temperatures have access to shelter, cooling, food, health care, psychosocial services, and mental health treatment.
1. Hanh, TN. Peace Is Every Breath: A Practice for Our Busy Lives. HarperOne; 2012.
2. Jones D. More than 50 million people in the U.S. are under excessive heat warnings. Updated June 12, 2022. Accessed June 20, 2022. https://www.michiganradioorg/2022-06-10/more-than-50-million-people-in-the-u-s-are-under-excessive-heat-warnings
3. US Global Change Research Program. Climate and Health Assessment. Temperature- Related Illness and Death. Accessed June 20, 2022. https://health2016.globalchange.gov/temperature-related-death-and-illness
4. US Department of Veterans Affairs. Extreme heat assistance available for veterans experiencing homelessness. Updated July 14, 2021. Accessed June 20, 2022. https://blogs.va.gov/VAntage/91819/extreme-heat-assistance-available-for-veterans-experiencing-homelessness
5. US Department of Veterans Affairs. Heat injuries. April 10, 2020. Accessed June 20, 2022. https://www.publichealth.va.gov/exposures/heat-injuries/index.asp
6. Hasemeyer D. Rising temperatures put U.S. troops at risk during training, report finds. November 10, 2019. Accessed June 20, 2022. https://www.nbcnews.com/science/environment/rising-temperatures-put-u-s-troops-risk-during-training-report-n1079156
7. Dahl K, Udvardy S. US military on the front lines of extreme heat. November 11, 2019. Updated January 4, 2020. Accessed June 20, 2022. https://www.ucsusa.org/resources/us-military-bases-risk-extreme-heat
8. Thompson R, Horingold R, Page L, Waite T. Associations between high ambient temperatures and heat waves with mental health outcomes: a systematic review. Public Health. 2018;161:171-191. doi:10.1016/j.puhe.2018.06.008
9. Kessler RC, Heeringa SG, Stein MB, et al; Army STARRS Collaborators. Thirty-day prevalence of DSM-IV mental disorders among non-deployed soldiers in the U.S. Army. JAMA Psychiatry. 2014;71(5):504-513. doi:10.1001/jamapsychiatry.2014.28
10. American Psychiatric Association. extreme heat contributes to worsening mental health, especially among vulnerable populations. June 30, 2021. Accessed June 20, 2022. https://psychiatry.org/news-room/news-releases/extreme-heat-contributes-to-worsening-mental-healt
11. Cooper R. The impacts of extreme heat on mental health. Psychiatric Times. July 29, 2019. Accessed June 20, 2022. https://www.psychiatrictimes.com/view/impacts-extreme-heat-mental-health
12. Anderson C. Heat and violence. Current Directions in Psychological Violence. 2011;10(1):38-42. doi.10.1177/0963721410397271
In June, an intense heatwave moved across the United States. According to the National Weather Service, about 50 million Americans were warned of excessively hot temperatures. In the Southwest, dozens of cities broke temperature records, and in New Mexico, my home state, terrible wildfires ravaged thousands of acres. Nor will the rest of the country be spared as the dome of heat is expected to move into the Midwest and even the Northeast before it is done.2 The ongoing COVID-19 pandemic and the heatwaves exacerbate each other.
The US Global Change Research Program studies the adverse effects of high temperatures on human health. High ambient heat is associated with cardiovascular, respiratory, renal, metabolic, vector- and food-borne illnesses, and malnutrition.3 Veterans, especially those who are older or homeless, are considered heat-vulnerable populations more susceptible to sunstroke, dehydration, and heat exhaustion. Last July, during record-breaking heat in many large cities, US Department of Veterans Affairs (VA) Secretary McDonough emphasized the availability of community and VA resources for veterans experiencing high temperatures, especially those who were homeless.4
The Veterans Health Administration (VHA) also reached out to service members who were deployed to the baking deserts of Iraq and Afghanistan, advising them that they may experience service-related heat stroke or exhaustion.5 Today’s military confronts many challenges in training troops in hot temperatures at home and in combat overseas.6 The 2019 report from the advocacy and research organization, the Union of Concerned Scientists (UCS) reported the need to ensure the preparedness of the fighting force and that increasing temperatures from climate change will make it harder to balance this mission with protecting the health of service members. The study estimated there were 17 heat-related deaths and a 60% jump in heat-related injuries in the previous decade. More worrisome, UCS predicted that if the temperature trend is not abated, by 2050, military bases will experience an additional month where the heat index will feel like it is 100 °F or more.7
In comparison, less attention has been focused on the adverse effects of high temperatures on mental health. Most of us recognize that too many hot days in the height of summer may cause fatigue, impatience, restlessness, and difficulty concentrating. A 2018 systematic review reported a strong association between high ambient temperature and suicide.8 Suicide has been among the highest public health priorities in the VHA and the military. There is also evidence of the correlation between emergency department (ED) visits for mental health conditions in non-VA hospitals and scorching days and sweltering nights. An analysis of data of > 3 million ED visits involving > 2 million insured patients revealed increased ED visits during periods of extreme heat for stress, substance use, somatoform, anxiety, mood, schizophrenia, schizotypal and delusional disorders, as well as self-harming behaviors. The association is likely even stronger in service members. The largest study ever conducted on the mental health of service members, the Army Study to Assess Risk and Resilience in Servicemembers (ARMY STARRS), found higher rates of mental health disorders than in the civilian population.9
What is the clinical science behind this long-established link between heat and mental health disorders? High temperatures disrupt sleep, interfere with memory and attention, and increase irritability and depression especially in persons with extant mental health disorders. Individuals with schizophrenia may have difficulty with temperature regulation, a problem antipsychotic and antidepressant medications may exacerbate. Extreme heat leads to extreme behavior, including domestic violence, chemical coping, and aggression. Individuals diagnosed with dementia may lack the mental wherewithal and economic resources to prepare for and respond to extreme heat, leading to higher morbidity and mortality.10,11 The so called heat hypothesis holds that extreme high temperatures increase hostile feelings and aggressive thoughts that trigger other directed violence.12
For many, summer is the most enjoyable time of year “when the livin’ is easy,” as the George Gershwin song claims. We can relax in air-conditioned homes or sit by a swimming pool, sipping iced tea. As federal practitioners, and even more as humans, we need to realize that our patients, those on active duty, veterans, and the underserved populations who are the mission of the US Commissioned Corps and the Indian Health Service, are not as fortunate. As temperatures climb, we must redouble our efforts to educate our patients about the dangers of extreme heat and advocate for policies and procedures in our respective federal agencies that will positively impact climate change.
During clinical encounters with patients with mental health conditions, we should be mindful of the potential increase in substance use, suicidal ideation, aggressive impulses, and medication adverse effects when temperatures are high. Most important, we must raise awareness and participate in public health initiatives to ensure that populations whose prior service, current duty, or health disparities place them at greater risk of harm from increasing temperatures have access to shelter, cooling, food, health care, psychosocial services, and mental health treatment.
In June, an intense heatwave moved across the United States. According to the National Weather Service, about 50 million Americans were warned of excessively hot temperatures. In the Southwest, dozens of cities broke temperature records, and in New Mexico, my home state, terrible wildfires ravaged thousands of acres. Nor will the rest of the country be spared as the dome of heat is expected to move into the Midwest and even the Northeast before it is done.2 The ongoing COVID-19 pandemic and the heatwaves exacerbate each other.
The US Global Change Research Program studies the adverse effects of high temperatures on human health. High ambient heat is associated with cardiovascular, respiratory, renal, metabolic, vector- and food-borne illnesses, and malnutrition.3 Veterans, especially those who are older or homeless, are considered heat-vulnerable populations more susceptible to sunstroke, dehydration, and heat exhaustion. Last July, during record-breaking heat in many large cities, US Department of Veterans Affairs (VA) Secretary McDonough emphasized the availability of community and VA resources for veterans experiencing high temperatures, especially those who were homeless.4
The Veterans Health Administration (VHA) also reached out to service members who were deployed to the baking deserts of Iraq and Afghanistan, advising them that they may experience service-related heat stroke or exhaustion.5 Today’s military confronts many challenges in training troops in hot temperatures at home and in combat overseas.6 The 2019 report from the advocacy and research organization, the Union of Concerned Scientists (UCS) reported the need to ensure the preparedness of the fighting force and that increasing temperatures from climate change will make it harder to balance this mission with protecting the health of service members. The study estimated there were 17 heat-related deaths and a 60% jump in heat-related injuries in the previous decade. More worrisome, UCS predicted that if the temperature trend is not abated, by 2050, military bases will experience an additional month where the heat index will feel like it is 100 °F or more.7
In comparison, less attention has been focused on the adverse effects of high temperatures on mental health. Most of us recognize that too many hot days in the height of summer may cause fatigue, impatience, restlessness, and difficulty concentrating. A 2018 systematic review reported a strong association between high ambient temperature and suicide.8 Suicide has been among the highest public health priorities in the VHA and the military. There is also evidence of the correlation between emergency department (ED) visits for mental health conditions in non-VA hospitals and scorching days and sweltering nights. An analysis of data of > 3 million ED visits involving > 2 million insured patients revealed increased ED visits during periods of extreme heat for stress, substance use, somatoform, anxiety, mood, schizophrenia, schizotypal and delusional disorders, as well as self-harming behaviors. The association is likely even stronger in service members. The largest study ever conducted on the mental health of service members, the Army Study to Assess Risk and Resilience in Servicemembers (ARMY STARRS), found higher rates of mental health disorders than in the civilian population.9
What is the clinical science behind this long-established link between heat and mental health disorders? High temperatures disrupt sleep, interfere with memory and attention, and increase irritability and depression especially in persons with extant mental health disorders. Individuals with schizophrenia may have difficulty with temperature regulation, a problem antipsychotic and antidepressant medications may exacerbate. Extreme heat leads to extreme behavior, including domestic violence, chemical coping, and aggression. Individuals diagnosed with dementia may lack the mental wherewithal and economic resources to prepare for and respond to extreme heat, leading to higher morbidity and mortality.10,11 The so called heat hypothesis holds that extreme high temperatures increase hostile feelings and aggressive thoughts that trigger other directed violence.12
For many, summer is the most enjoyable time of year “when the livin’ is easy,” as the George Gershwin song claims. We can relax in air-conditioned homes or sit by a swimming pool, sipping iced tea. As federal practitioners, and even more as humans, we need to realize that our patients, those on active duty, veterans, and the underserved populations who are the mission of the US Commissioned Corps and the Indian Health Service, are not as fortunate. As temperatures climb, we must redouble our efforts to educate our patients about the dangers of extreme heat and advocate for policies and procedures in our respective federal agencies that will positively impact climate change.
During clinical encounters with patients with mental health conditions, we should be mindful of the potential increase in substance use, suicidal ideation, aggressive impulses, and medication adverse effects when temperatures are high. Most important, we must raise awareness and participate in public health initiatives to ensure that populations whose prior service, current duty, or health disparities place them at greater risk of harm from increasing temperatures have access to shelter, cooling, food, health care, psychosocial services, and mental health treatment.
1. Hanh, TN. Peace Is Every Breath: A Practice for Our Busy Lives. HarperOne; 2012.
2. Jones D. More than 50 million people in the U.S. are under excessive heat warnings. Updated June 12, 2022. Accessed June 20, 2022. https://www.michiganradioorg/2022-06-10/more-than-50-million-people-in-the-u-s-are-under-excessive-heat-warnings
3. US Global Change Research Program. Climate and Health Assessment. Temperature- Related Illness and Death. Accessed June 20, 2022. https://health2016.globalchange.gov/temperature-related-death-and-illness
4. US Department of Veterans Affairs. Extreme heat assistance available for veterans experiencing homelessness. Updated July 14, 2021. Accessed June 20, 2022. https://blogs.va.gov/VAntage/91819/extreme-heat-assistance-available-for-veterans-experiencing-homelessness
5. US Department of Veterans Affairs. Heat injuries. April 10, 2020. Accessed June 20, 2022. https://www.publichealth.va.gov/exposures/heat-injuries/index.asp
6. Hasemeyer D. Rising temperatures put U.S. troops at risk during training, report finds. November 10, 2019. Accessed June 20, 2022. https://www.nbcnews.com/science/environment/rising-temperatures-put-u-s-troops-risk-during-training-report-n1079156
7. Dahl K, Udvardy S. US military on the front lines of extreme heat. November 11, 2019. Updated January 4, 2020. Accessed June 20, 2022. https://www.ucsusa.org/resources/us-military-bases-risk-extreme-heat
8. Thompson R, Horingold R, Page L, Waite T. Associations between high ambient temperatures and heat waves with mental health outcomes: a systematic review. Public Health. 2018;161:171-191. doi:10.1016/j.puhe.2018.06.008
9. Kessler RC, Heeringa SG, Stein MB, et al; Army STARRS Collaborators. Thirty-day prevalence of DSM-IV mental disorders among non-deployed soldiers in the U.S. Army. JAMA Psychiatry. 2014;71(5):504-513. doi:10.1001/jamapsychiatry.2014.28
10. American Psychiatric Association. extreme heat contributes to worsening mental health, especially among vulnerable populations. June 30, 2021. Accessed June 20, 2022. https://psychiatry.org/news-room/news-releases/extreme-heat-contributes-to-worsening-mental-healt
11. Cooper R. The impacts of extreme heat on mental health. Psychiatric Times. July 29, 2019. Accessed June 20, 2022. https://www.psychiatrictimes.com/view/impacts-extreme-heat-mental-health
12. Anderson C. Heat and violence. Current Directions in Psychological Violence. 2011;10(1):38-42. doi.10.1177/0963721410397271
1. Hanh, TN. Peace Is Every Breath: A Practice for Our Busy Lives. HarperOne; 2012.
2. Jones D. More than 50 million people in the U.S. are under excessive heat warnings. Updated June 12, 2022. Accessed June 20, 2022. https://www.michiganradioorg/2022-06-10/more-than-50-million-people-in-the-u-s-are-under-excessive-heat-warnings
3. US Global Change Research Program. Climate and Health Assessment. Temperature- Related Illness and Death. Accessed June 20, 2022. https://health2016.globalchange.gov/temperature-related-death-and-illness
4. US Department of Veterans Affairs. Extreme heat assistance available for veterans experiencing homelessness. Updated July 14, 2021. Accessed June 20, 2022. https://blogs.va.gov/VAntage/91819/extreme-heat-assistance-available-for-veterans-experiencing-homelessness
5. US Department of Veterans Affairs. Heat injuries. April 10, 2020. Accessed June 20, 2022. https://www.publichealth.va.gov/exposures/heat-injuries/index.asp
6. Hasemeyer D. Rising temperatures put U.S. troops at risk during training, report finds. November 10, 2019. Accessed June 20, 2022. https://www.nbcnews.com/science/environment/rising-temperatures-put-u-s-troops-risk-during-training-report-n1079156
7. Dahl K, Udvardy S. US military on the front lines of extreme heat. November 11, 2019. Updated January 4, 2020. Accessed June 20, 2022. https://www.ucsusa.org/resources/us-military-bases-risk-extreme-heat
8. Thompson R, Horingold R, Page L, Waite T. Associations between high ambient temperatures and heat waves with mental health outcomes: a systematic review. Public Health. 2018;161:171-191. doi:10.1016/j.puhe.2018.06.008
9. Kessler RC, Heeringa SG, Stein MB, et al; Army STARRS Collaborators. Thirty-day prevalence of DSM-IV mental disorders among non-deployed soldiers in the U.S. Army. JAMA Psychiatry. 2014;71(5):504-513. doi:10.1001/jamapsychiatry.2014.28
10. American Psychiatric Association. extreme heat contributes to worsening mental health, especially among vulnerable populations. June 30, 2021. Accessed June 20, 2022. https://psychiatry.org/news-room/news-releases/extreme-heat-contributes-to-worsening-mental-healt
11. Cooper R. The impacts of extreme heat on mental health. Psychiatric Times. July 29, 2019. Accessed June 20, 2022. https://www.psychiatrictimes.com/view/impacts-extreme-heat-mental-health
12. Anderson C. Heat and violence. Current Directions in Psychological Violence. 2011;10(1):38-42. doi.10.1177/0963721410397271
For the Fourth of July, a neuroscientist reflects on patriotism
This week, we celebrate our nation’s birth in a national and individual display of our patriotic attachment to this country. — which includes our self-definition as Americans.
For each of us, personhood is an almost miraculous product of our brain’s plasticity — the brain’s ability to change chemically, structurally, and functionally, based on our life experiences — arising from near countless moments of change in the wiring of our brain.
The incredibly complex remodeling that created “you” is a product, of course, of your very complicated, unique passage in life. You have a repertoire of skills and ability; you have stories and understanding and a history of sensing and acting and thinking in the world that is, in detail, unique only to you and your experiences.
As your brain created its model of your world by recording “what goes with what” at each brief moment of time, your brain — that most complicated and wonderful of “machines” on planet Earth — also associated billions of moments of feeling and action and thought with their source, your Self.
Because we primarily construct our model of the world through our eyes and ears, it’s not surprising that the emergent Self that is located somewhere in the center of your head behind your eyes and between your ears. Through billions of contacts with the surfaces of your hide and sensory organs, you have embodied yourself.
Your sense of ‘us’
These same neurologic processes extend beyond our physical beings to incorporate other contributors to our well-being into our personhoods. Loving parents, siblings, friends — and others in your clans and tribes and nations — literally grow into your personhood by these same self-associating processes. These relationships are supported in mutual identity by all of the tokens and icons and charms and customs that collectively define you and enable a sense of “us.”
Put another way, Mother Nature (or, in another cultural perspective, our Creator) has designed our brains to incorporate all of those who are close to us — and more broadly, other individuals in our clan or tribe or nation — to be a part of each of us.
Humans are highly social creatures. When we rise up and risk our lives to defend our friends, family, or cultural “in-groups,” we are literally fighting to defend ourselves — because those other individuals have grown into our very being. In defending them, we are literally defending a part of ourselves.
From one human perspective, this attachment to family and clan and tribe and nation is obviously key for our survival. We are an individually vulnerable but collectively powerful species, and attachment and mutual support are a key to our personal and collective successes in life.
From another perspective, there is also a dark side to this “gift of nature.”
We draw lines in substantially arbitrary locations across the surface of planet Earth, or we may define our self as belonging to a group in a political or social or religious context, or sect. Our tribalism can support a generally strong level of support and succor for fellow humans on our side of that line, while we regard those just across the line as undeserving of our support. If they offend us, they may become targets of our capacity for cruelty.
Our allegiances can be both wonderful and harmful.
The individuality of us
As we celebrate this holiday — a favorite day on my personal calendar — I am compelled to reflect on the fact that America was designed to be fractious. We Americans are not required to all operate like “peas in the pod.”
While we, as a nation, often fail to live up to our ideals, when we pursue the highest standards of liberty, we celebrate diversity, difference, and the ability of each member of our tribe to find their own path.
In a very real sense, the great American “invention” was to create a nation in which we could all find a wonderful place of our own, with the sympathy and protection of fellow citizens, and with liberty and justice for all.
Happy Independence Day to my American tribe!
Michael Merzenich, PhD, is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is professor emeritus at UCSF and a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Posit Science Corporation; Stronger Brains Inc. Serve(d) as a speaker or a member of a speakers bureau for: Posit Science Corporation; Stronger Brains Inc. Received research grant from: National Institutes of Health Have a 5% or greater equity interest in: Posit Science Corporation; Stronger Brains Inc. Received income in an amount equal to or greater than $250 from: Posit Science Corporation; Stronger Brains Inc.; National Institutes of Health.
A version of this article first appeared on Medscape.com.
This week, we celebrate our nation’s birth in a national and individual display of our patriotic attachment to this country. — which includes our self-definition as Americans.
For each of us, personhood is an almost miraculous product of our brain’s plasticity — the brain’s ability to change chemically, structurally, and functionally, based on our life experiences — arising from near countless moments of change in the wiring of our brain.
The incredibly complex remodeling that created “you” is a product, of course, of your very complicated, unique passage in life. You have a repertoire of skills and ability; you have stories and understanding and a history of sensing and acting and thinking in the world that is, in detail, unique only to you and your experiences.
As your brain created its model of your world by recording “what goes with what” at each brief moment of time, your brain — that most complicated and wonderful of “machines” on planet Earth — also associated billions of moments of feeling and action and thought with their source, your Self.
Because we primarily construct our model of the world through our eyes and ears, it’s not surprising that the emergent Self that is located somewhere in the center of your head behind your eyes and between your ears. Through billions of contacts with the surfaces of your hide and sensory organs, you have embodied yourself.
Your sense of ‘us’
These same neurologic processes extend beyond our physical beings to incorporate other contributors to our well-being into our personhoods. Loving parents, siblings, friends — and others in your clans and tribes and nations — literally grow into your personhood by these same self-associating processes. These relationships are supported in mutual identity by all of the tokens and icons and charms and customs that collectively define you and enable a sense of “us.”
Put another way, Mother Nature (or, in another cultural perspective, our Creator) has designed our brains to incorporate all of those who are close to us — and more broadly, other individuals in our clan or tribe or nation — to be a part of each of us.
Humans are highly social creatures. When we rise up and risk our lives to defend our friends, family, or cultural “in-groups,” we are literally fighting to defend ourselves — because those other individuals have grown into our very being. In defending them, we are literally defending a part of ourselves.
From one human perspective, this attachment to family and clan and tribe and nation is obviously key for our survival. We are an individually vulnerable but collectively powerful species, and attachment and mutual support are a key to our personal and collective successes in life.
From another perspective, there is also a dark side to this “gift of nature.”
We draw lines in substantially arbitrary locations across the surface of planet Earth, or we may define our self as belonging to a group in a political or social or religious context, or sect. Our tribalism can support a generally strong level of support and succor for fellow humans on our side of that line, while we regard those just across the line as undeserving of our support. If they offend us, they may become targets of our capacity for cruelty.
Our allegiances can be both wonderful and harmful.
The individuality of us
As we celebrate this holiday — a favorite day on my personal calendar — I am compelled to reflect on the fact that America was designed to be fractious. We Americans are not required to all operate like “peas in the pod.”
While we, as a nation, often fail to live up to our ideals, when we pursue the highest standards of liberty, we celebrate diversity, difference, and the ability of each member of our tribe to find their own path.
In a very real sense, the great American “invention” was to create a nation in which we could all find a wonderful place of our own, with the sympathy and protection of fellow citizens, and with liberty and justice for all.
Happy Independence Day to my American tribe!
Michael Merzenich, PhD, is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is professor emeritus at UCSF and a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Posit Science Corporation; Stronger Brains Inc. Serve(d) as a speaker or a member of a speakers bureau for: Posit Science Corporation; Stronger Brains Inc. Received research grant from: National Institutes of Health Have a 5% or greater equity interest in: Posit Science Corporation; Stronger Brains Inc. Received income in an amount equal to or greater than $250 from: Posit Science Corporation; Stronger Brains Inc.; National Institutes of Health.
A version of this article first appeared on Medscape.com.
This week, we celebrate our nation’s birth in a national and individual display of our patriotic attachment to this country. — which includes our self-definition as Americans.
For each of us, personhood is an almost miraculous product of our brain’s plasticity — the brain’s ability to change chemically, structurally, and functionally, based on our life experiences — arising from near countless moments of change in the wiring of our brain.
The incredibly complex remodeling that created “you” is a product, of course, of your very complicated, unique passage in life. You have a repertoire of skills and ability; you have stories and understanding and a history of sensing and acting and thinking in the world that is, in detail, unique only to you and your experiences.
As your brain created its model of your world by recording “what goes with what” at each brief moment of time, your brain — that most complicated and wonderful of “machines” on planet Earth — also associated billions of moments of feeling and action and thought with their source, your Self.
Because we primarily construct our model of the world through our eyes and ears, it’s not surprising that the emergent Self that is located somewhere in the center of your head behind your eyes and between your ears. Through billions of contacts with the surfaces of your hide and sensory organs, you have embodied yourself.
Your sense of ‘us’
These same neurologic processes extend beyond our physical beings to incorporate other contributors to our well-being into our personhoods. Loving parents, siblings, friends — and others in your clans and tribes and nations — literally grow into your personhood by these same self-associating processes. These relationships are supported in mutual identity by all of the tokens and icons and charms and customs that collectively define you and enable a sense of “us.”
Put another way, Mother Nature (or, in another cultural perspective, our Creator) has designed our brains to incorporate all of those who are close to us — and more broadly, other individuals in our clan or tribe or nation — to be a part of each of us.
Humans are highly social creatures. When we rise up and risk our lives to defend our friends, family, or cultural “in-groups,” we are literally fighting to defend ourselves — because those other individuals have grown into our very being. In defending them, we are literally defending a part of ourselves.
From one human perspective, this attachment to family and clan and tribe and nation is obviously key for our survival. We are an individually vulnerable but collectively powerful species, and attachment and mutual support are a key to our personal and collective successes in life.
From another perspective, there is also a dark side to this “gift of nature.”
We draw lines in substantially arbitrary locations across the surface of planet Earth, or we may define our self as belonging to a group in a political or social or religious context, or sect. Our tribalism can support a generally strong level of support and succor for fellow humans on our side of that line, while we regard those just across the line as undeserving of our support. If they offend us, they may become targets of our capacity for cruelty.
Our allegiances can be both wonderful and harmful.
The individuality of us
As we celebrate this holiday — a favorite day on my personal calendar — I am compelled to reflect on the fact that America was designed to be fractious. We Americans are not required to all operate like “peas in the pod.”
While we, as a nation, often fail to live up to our ideals, when we pursue the highest standards of liberty, we celebrate diversity, difference, and the ability of each member of our tribe to find their own path.
In a very real sense, the great American “invention” was to create a nation in which we could all find a wonderful place of our own, with the sympathy and protection of fellow citizens, and with liberty and justice for all.
Happy Independence Day to my American tribe!
Michael Merzenich, PhD, is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is professor emeritus at UCSF and a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Posit Science Corporation; Stronger Brains Inc. Serve(d) as a speaker or a member of a speakers bureau for: Posit Science Corporation; Stronger Brains Inc. Received research grant from: National Institutes of Health Have a 5% or greater equity interest in: Posit Science Corporation; Stronger Brains Inc. Received income in an amount equal to or greater than $250 from: Posit Science Corporation; Stronger Brains Inc.; National Institutes of Health.
A version of this article first appeared on Medscape.com.
Neurotransmitter-based diagnosis and treatment: A hypothesis (Part 3)
Optimal diagnosis and treatment of psychiatric illness requires clinicians to be able to connect mental and physical symptoms. Direct brain neurotransmitter testing is presently in its infancy and the science of defining the underlying mechanisms of psychiatric disorders lags behind the obvious clinical needs. We are not yet equipped to clearly recognize which neurotransmitters cause which symptoms. In this article series, we suggest an indirect way of judging neurotransmitter activity by recognizing specific mental and physical symptoms connected by common biology. Here we present hypothetical clinical cases to emphasize a possible way of analyzing symptoms in order to identify underlying pathology and guide more effective treatment. The descriptions we present in this series do not reflect the entire set of symptoms caused by the neurotransmitters we discuss; we created them based on what is presently known (or suspected). Additional research is needed to confirm or disprove the hypothesis we present. We argue that in cases of multiple psychiatric disorders and chronic pain, the development and approval of medications currently is based on an umbrella descriptive diagnoses, and disregards the various underlying causes of such conditions. Similar to how the many types of pneumonias are treated differently depending on the infective agent, we suggested the same possible causative approach to various types of depression and pain.
Part 1 of this series (
GABA excess (Table 11-9)
Ms. V is brought to your office by a friend. She complains of pain all over her body, itchiness, inability to focus, and dizziness.1,5,6,9 She is puzzled by how little pain she feels when she cuts her finger but by how much pain she is in every day, though her clinicians have not discovered a reason for her pain.1,6,9 She states that her fatigue is so severe that she can sleep 15 hours a day.1-6,9 Her obstructive and central sleep apnea have been treated, but this did not improve her fatigue.3,5,9 She is forgetful and has been diagnosed with depression, though she says she does not feel depressed.1,5,6 Nothing is pleasant to her, but she is prone to abnormal excitement and unpredictable behavior.1,4,6,7
A physical exam shows slow breathing, bradycardia, decreased deep tendon reflexes, and decreased muscle tone.1,5,6,9 Ms. V complains of double vision1,5,6,9 and problems with gait and balance,5,6,9 as well as tremors.1,4-7 She experienced enuresis well into adulthood1,5,6,9 and is prone to weight gain, dyspepsia, and constipation.8,9 She cannot understand people who have anxiety, and is prone to melancholy.4-6,9 Ms. V had been treated with electroconvulsive therapy in the past but states that she “had to have so much electricity, they gave up on me.”
Impression. Ms. V exhibits multiple symptoms associated with GABA excess. Dopaminergic medications such as methylphenidate or amphetamines may be helpful, as they suppress GABA. GABAergic medications and supplements should be avoided in such a patient. Noradrenergic medications including antidepressants with corresponding activity or vasopressors may be beneficial. Suppression of glutamate increases GABA, which is why ketamine in any formulation should be avoided in a patient such as Ms. V.
GABA deficiency (Table 11-4,6,9-17)
Mr. N complains of depression,1,3,4,6,12,16 pain all over his body, tingling in his hands and feet,1,6,9 a constant dull headache,2 and severe insomnia.2,3,9,10 He cannot control his anxiety and, in general, has problems relaxing. In the office, he is jumpy, tremulous, and fidgety during the interview and examination.1,3,4,6,9,12 His muscle tone is high1,9,11 and he feels stiff.6,9 Mr. N’s pupils are narrow1,9; he is hyper-reflexive1,9,11 and reports “Klonopin withdrawal seizures.”1,6,9 He loves alcohol because “it makes me feel good” and helps with his mind, which otherwise “never stops.”1,6,13 Mr. N is frequently anxious and very sensitive to pain, especially when he is upset. He was diagnosed with fibromyalgia by his primary care doctor, who says that irritable bowel is common in patients like him.1,6 His anxiety disables him.1-4,6,9-12 His sister reports that in addition to having difficulty relaxing, Mr. N is easily frustrated and sleeps poorly because he says he has racing thoughts.10 She mentions that her brother’s gambling addiction endangered his finances on several occasions4,12,15 and he was suspected of having autism spectrum disorder.4,12 Mr. N is frequently overwhelmed, including during your interview.1,3,4,6 He is sensitive to light and noise1,9 and complains of palpitations1,3,4,6,9 and frequent shortness of breath.1,3,4,9 He mentions his hands and feet often are cold, especially when he is anxious.1,3,4,6,9 Not eating at regular times makes his symptoms even worse. Mr. N commonly feels depressed, but his anxiety is more bothersome.1,3,4,6,12,16 His ongoing complaints include difficulty concentrating and memory problems,3,4,12,13 as well as a constant feeling of being overwhelmed.1,3,4,6 His restless leg syndrome requires ongoing treatment.1,9,14 Though uncommon, Mr. N has episodes of slowing and weakness, which are associated with growth hormone problems.16 In the past, he experienced gut motility dysregulation9,10 and prolonged bleeding that worried his doctors.17
Impression. Mr. N shows multiple symptoms associated with GABA deficiency. The deficiency of GABA activity ultimately causes an increase in norepinephrine and dopamine firing; therefore, symptoms of GABA deficiency are partially aligned with symptoms of dopamine and norepinephrine excess. GABAergic medications would be most beneficial for such patients. Anticonvulsants (eg, gabapentin and pregabalin) are preferable. Acamprostate may be considered. For long-term use, benzodiapines are as problematic as opioids and should be avoided, if possible. The use of opioids in such patients is especially counterproductive. Some supplements and vitamins may enhance GABA activity. Avoiding bupropion and stimulants would be wise. Ketamine in any formulation would be a good choice in this scenario. Sedating antipsychotic medications have a promise for patients such as Mr. N. The muscle relaxant baclofen frequently helps with these patients’ pain, anxiety, and sleep.
Continue to: Glutamate excess
Glutamate excess (Table 29,18-30)
Mr. B is anxious and bites his fingernails and cheek while you interview him.18 He has scars on his lower arms that were caused by years of picking his skin.18 He complains of headache28-30 and deep muscle, whole body,19-23 and abdominal pain.20 Both hyperesthesia (he calls it “fibromyalgia”)9,19,20,22 and irritable bowel syndrome flare up if he eats Chinese food that contains monosodium glutamate.21 This also increases nausea, vomiting, and hypertensive episodes.9,19,20,22,24,26 Mr. B developed and received treatment for opioid use disorder after being prescribed morphine for the treatment of fibromyalgia.22 He is being treated for posttraumatic stress disorder at the VA hospital and is bitter that his flashbacks are not controlled.23 Once, he experienced a frank psychosis.26 He commonly experiences dissociative symptoms and suicidality.23,26 The sensations of crawling skin,18 panic attacks, and nightmares complicate his life.23 Mr. B is angry that his “incompetent” psychiatrist stopped his diazepam and that it “almost killed him” by causing delirium.24 He suffers from severe neuropathic pain in his feet and says that his pain, depression, and anxiety respond especially well to ketamine treatment.9,23,26 He is prone to euphoria and has had several manic episodes.26 In childhood, his parents brought him to a psychiatrist to address episodes of head-banging and self-hitting.18 Mr. B developed seizures; presently, they are controlled, but he remains chronically dizzy.9,24,25,27 He claims that his headaches and migraines respond only to methadone and that sumatriptan makes them worse, especially in prolonged treatment.28-30 He is tachycardic, tremulous, and makes you feel deeply uneasy.9,24
Impression. Mr. B has many symptoms of glutamate hyperactivity. The use of N-methyl-
Glutamate deficiency (Table 29,32-38)
Mr. Z feels dull, fatigued, and unhappy.32,33,37 He is overweight and moves slowly. Sometimes he is so slow and clumsy that he seems obtunded.9,36,37 He states that his peripheral neuropathy does not cause him pain, though his neurodiagnostic results are unfavorable.32 Mr. Z’s overall pain threshold is high, and he is unhappy with people who complain about pain because “who cares?”32 His memory and concentration were never good.33,37,38 He suffers from insomnia and is frequently miserable and disheartened.32,33,38 People view him as melancholic.33,37 Mr. Z is mildly depressed, but he experiences aggressive outbursts37,38 and bouts of anxiety,32,33,36,38 psychosis, and mania.33,37,38 He is visibly confused37 and says it is easy for him to get disoriented and lost.37,38 His medical history includes long-term constipation and several episodes of ileus.9,34,35 His childhood-onset seizures are controlled presently.33 He complains of frequent bouts of dizziness and headache.32,34,35 On physical exam, Mr. Z has dry mouth, hypotension, diminished deep tendon reflexes, and bradycardia.9,34,35 He sought a consultation from an ophthalmologist to evaluate an eye movement problem.33,36 No cause was found, but the ophthalmologist thought this problem might have the same underlying mechanism as his dysarthria.33 Mr. Z’s balance is bothersome, but his podiatrist was unable to help him to correct his abnormal gait.33-36 A friend who came with Mr. Z mentioned she had noticed personality changes in him over the last several months.37
Impression. Mr. Z exhibits multiple signs of low glutamatergic function. Amino acid taurine has been shown in rodents to increase brain levels of both GABA and glutamate. Glutamate is metabolized into GABA, so low glutamate and low GABA symptoms overlap. Glutamine, which is present in meat, fish, eggs, dairy, wheat, and some vegetables, is converted in the body into glutamate and may be considered for a patient with low glutamate function. The medication approach to such a patient would be similar to the treatment of a low GABA patient and includes glutamate-enhancing magnesium and dextromethorphan.
Rarely is just 1 neurotransmitter involved
Most real-world patients have mixed presentations with more than 1 neurotransmitter implicated in the pathology of their symptoms. A clinician’s ability to dissect the clinical picture and select an appropriate treatment must be based on history and observed behavior because no lab results or reliable tests are presently available.
Continue to: The most studied...
The most studied neurotransmitter in depression and anxiety is serotonin, and for many years psychiatrists have paid too much attention to it. Similarly, pain physicians have been overly focused on the opioid system. Excessive attention to these neurochemicals has overshadowed multiple other (no less impactful) neurotransmitters. Dopamine is frequently not attended to by many physicians who treat chronic pain. Psychiatrists also may overlook underlying endorphin or glutamate dysfunction in patients with psychiatric illness.
Nonpharmacologic approaches can affect neurotransmitters
With all the emphasis on pharmacologic treatments, it is important to remember that nonpharmacologic modalities such as exercise, diet, hydrotherapy, acupuncture, and psychotherapy can help normalize neurotransmitter function in the brain and ultimately help patients with chronic conditions. Careful use of nutritional supplements and vitamins may also be beneficial.
A hypothesis for future research
Multiple peripheral and central mechanisms define various chronic pain and psychiatric symptoms and disorders, including depression, anxiety, and fibromyalgia. The variety of mechanisms of pathologic mood and pain perception may be expressed to a different extent and in countless combinations in individual patients. This, in part, explains the variable responses to the same treatment observed in similar patients, or even in the same patient.
Clinicians should always remember that depression and anxiety as well as chronic pain (including fibromyalgia and chronic headache) are not a representation of a single condition but are the result of an assembly of different syndromes; therefore, 1 treatment does not fit all patients. Pain is ultimately recognized and comprehended centrally, making it very much a neuropsychiatric field. The optimal treatment for 2 patients with similar pain or psychiatric symptoms may be drastically different due to different underlying mechanisms that can be distinguished by looking at the symptoms other than “pain” or “depression.”
Remembering that every neurotransmitter deficiency or excess has an identifiable clinical correlation is important. Basing a treatment approach on a specific clinical presentation in a particular depressed or chronic pain patient would assure a more successful and reliable outcome.
Continue to: This 3-part series...
This 3-part series was designed to bring attention to a notion that diagnosis and treatment of diverse conditions such as “depression,” “anxiety,” or “chronic pain” should be based on clinically identifiable symptoms that may suggest specific neurotransmitter(s) involved in a specific type of each of these conditions. However, there are no well-recognized, well-established, reliable, or validated syndromes described in this series. The collection of symptoms associated with the various neurotransmitters described in this series is not complete. We have assembled what is described in the literature as a suggestion for future research.
Bottom Line
Both high and low levels of gamma aminobutyric acid (GABA) and glutamate may be associated with certain psychiatric and medical symptoms and disorders. An astute clinician may judge which neurotransmitter is dysfunctional based on the patient’s presentation, and tailor treatment accordingly.
Related Resources
- Arbuck DM, Salmerón JM, Mueller R. Neurotransmitter-based diagnosis and treatment: a hypothesis (part 1). Current Psychiatry. 2022;21(5):30-36. doi:10.12788/cp.0242
- Arbuck DM, Salmerón JM, Mueller R. Neurotransmitter-based diagnosis and treatment: a hypothesis (part 2). Current Psychiatry. 2022;21(6):28-33. doi:10.12788/cp.0253
Drug Brand Names
Acamprostate • Campral
Amantadine • Gocovri
Bupropion • Wellbutrin
Clonazepam • Klonopin
Clonidine • Catapres
Diazepam • Valium
Gabapentin • Neurontin
Ketamine • Ketalar
Memantine • Namenda
Methylphenidate • Concerta
Morphine • Kadian
Pregabalin • Lyrica
Sumatriptan • Imitrex
Tizanidine • Zanaflex
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15. Mick I, Ramos AC, Myers J, et al. Evidence for GABA-A receptor dysregulation in gambling disorder: correlation with impulsivity. Addict Biol. 2017;22(6):1601-1609.
16. Brambilla P, Perez J, Barale F, et al. Gabaergic dysfunction in mood disorders. Molecular Psychiatry. 2003;8:721-737.
17. Kaneez FS, Saeed SA. Investigating GABA and its function in platelets as compared to neurons. Platelets. 2009;20(5):328-333.
18. Paholpak P, Mendez MF. Trichotillomania as a manifestation of dementia. Case Rep Psychiatry. 2016;2016:9782702.
19. Miranda A, Peles S, Rudolph C, et al. Altered visceral sensation in response to somatic pain in the rat. Gastroenterology. 2004;126(4):1082-1089.
20. Skyba DA, King EW, Sluka KA. Effects of NMDA and non-NMDA ionotropic glutamate receptor antagonists on the development and maintenance of hyperalgesia induced by repeated intramuscular injection of acidic saline. Pain. 2002;98(1-2):69-78.
21. Holton KF, Taren DL, Thomson CA, et al. The effect of dietary glutamate on fibromyalgia and irritable bowel symptoms. Clin Exp Rheumatol. 2012;30(6 Suppl 74):10-70.
22. Sekiya Y, Nakagawa T, Ozawa T, et al. Facilitation of morphine withdrawal symptoms and morphine-induced conditioned place preference by a glutamate transporter inhibitor DL-threo-beta-benzyloxy aspartate in rats. Eur J Pharmacol. 2004;485(1-3):201-210.
23. Bestha D, Soliman L, Blankenship K. et al. The walking wounded: emerging treatments for PTSD. Curr Psychiatry Rep. 2018;20(10):94.
24. Tsuda M, Shimizu N, Suzuki T. Contribution of glutamate receptors to benzodiazepine withdrawal signs. Jpn J Pharmacol. 1999;81(1):1-6.
25. Spravato [package insert]. Janssen Pharmaceuticals, Inc; 2019.
26. Mattingly GW, Anderson RH. Intranasal ketamine. Current Psychiatry. 2019;18(5):31-38.
27. Buckingham SC, Campbell SL, Haas BR, et al. Glutamate release by primary brain tumors induces epileptic activity. Nat Med. 2011;17(10):1269-1275.
28. Ferrari A, Spaccapelo L, Pinetti D, et al. Effective prophylactic treatment of migraines lower plasma glutamate levels. Cephalalgia. 2009;29(4):423-429.
29. Vieira DS, Naffah-Mazzacoratti Mda G, Zukerman E, et al. Glutamate levels in cerebrospinal fluid and triptans overuse in chronic migraine. Headache. 2007;47(6):842-847.
30. Chan K, MaassenVanDenBrink A. Glutamate receptor antagonists in the management of migraine. Drugs. 2014;74:1165-1176.
31. Pappa S, Tsouli S, Apostolou G, et al. Effects of amantadine on tardive dyskinesia: a randomized, double-blind, placebo-controlled study. Clin Neuropharmacol. 2010;33(6):271-275.
32. Kraal AZ, Arvanitis NR, Jaeger AP, et al. Could dietary glutamate play a role in psychiatric distress? Neuro Psych. 2020;79:13-19.
33. Levite M. Glutamate receptor antibodies in neurological diseases: anti-AMPA-GluR3 antibodies, Anti-NMDA-NR1 antibodies, Anti-NMDA-NR2A/B antibodies, Anti-mGluR1 antibodies or Anti-mGluR5 antibodies are present in subpopulations of patients with either: epilepsy, encephalitis, cerebellar ataxia, systemic lupus erythematosus (SLE) and neuropsychiatric SLE, Sjogren’s syndrome, schizophrenia, mania or stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor’s expression, impair glutamate-induced signaling and function, activate blood brain barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and ataxia in animal models, and can be removed or silenced in some patients by immunotherapy. J Neural Transm (Vienna). 2014;121(8):1029-1075.
34. Lancaster E. CNS syndromes associated with antibodies against metabotropic receptors. Curr Opin Neurol. 2017;30:354-360.
35. Sillevis Smitt P, Kinoshita A, De Leeuw B, et al. Paraneoplastic cerebellar ataxia due to autoantibodies against a glutamate receptor. N Engl J Med. 2000;342(1):21-27.
36. Marignier R, Chenevier F, Rogemond V, et al. Metabotropic glutamate receptor type 1 autoantibody-associated cerebellitis: a primary autoimmune disease? Arch Neurol. 2010;67(5):627-630.
37. Lancaster E, Martinez-Hernandez E, Titulaer MJ, et al. Antibodies to metabotropic glutamate receptor 5 in the Ophelia syndrome. Neurology. 2011;77:1698-1701.
38. Mat A, Adler H, Merwick A, et al. Ophelia syndrome with metabotropic glutamate receptor 5 antibodies in CSF. Neurology. 2013;80(14):1349-1350.
Optimal diagnosis and treatment of psychiatric illness requires clinicians to be able to connect mental and physical symptoms. Direct brain neurotransmitter testing is presently in its infancy and the science of defining the underlying mechanisms of psychiatric disorders lags behind the obvious clinical needs. We are not yet equipped to clearly recognize which neurotransmitters cause which symptoms. In this article series, we suggest an indirect way of judging neurotransmitter activity by recognizing specific mental and physical symptoms connected by common biology. Here we present hypothetical clinical cases to emphasize a possible way of analyzing symptoms in order to identify underlying pathology and guide more effective treatment. The descriptions we present in this series do not reflect the entire set of symptoms caused by the neurotransmitters we discuss; we created them based on what is presently known (or suspected). Additional research is needed to confirm or disprove the hypothesis we present. We argue that in cases of multiple psychiatric disorders and chronic pain, the development and approval of medications currently is based on an umbrella descriptive diagnoses, and disregards the various underlying causes of such conditions. Similar to how the many types of pneumonias are treated differently depending on the infective agent, we suggested the same possible causative approach to various types of depression and pain.
Part 1 of this series (
GABA excess (Table 11-9)
Ms. V is brought to your office by a friend. She complains of pain all over her body, itchiness, inability to focus, and dizziness.1,5,6,9 She is puzzled by how little pain she feels when she cuts her finger but by how much pain she is in every day, though her clinicians have not discovered a reason for her pain.1,6,9 She states that her fatigue is so severe that she can sleep 15 hours a day.1-6,9 Her obstructive and central sleep apnea have been treated, but this did not improve her fatigue.3,5,9 She is forgetful and has been diagnosed with depression, though she says she does not feel depressed.1,5,6 Nothing is pleasant to her, but she is prone to abnormal excitement and unpredictable behavior.1,4,6,7
A physical exam shows slow breathing, bradycardia, decreased deep tendon reflexes, and decreased muscle tone.1,5,6,9 Ms. V complains of double vision1,5,6,9 and problems with gait and balance,5,6,9 as well as tremors.1,4-7 She experienced enuresis well into adulthood1,5,6,9 and is prone to weight gain, dyspepsia, and constipation.8,9 She cannot understand people who have anxiety, and is prone to melancholy.4-6,9 Ms. V had been treated with electroconvulsive therapy in the past but states that she “had to have so much electricity, they gave up on me.”
Impression. Ms. V exhibits multiple symptoms associated with GABA excess. Dopaminergic medications such as methylphenidate or amphetamines may be helpful, as they suppress GABA. GABAergic medications and supplements should be avoided in such a patient. Noradrenergic medications including antidepressants with corresponding activity or vasopressors may be beneficial. Suppression of glutamate increases GABA, which is why ketamine in any formulation should be avoided in a patient such as Ms. V.
GABA deficiency (Table 11-4,6,9-17)
Mr. N complains of depression,1,3,4,6,12,16 pain all over his body, tingling in his hands and feet,1,6,9 a constant dull headache,2 and severe insomnia.2,3,9,10 He cannot control his anxiety and, in general, has problems relaxing. In the office, he is jumpy, tremulous, and fidgety during the interview and examination.1,3,4,6,9,12 His muscle tone is high1,9,11 and he feels stiff.6,9 Mr. N’s pupils are narrow1,9; he is hyper-reflexive1,9,11 and reports “Klonopin withdrawal seizures.”1,6,9 He loves alcohol because “it makes me feel good” and helps with his mind, which otherwise “never stops.”1,6,13 Mr. N is frequently anxious and very sensitive to pain, especially when he is upset. He was diagnosed with fibromyalgia by his primary care doctor, who says that irritable bowel is common in patients like him.1,6 His anxiety disables him.1-4,6,9-12 His sister reports that in addition to having difficulty relaxing, Mr. N is easily frustrated and sleeps poorly because he says he has racing thoughts.10 She mentions that her brother’s gambling addiction endangered his finances on several occasions4,12,15 and he was suspected of having autism spectrum disorder.4,12 Mr. N is frequently overwhelmed, including during your interview.1,3,4,6 He is sensitive to light and noise1,9 and complains of palpitations1,3,4,6,9 and frequent shortness of breath.1,3,4,9 He mentions his hands and feet often are cold, especially when he is anxious.1,3,4,6,9 Not eating at regular times makes his symptoms even worse. Mr. N commonly feels depressed, but his anxiety is more bothersome.1,3,4,6,12,16 His ongoing complaints include difficulty concentrating and memory problems,3,4,12,13 as well as a constant feeling of being overwhelmed.1,3,4,6 His restless leg syndrome requires ongoing treatment.1,9,14 Though uncommon, Mr. N has episodes of slowing and weakness, which are associated with growth hormone problems.16 In the past, he experienced gut motility dysregulation9,10 and prolonged bleeding that worried his doctors.17
Impression. Mr. N shows multiple symptoms associated with GABA deficiency. The deficiency of GABA activity ultimately causes an increase in norepinephrine and dopamine firing; therefore, symptoms of GABA deficiency are partially aligned with symptoms of dopamine and norepinephrine excess. GABAergic medications would be most beneficial for such patients. Anticonvulsants (eg, gabapentin and pregabalin) are preferable. Acamprostate may be considered. For long-term use, benzodiapines are as problematic as opioids and should be avoided, if possible. The use of opioids in such patients is especially counterproductive. Some supplements and vitamins may enhance GABA activity. Avoiding bupropion and stimulants would be wise. Ketamine in any formulation would be a good choice in this scenario. Sedating antipsychotic medications have a promise for patients such as Mr. N. The muscle relaxant baclofen frequently helps with these patients’ pain, anxiety, and sleep.
Continue to: Glutamate excess
Glutamate excess (Table 29,18-30)
Mr. B is anxious and bites his fingernails and cheek while you interview him.18 He has scars on his lower arms that were caused by years of picking his skin.18 He complains of headache28-30 and deep muscle, whole body,19-23 and abdominal pain.20 Both hyperesthesia (he calls it “fibromyalgia”)9,19,20,22 and irritable bowel syndrome flare up if he eats Chinese food that contains monosodium glutamate.21 This also increases nausea, vomiting, and hypertensive episodes.9,19,20,22,24,26 Mr. B developed and received treatment for opioid use disorder after being prescribed morphine for the treatment of fibromyalgia.22 He is being treated for posttraumatic stress disorder at the VA hospital and is bitter that his flashbacks are not controlled.23 Once, he experienced a frank psychosis.26 He commonly experiences dissociative symptoms and suicidality.23,26 The sensations of crawling skin,18 panic attacks, and nightmares complicate his life.23 Mr. B is angry that his “incompetent” psychiatrist stopped his diazepam and that it “almost killed him” by causing delirium.24 He suffers from severe neuropathic pain in his feet and says that his pain, depression, and anxiety respond especially well to ketamine treatment.9,23,26 He is prone to euphoria and has had several manic episodes.26 In childhood, his parents brought him to a psychiatrist to address episodes of head-banging and self-hitting.18 Mr. B developed seizures; presently, they are controlled, but he remains chronically dizzy.9,24,25,27 He claims that his headaches and migraines respond only to methadone and that sumatriptan makes them worse, especially in prolonged treatment.28-30 He is tachycardic, tremulous, and makes you feel deeply uneasy.9,24
Impression. Mr. B has many symptoms of glutamate hyperactivity. The use of N-methyl-
Glutamate deficiency (Table 29,32-38)
Mr. Z feels dull, fatigued, and unhappy.32,33,37 He is overweight and moves slowly. Sometimes he is so slow and clumsy that he seems obtunded.9,36,37 He states that his peripheral neuropathy does not cause him pain, though his neurodiagnostic results are unfavorable.32 Mr. Z’s overall pain threshold is high, and he is unhappy with people who complain about pain because “who cares?”32 His memory and concentration were never good.33,37,38 He suffers from insomnia and is frequently miserable and disheartened.32,33,38 People view him as melancholic.33,37 Mr. Z is mildly depressed, but he experiences aggressive outbursts37,38 and bouts of anxiety,32,33,36,38 psychosis, and mania.33,37,38 He is visibly confused37 and says it is easy for him to get disoriented and lost.37,38 His medical history includes long-term constipation and several episodes of ileus.9,34,35 His childhood-onset seizures are controlled presently.33 He complains of frequent bouts of dizziness and headache.32,34,35 On physical exam, Mr. Z has dry mouth, hypotension, diminished deep tendon reflexes, and bradycardia.9,34,35 He sought a consultation from an ophthalmologist to evaluate an eye movement problem.33,36 No cause was found, but the ophthalmologist thought this problem might have the same underlying mechanism as his dysarthria.33 Mr. Z’s balance is bothersome, but his podiatrist was unable to help him to correct his abnormal gait.33-36 A friend who came with Mr. Z mentioned she had noticed personality changes in him over the last several months.37
Impression. Mr. Z exhibits multiple signs of low glutamatergic function. Amino acid taurine has been shown in rodents to increase brain levels of both GABA and glutamate. Glutamate is metabolized into GABA, so low glutamate and low GABA symptoms overlap. Glutamine, which is present in meat, fish, eggs, dairy, wheat, and some vegetables, is converted in the body into glutamate and may be considered for a patient with low glutamate function. The medication approach to such a patient would be similar to the treatment of a low GABA patient and includes glutamate-enhancing magnesium and dextromethorphan.
Rarely is just 1 neurotransmitter involved
Most real-world patients have mixed presentations with more than 1 neurotransmitter implicated in the pathology of their symptoms. A clinician’s ability to dissect the clinical picture and select an appropriate treatment must be based on history and observed behavior because no lab results or reliable tests are presently available.
Continue to: The most studied...
The most studied neurotransmitter in depression and anxiety is serotonin, and for many years psychiatrists have paid too much attention to it. Similarly, pain physicians have been overly focused on the opioid system. Excessive attention to these neurochemicals has overshadowed multiple other (no less impactful) neurotransmitters. Dopamine is frequently not attended to by many physicians who treat chronic pain. Psychiatrists also may overlook underlying endorphin or glutamate dysfunction in patients with psychiatric illness.
Nonpharmacologic approaches can affect neurotransmitters
With all the emphasis on pharmacologic treatments, it is important to remember that nonpharmacologic modalities such as exercise, diet, hydrotherapy, acupuncture, and psychotherapy can help normalize neurotransmitter function in the brain and ultimately help patients with chronic conditions. Careful use of nutritional supplements and vitamins may also be beneficial.
A hypothesis for future research
Multiple peripheral and central mechanisms define various chronic pain and psychiatric symptoms and disorders, including depression, anxiety, and fibromyalgia. The variety of mechanisms of pathologic mood and pain perception may be expressed to a different extent and in countless combinations in individual patients. This, in part, explains the variable responses to the same treatment observed in similar patients, or even in the same patient.
Clinicians should always remember that depression and anxiety as well as chronic pain (including fibromyalgia and chronic headache) are not a representation of a single condition but are the result of an assembly of different syndromes; therefore, 1 treatment does not fit all patients. Pain is ultimately recognized and comprehended centrally, making it very much a neuropsychiatric field. The optimal treatment for 2 patients with similar pain or psychiatric symptoms may be drastically different due to different underlying mechanisms that can be distinguished by looking at the symptoms other than “pain” or “depression.”
Remembering that every neurotransmitter deficiency or excess has an identifiable clinical correlation is important. Basing a treatment approach on a specific clinical presentation in a particular depressed or chronic pain patient would assure a more successful and reliable outcome.
Continue to: This 3-part series...
This 3-part series was designed to bring attention to a notion that diagnosis and treatment of diverse conditions such as “depression,” “anxiety,” or “chronic pain” should be based on clinically identifiable symptoms that may suggest specific neurotransmitter(s) involved in a specific type of each of these conditions. However, there are no well-recognized, well-established, reliable, or validated syndromes described in this series. The collection of symptoms associated with the various neurotransmitters described in this series is not complete. We have assembled what is described in the literature as a suggestion for future research.
Bottom Line
Both high and low levels of gamma aminobutyric acid (GABA) and glutamate may be associated with certain psychiatric and medical symptoms and disorders. An astute clinician may judge which neurotransmitter is dysfunctional based on the patient’s presentation, and tailor treatment accordingly.
Related Resources
- Arbuck DM, Salmerón JM, Mueller R. Neurotransmitter-based diagnosis and treatment: a hypothesis (part 1). Current Psychiatry. 2022;21(5):30-36. doi:10.12788/cp.0242
- Arbuck DM, Salmerón JM, Mueller R. Neurotransmitter-based diagnosis and treatment: a hypothesis (part 2). Current Psychiatry. 2022;21(6):28-33. doi:10.12788/cp.0253
Drug Brand Names
Acamprostate • Campral
Amantadine • Gocovri
Bupropion • Wellbutrin
Clonazepam • Klonopin
Clonidine • Catapres
Diazepam • Valium
Gabapentin • Neurontin
Ketamine • Ketalar
Memantine • Namenda
Methylphenidate • Concerta
Morphine • Kadian
Pregabalin • Lyrica
Sumatriptan • Imitrex
Tizanidine • Zanaflex
Optimal diagnosis and treatment of psychiatric illness requires clinicians to be able to connect mental and physical symptoms. Direct brain neurotransmitter testing is presently in its infancy and the science of defining the underlying mechanisms of psychiatric disorders lags behind the obvious clinical needs. We are not yet equipped to clearly recognize which neurotransmitters cause which symptoms. In this article series, we suggest an indirect way of judging neurotransmitter activity by recognizing specific mental and physical symptoms connected by common biology. Here we present hypothetical clinical cases to emphasize a possible way of analyzing symptoms in order to identify underlying pathology and guide more effective treatment. The descriptions we present in this series do not reflect the entire set of symptoms caused by the neurotransmitters we discuss; we created them based on what is presently known (or suspected). Additional research is needed to confirm or disprove the hypothesis we present. We argue that in cases of multiple psychiatric disorders and chronic pain, the development and approval of medications currently is based on an umbrella descriptive diagnoses, and disregards the various underlying causes of such conditions. Similar to how the many types of pneumonias are treated differently depending on the infective agent, we suggested the same possible causative approach to various types of depression and pain.
Part 1 of this series (
GABA excess (Table 11-9)
Ms. V is brought to your office by a friend. She complains of pain all over her body, itchiness, inability to focus, and dizziness.1,5,6,9 She is puzzled by how little pain she feels when she cuts her finger but by how much pain she is in every day, though her clinicians have not discovered a reason for her pain.1,6,9 She states that her fatigue is so severe that she can sleep 15 hours a day.1-6,9 Her obstructive and central sleep apnea have been treated, but this did not improve her fatigue.3,5,9 She is forgetful and has been diagnosed with depression, though she says she does not feel depressed.1,5,6 Nothing is pleasant to her, but she is prone to abnormal excitement and unpredictable behavior.1,4,6,7
A physical exam shows slow breathing, bradycardia, decreased deep tendon reflexes, and decreased muscle tone.1,5,6,9 Ms. V complains of double vision1,5,6,9 and problems with gait and balance,5,6,9 as well as tremors.1,4-7 She experienced enuresis well into adulthood1,5,6,9 and is prone to weight gain, dyspepsia, and constipation.8,9 She cannot understand people who have anxiety, and is prone to melancholy.4-6,9 Ms. V had been treated with electroconvulsive therapy in the past but states that she “had to have so much electricity, they gave up on me.”
Impression. Ms. V exhibits multiple symptoms associated with GABA excess. Dopaminergic medications such as methylphenidate or amphetamines may be helpful, as they suppress GABA. GABAergic medications and supplements should be avoided in such a patient. Noradrenergic medications including antidepressants with corresponding activity or vasopressors may be beneficial. Suppression of glutamate increases GABA, which is why ketamine in any formulation should be avoided in a patient such as Ms. V.
GABA deficiency (Table 11-4,6,9-17)
Mr. N complains of depression,1,3,4,6,12,16 pain all over his body, tingling in his hands and feet,1,6,9 a constant dull headache,2 and severe insomnia.2,3,9,10 He cannot control his anxiety and, in general, has problems relaxing. In the office, he is jumpy, tremulous, and fidgety during the interview and examination.1,3,4,6,9,12 His muscle tone is high1,9,11 and he feels stiff.6,9 Mr. N’s pupils are narrow1,9; he is hyper-reflexive1,9,11 and reports “Klonopin withdrawal seizures.”1,6,9 He loves alcohol because “it makes me feel good” and helps with his mind, which otherwise “never stops.”1,6,13 Mr. N is frequently anxious and very sensitive to pain, especially when he is upset. He was diagnosed with fibromyalgia by his primary care doctor, who says that irritable bowel is common in patients like him.1,6 His anxiety disables him.1-4,6,9-12 His sister reports that in addition to having difficulty relaxing, Mr. N is easily frustrated and sleeps poorly because he says he has racing thoughts.10 She mentions that her brother’s gambling addiction endangered his finances on several occasions4,12,15 and he was suspected of having autism spectrum disorder.4,12 Mr. N is frequently overwhelmed, including during your interview.1,3,4,6 He is sensitive to light and noise1,9 and complains of palpitations1,3,4,6,9 and frequent shortness of breath.1,3,4,9 He mentions his hands and feet often are cold, especially when he is anxious.1,3,4,6,9 Not eating at regular times makes his symptoms even worse. Mr. N commonly feels depressed, but his anxiety is more bothersome.1,3,4,6,12,16 His ongoing complaints include difficulty concentrating and memory problems,3,4,12,13 as well as a constant feeling of being overwhelmed.1,3,4,6 His restless leg syndrome requires ongoing treatment.1,9,14 Though uncommon, Mr. N has episodes of slowing and weakness, which are associated with growth hormone problems.16 In the past, he experienced gut motility dysregulation9,10 and prolonged bleeding that worried his doctors.17
Impression. Mr. N shows multiple symptoms associated with GABA deficiency. The deficiency of GABA activity ultimately causes an increase in norepinephrine and dopamine firing; therefore, symptoms of GABA deficiency are partially aligned with symptoms of dopamine and norepinephrine excess. GABAergic medications would be most beneficial for such patients. Anticonvulsants (eg, gabapentin and pregabalin) are preferable. Acamprostate may be considered. For long-term use, benzodiapines are as problematic as opioids and should be avoided, if possible. The use of opioids in such patients is especially counterproductive. Some supplements and vitamins may enhance GABA activity. Avoiding bupropion and stimulants would be wise. Ketamine in any formulation would be a good choice in this scenario. Sedating antipsychotic medications have a promise for patients such as Mr. N. The muscle relaxant baclofen frequently helps with these patients’ pain, anxiety, and sleep.
Continue to: Glutamate excess
Glutamate excess (Table 29,18-30)
Mr. B is anxious and bites his fingernails and cheek while you interview him.18 He has scars on his lower arms that were caused by years of picking his skin.18 He complains of headache28-30 and deep muscle, whole body,19-23 and abdominal pain.20 Both hyperesthesia (he calls it “fibromyalgia”)9,19,20,22 and irritable bowel syndrome flare up if he eats Chinese food that contains monosodium glutamate.21 This also increases nausea, vomiting, and hypertensive episodes.9,19,20,22,24,26 Mr. B developed and received treatment for opioid use disorder after being prescribed morphine for the treatment of fibromyalgia.22 He is being treated for posttraumatic stress disorder at the VA hospital and is bitter that his flashbacks are not controlled.23 Once, he experienced a frank psychosis.26 He commonly experiences dissociative symptoms and suicidality.23,26 The sensations of crawling skin,18 panic attacks, and nightmares complicate his life.23 Mr. B is angry that his “incompetent” psychiatrist stopped his diazepam and that it “almost killed him” by causing delirium.24 He suffers from severe neuropathic pain in his feet and says that his pain, depression, and anxiety respond especially well to ketamine treatment.9,23,26 He is prone to euphoria and has had several manic episodes.26 In childhood, his parents brought him to a psychiatrist to address episodes of head-banging and self-hitting.18 Mr. B developed seizures; presently, they are controlled, but he remains chronically dizzy.9,24,25,27 He claims that his headaches and migraines respond only to methadone and that sumatriptan makes them worse, especially in prolonged treatment.28-30 He is tachycardic, tremulous, and makes you feel deeply uneasy.9,24
Impression. Mr. B has many symptoms of glutamate hyperactivity. The use of N-methyl-
Glutamate deficiency (Table 29,32-38)
Mr. Z feels dull, fatigued, and unhappy.32,33,37 He is overweight and moves slowly. Sometimes he is so slow and clumsy that he seems obtunded.9,36,37 He states that his peripheral neuropathy does not cause him pain, though his neurodiagnostic results are unfavorable.32 Mr. Z’s overall pain threshold is high, and he is unhappy with people who complain about pain because “who cares?”32 His memory and concentration were never good.33,37,38 He suffers from insomnia and is frequently miserable and disheartened.32,33,38 People view him as melancholic.33,37 Mr. Z is mildly depressed, but he experiences aggressive outbursts37,38 and bouts of anxiety,32,33,36,38 psychosis, and mania.33,37,38 He is visibly confused37 and says it is easy for him to get disoriented and lost.37,38 His medical history includes long-term constipation and several episodes of ileus.9,34,35 His childhood-onset seizures are controlled presently.33 He complains of frequent bouts of dizziness and headache.32,34,35 On physical exam, Mr. Z has dry mouth, hypotension, diminished deep tendon reflexes, and bradycardia.9,34,35 He sought a consultation from an ophthalmologist to evaluate an eye movement problem.33,36 No cause was found, but the ophthalmologist thought this problem might have the same underlying mechanism as his dysarthria.33 Mr. Z’s balance is bothersome, but his podiatrist was unable to help him to correct his abnormal gait.33-36 A friend who came with Mr. Z mentioned she had noticed personality changes in him over the last several months.37
Impression. Mr. Z exhibits multiple signs of low glutamatergic function. Amino acid taurine has been shown in rodents to increase brain levels of both GABA and glutamate. Glutamate is metabolized into GABA, so low glutamate and low GABA symptoms overlap. Glutamine, which is present in meat, fish, eggs, dairy, wheat, and some vegetables, is converted in the body into glutamate and may be considered for a patient with low glutamate function. The medication approach to such a patient would be similar to the treatment of a low GABA patient and includes glutamate-enhancing magnesium and dextromethorphan.
Rarely is just 1 neurotransmitter involved
Most real-world patients have mixed presentations with more than 1 neurotransmitter implicated in the pathology of their symptoms. A clinician’s ability to dissect the clinical picture and select an appropriate treatment must be based on history and observed behavior because no lab results or reliable tests are presently available.
Continue to: The most studied...
The most studied neurotransmitter in depression and anxiety is serotonin, and for many years psychiatrists have paid too much attention to it. Similarly, pain physicians have been overly focused on the opioid system. Excessive attention to these neurochemicals has overshadowed multiple other (no less impactful) neurotransmitters. Dopamine is frequently not attended to by many physicians who treat chronic pain. Psychiatrists also may overlook underlying endorphin or glutamate dysfunction in patients with psychiatric illness.
Nonpharmacologic approaches can affect neurotransmitters
With all the emphasis on pharmacologic treatments, it is important to remember that nonpharmacologic modalities such as exercise, diet, hydrotherapy, acupuncture, and psychotherapy can help normalize neurotransmitter function in the brain and ultimately help patients with chronic conditions. Careful use of nutritional supplements and vitamins may also be beneficial.
A hypothesis for future research
Multiple peripheral and central mechanisms define various chronic pain and psychiatric symptoms and disorders, including depression, anxiety, and fibromyalgia. The variety of mechanisms of pathologic mood and pain perception may be expressed to a different extent and in countless combinations in individual patients. This, in part, explains the variable responses to the same treatment observed in similar patients, or even in the same patient.
Clinicians should always remember that depression and anxiety as well as chronic pain (including fibromyalgia and chronic headache) are not a representation of a single condition but are the result of an assembly of different syndromes; therefore, 1 treatment does not fit all patients. Pain is ultimately recognized and comprehended centrally, making it very much a neuropsychiatric field. The optimal treatment for 2 patients with similar pain or psychiatric symptoms may be drastically different due to different underlying mechanisms that can be distinguished by looking at the symptoms other than “pain” or “depression.”
Remembering that every neurotransmitter deficiency or excess has an identifiable clinical correlation is important. Basing a treatment approach on a specific clinical presentation in a particular depressed or chronic pain patient would assure a more successful and reliable outcome.
Continue to: This 3-part series...
This 3-part series was designed to bring attention to a notion that diagnosis and treatment of diverse conditions such as “depression,” “anxiety,” or “chronic pain” should be based on clinically identifiable symptoms that may suggest specific neurotransmitter(s) involved in a specific type of each of these conditions. However, there are no well-recognized, well-established, reliable, or validated syndromes described in this series. The collection of symptoms associated with the various neurotransmitters described in this series is not complete. We have assembled what is described in the literature as a suggestion for future research.
Bottom Line
Both high and low levels of gamma aminobutyric acid (GABA) and glutamate may be associated with certain psychiatric and medical symptoms and disorders. An astute clinician may judge which neurotransmitter is dysfunctional based on the patient’s presentation, and tailor treatment accordingly.
Related Resources
- Arbuck DM, Salmerón JM, Mueller R. Neurotransmitter-based diagnosis and treatment: a hypothesis (part 1). Current Psychiatry. 2022;21(5):30-36. doi:10.12788/cp.0242
- Arbuck DM, Salmerón JM, Mueller R. Neurotransmitter-based diagnosis and treatment: a hypothesis (part 2). Current Psychiatry. 2022;21(6):28-33. doi:10.12788/cp.0253
Drug Brand Names
Acamprostate • Campral
Amantadine • Gocovri
Bupropion • Wellbutrin
Clonazepam • Klonopin
Clonidine • Catapres
Diazepam • Valium
Gabapentin • Neurontin
Ketamine • Ketalar
Memantine • Namenda
Methylphenidate • Concerta
Morphine • Kadian
Pregabalin • Lyrica
Sumatriptan • Imitrex
Tizanidine • Zanaflex
1. Petroff OA. GABA and glutamate in the human brain. Neuroscientist. 2002;8(6):562-573.
2. Winkelman JW, Buxton OM, Jensen JE, et al. Reduced brain GABA in primary insomnia: preliminary data from 4T proton magnetic resonance spectroscopy (1H-MRS). Sleep. 2008;31(11):1499-1506.
3. Pereira AC, Mao X, Jiang CS, et al. Dorsolateral prefrontal cortex GABA deficit in older adults with sleep-disordered breathing. Proc Natl Acad Sci U S A. 2017;114(38):10250-10255.
4. Schür RR, Draisma LW, Wijnen JP, et al. Brain GABA levels across psychiatric disorders: a systematic literature review and meta-analysis of (1) H-MRS studies. Hum Brain Mapp. 2016;37(9):3337-3352.
5. Evoy KE, Morrison MD, Saklad SR. Abuse and misuse of pregabalin and gabapentin. Drugs. 2017;77(4):403-426.
6. Mersfelder TL, Nichols WH. Gabapentin: abuse, dependence, and withdrawal. Ann Pharmacother. 2016;50(3):229-233.
7. Bremner JD. Traumatic stress: effects on the brain. Dialogues Clin Neurosci. 2006;8(4):445-461.
8. Kelly JR, Kennedy PJ, Cryan JF, et al. Breaking down the barriers: the gut microbiome, intestinal permeability, and stress-related psychiatric disorders. Front Cell Neurosci. 2015;9:392.
9. Guyton AC, Hall JE. Guyton and Hall Textbook of Medical Physiology. 12th ed. Elsevier; 2011:550-551,692-693.
10. Evrensel A, Ceylan ME. The gut-brain axis: the missing link in depression. Clin Psychopharmacol Neurosci. 2015;13(3):239-244.
11. Vianello M, Tavolato B, Giometto B. Glutamic acid decarboxylase autoantibodies and neurological disorders. Neurol Sci. 2002;23(4):145-151.
12. Marin O. Interneuron dysfunction in psychiatric disorders. Nat Rev Neurosci. 2012;13(2):107-120.
13. Huang D, Liu D, Yin J, et al. Glutamate-glutamine and GABA in the brain of normal aged and patients with cognitive impairment. Eur Radiol. 2017;27(7):2698-2705.
14. Jiménez-Jiménez FJ, Alonso-Navarro H, García-Martín E, et al. Neurochemical features of idiopathic restless legs syndrome. Sleep Med Rev. 2019;45:70-87.
15. Mick I, Ramos AC, Myers J, et al. Evidence for GABA-A receptor dysregulation in gambling disorder: correlation with impulsivity. Addict Biol. 2017;22(6):1601-1609.
16. Brambilla P, Perez J, Barale F, et al. Gabaergic dysfunction in mood disorders. Molecular Psychiatry. 2003;8:721-737.
17. Kaneez FS, Saeed SA. Investigating GABA and its function in platelets as compared to neurons. Platelets. 2009;20(5):328-333.
18. Paholpak P, Mendez MF. Trichotillomania as a manifestation of dementia. Case Rep Psychiatry. 2016;2016:9782702.
19. Miranda A, Peles S, Rudolph C, et al. Altered visceral sensation in response to somatic pain in the rat. Gastroenterology. 2004;126(4):1082-1089.
20. Skyba DA, King EW, Sluka KA. Effects of NMDA and non-NMDA ionotropic glutamate receptor antagonists on the development and maintenance of hyperalgesia induced by repeated intramuscular injection of acidic saline. Pain. 2002;98(1-2):69-78.
21. Holton KF, Taren DL, Thomson CA, et al. The effect of dietary glutamate on fibromyalgia and irritable bowel symptoms. Clin Exp Rheumatol. 2012;30(6 Suppl 74):10-70.
22. Sekiya Y, Nakagawa T, Ozawa T, et al. Facilitation of morphine withdrawal symptoms and morphine-induced conditioned place preference by a glutamate transporter inhibitor DL-threo-beta-benzyloxy aspartate in rats. Eur J Pharmacol. 2004;485(1-3):201-210.
23. Bestha D, Soliman L, Blankenship K. et al. The walking wounded: emerging treatments for PTSD. Curr Psychiatry Rep. 2018;20(10):94.
24. Tsuda M, Shimizu N, Suzuki T. Contribution of glutamate receptors to benzodiazepine withdrawal signs. Jpn J Pharmacol. 1999;81(1):1-6.
25. Spravato [package insert]. Janssen Pharmaceuticals, Inc; 2019.
26. Mattingly GW, Anderson RH. Intranasal ketamine. Current Psychiatry. 2019;18(5):31-38.
27. Buckingham SC, Campbell SL, Haas BR, et al. Glutamate release by primary brain tumors induces epileptic activity. Nat Med. 2011;17(10):1269-1275.
28. Ferrari A, Spaccapelo L, Pinetti D, et al. Effective prophylactic treatment of migraines lower plasma glutamate levels. Cephalalgia. 2009;29(4):423-429.
29. Vieira DS, Naffah-Mazzacoratti Mda G, Zukerman E, et al. Glutamate levels in cerebrospinal fluid and triptans overuse in chronic migraine. Headache. 2007;47(6):842-847.
30. Chan K, MaassenVanDenBrink A. Glutamate receptor antagonists in the management of migraine. Drugs. 2014;74:1165-1176.
31. Pappa S, Tsouli S, Apostolou G, et al. Effects of amantadine on tardive dyskinesia: a randomized, double-blind, placebo-controlled study. Clin Neuropharmacol. 2010;33(6):271-275.
32. Kraal AZ, Arvanitis NR, Jaeger AP, et al. Could dietary glutamate play a role in psychiatric distress? Neuro Psych. 2020;79:13-19.
33. Levite M. Glutamate receptor antibodies in neurological diseases: anti-AMPA-GluR3 antibodies, Anti-NMDA-NR1 antibodies, Anti-NMDA-NR2A/B antibodies, Anti-mGluR1 antibodies or Anti-mGluR5 antibodies are present in subpopulations of patients with either: epilepsy, encephalitis, cerebellar ataxia, systemic lupus erythematosus (SLE) and neuropsychiatric SLE, Sjogren’s syndrome, schizophrenia, mania or stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor’s expression, impair glutamate-induced signaling and function, activate blood brain barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and ataxia in animal models, and can be removed or silenced in some patients by immunotherapy. J Neural Transm (Vienna). 2014;121(8):1029-1075.
34. Lancaster E. CNS syndromes associated with antibodies against metabotropic receptors. Curr Opin Neurol. 2017;30:354-360.
35. Sillevis Smitt P, Kinoshita A, De Leeuw B, et al. Paraneoplastic cerebellar ataxia due to autoantibodies against a glutamate receptor. N Engl J Med. 2000;342(1):21-27.
36. Marignier R, Chenevier F, Rogemond V, et al. Metabotropic glutamate receptor type 1 autoantibody-associated cerebellitis: a primary autoimmune disease? Arch Neurol. 2010;67(5):627-630.
37. Lancaster E, Martinez-Hernandez E, Titulaer MJ, et al. Antibodies to metabotropic glutamate receptor 5 in the Ophelia syndrome. Neurology. 2011;77:1698-1701.
38. Mat A, Adler H, Merwick A, et al. Ophelia syndrome with metabotropic glutamate receptor 5 antibodies in CSF. Neurology. 2013;80(14):1349-1350.
1. Petroff OA. GABA and glutamate in the human brain. Neuroscientist. 2002;8(6):562-573.
2. Winkelman JW, Buxton OM, Jensen JE, et al. Reduced brain GABA in primary insomnia: preliminary data from 4T proton magnetic resonance spectroscopy (1H-MRS). Sleep. 2008;31(11):1499-1506.
3. Pereira AC, Mao X, Jiang CS, et al. Dorsolateral prefrontal cortex GABA deficit in older adults with sleep-disordered breathing. Proc Natl Acad Sci U S A. 2017;114(38):10250-10255.
4. Schür RR, Draisma LW, Wijnen JP, et al. Brain GABA levels across psychiatric disorders: a systematic literature review and meta-analysis of (1) H-MRS studies. Hum Brain Mapp. 2016;37(9):3337-3352.
5. Evoy KE, Morrison MD, Saklad SR. Abuse and misuse of pregabalin and gabapentin. Drugs. 2017;77(4):403-426.
6. Mersfelder TL, Nichols WH. Gabapentin: abuse, dependence, and withdrawal. Ann Pharmacother. 2016;50(3):229-233.
7. Bremner JD. Traumatic stress: effects on the brain. Dialogues Clin Neurosci. 2006;8(4):445-461.
8. Kelly JR, Kennedy PJ, Cryan JF, et al. Breaking down the barriers: the gut microbiome, intestinal permeability, and stress-related psychiatric disorders. Front Cell Neurosci. 2015;9:392.
9. Guyton AC, Hall JE. Guyton and Hall Textbook of Medical Physiology. 12th ed. Elsevier; 2011:550-551,692-693.
10. Evrensel A, Ceylan ME. The gut-brain axis: the missing link in depression. Clin Psychopharmacol Neurosci. 2015;13(3):239-244.
11. Vianello M, Tavolato B, Giometto B. Glutamic acid decarboxylase autoantibodies and neurological disorders. Neurol Sci. 2002;23(4):145-151.
12. Marin O. Interneuron dysfunction in psychiatric disorders. Nat Rev Neurosci. 2012;13(2):107-120.
13. Huang D, Liu D, Yin J, et al. Glutamate-glutamine and GABA in the brain of normal aged and patients with cognitive impairment. Eur Radiol. 2017;27(7):2698-2705.
14. Jiménez-Jiménez FJ, Alonso-Navarro H, García-Martín E, et al. Neurochemical features of idiopathic restless legs syndrome. Sleep Med Rev. 2019;45:70-87.
15. Mick I, Ramos AC, Myers J, et al. Evidence for GABA-A receptor dysregulation in gambling disorder: correlation with impulsivity. Addict Biol. 2017;22(6):1601-1609.
16. Brambilla P, Perez J, Barale F, et al. Gabaergic dysfunction in mood disorders. Molecular Psychiatry. 2003;8:721-737.
17. Kaneez FS, Saeed SA. Investigating GABA and its function in platelets as compared to neurons. Platelets. 2009;20(5):328-333.
18. Paholpak P, Mendez MF. Trichotillomania as a manifestation of dementia. Case Rep Psychiatry. 2016;2016:9782702.
19. Miranda A, Peles S, Rudolph C, et al. Altered visceral sensation in response to somatic pain in the rat. Gastroenterology. 2004;126(4):1082-1089.
20. Skyba DA, King EW, Sluka KA. Effects of NMDA and non-NMDA ionotropic glutamate receptor antagonists on the development and maintenance of hyperalgesia induced by repeated intramuscular injection of acidic saline. Pain. 2002;98(1-2):69-78.
21. Holton KF, Taren DL, Thomson CA, et al. The effect of dietary glutamate on fibromyalgia and irritable bowel symptoms. Clin Exp Rheumatol. 2012;30(6 Suppl 74):10-70.
22. Sekiya Y, Nakagawa T, Ozawa T, et al. Facilitation of morphine withdrawal symptoms and morphine-induced conditioned place preference by a glutamate transporter inhibitor DL-threo-beta-benzyloxy aspartate in rats. Eur J Pharmacol. 2004;485(1-3):201-210.
23. Bestha D, Soliman L, Blankenship K. et al. The walking wounded: emerging treatments for PTSD. Curr Psychiatry Rep. 2018;20(10):94.
24. Tsuda M, Shimizu N, Suzuki T. Contribution of glutamate receptors to benzodiazepine withdrawal signs. Jpn J Pharmacol. 1999;81(1):1-6.
25. Spravato [package insert]. Janssen Pharmaceuticals, Inc; 2019.
26. Mattingly GW, Anderson RH. Intranasal ketamine. Current Psychiatry. 2019;18(5):31-38.
27. Buckingham SC, Campbell SL, Haas BR, et al. Glutamate release by primary brain tumors induces epileptic activity. Nat Med. 2011;17(10):1269-1275.
28. Ferrari A, Spaccapelo L, Pinetti D, et al. Effective prophylactic treatment of migraines lower plasma glutamate levels. Cephalalgia. 2009;29(4):423-429.
29. Vieira DS, Naffah-Mazzacoratti Mda G, Zukerman E, et al. Glutamate levels in cerebrospinal fluid and triptans overuse in chronic migraine. Headache. 2007;47(6):842-847.
30. Chan K, MaassenVanDenBrink A. Glutamate receptor antagonists in the management of migraine. Drugs. 2014;74:1165-1176.
31. Pappa S, Tsouli S, Apostolou G, et al. Effects of amantadine on tardive dyskinesia: a randomized, double-blind, placebo-controlled study. Clin Neuropharmacol. 2010;33(6):271-275.
32. Kraal AZ, Arvanitis NR, Jaeger AP, et al. Could dietary glutamate play a role in psychiatric distress? Neuro Psych. 2020;79:13-19.
33. Levite M. Glutamate receptor antibodies in neurological diseases: anti-AMPA-GluR3 antibodies, Anti-NMDA-NR1 antibodies, Anti-NMDA-NR2A/B antibodies, Anti-mGluR1 antibodies or Anti-mGluR5 antibodies are present in subpopulations of patients with either: epilepsy, encephalitis, cerebellar ataxia, systemic lupus erythematosus (SLE) and neuropsychiatric SLE, Sjogren’s syndrome, schizophrenia, mania or stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor’s expression, impair glutamate-induced signaling and function, activate blood brain barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and ataxia in animal models, and can be removed or silenced in some patients by immunotherapy. J Neural Transm (Vienna). 2014;121(8):1029-1075.
34. Lancaster E. CNS syndromes associated with antibodies against metabotropic receptors. Curr Opin Neurol. 2017;30:354-360.
35. Sillevis Smitt P, Kinoshita A, De Leeuw B, et al. Paraneoplastic cerebellar ataxia due to autoantibodies against a glutamate receptor. N Engl J Med. 2000;342(1):21-27.
36. Marignier R, Chenevier F, Rogemond V, et al. Metabotropic glutamate receptor type 1 autoantibody-associated cerebellitis: a primary autoimmune disease? Arch Neurol. 2010;67(5):627-630.
37. Lancaster E, Martinez-Hernandez E, Titulaer MJ, et al. Antibodies to metabotropic glutamate receptor 5 in the Ophelia syndrome. Neurology. 2011;77:1698-1701.
38. Mat A, Adler H, Merwick A, et al. Ophelia syndrome with metabotropic glutamate receptor 5 antibodies in CSF. Neurology. 2013;80(14):1349-1350.
3 steps to bend the curve of schizophrenia
Schizophrenia is arguably the most serious psychiatric brain syndrome. It disables teens and young adults and robs them of their potential and life dreams. It is widely regarded as a hopeless illness.
But it does not have to be. The reason most patients with schizophrenia do not return to their baseline is because obsolete clinical management approaches, a carryover from the last century, continue to be used.
Approximately 20 years ago, psychiatric researchers made a major discovery: psychosis is a neurotoxic state, and each psychotic episode is associated with significant brain damage in both gray and white matter.1 Based on that discovery, a more rational management of schizophrenia has emerged, focused on protecting patients from experiencing psychotic recurrence after the first-episode psychosis (FEP). In the past century, this strategy did not exist because psychiatrists were in a state of scientific ignorance, completely unaware that the malignant component of schizophrenia that leads to disability is psychotic relapses, the primary cause of which is very poor medication adherence after hospital discharge following the FEP.
Based on the emerging scientific evidence, here are 3 essential principles to halt the deterioration and bend the curve of outcomes in schizophrenia:
1. Minimize the duration of untreated psychosis (DUP)
Numerous studies have shown that the longer the DUP, the worse the outcome in schizophrenia.2,3 It is therefore vital to shorten the DUP spanning the emergence of psychotic symptoms at home, prior to the first hospital admission.4 The DUP is often prolonged from weeks to months by a combination of anosognosia by the patient, who fails to recognize how pathological their hallucinations and delusions are, plus the stigma of mental illness, which leads parents to delay bringing their son or daughter for psychiatric evaluation and treatment.
Another reason for a prolonged DUP is the legal system’s governing of the initiation of antipsychotic medications for an acutely psychotic patient who does not believe he/she is sick, and who adamantly refuses to receive medications. Laws passed decades ago have not kept up with scientific advances about brain damage during the DUP. Instead of delegating the rapid administration of an antipsychotic medication to the psychiatric physician who evaluated and diagnosed a patient with acute psychosis, the legal system further prolongs the DUP by requiring the psychiatrist to go to court and have a judge order the administration of antipsychotic medications. Such a legal requirement that delays urgently needed treatment has never been imposed on neurologists when administering medication to an obtunded stroke patient. Yet psychosis damages brain tissue and must be treated as urgently as stroke.5
Perhaps the most common reason for a long DUP is the recurrent relapses of psychosis, almost always caused by the high nonadherence rate among patients with schizophrenia due to multiple factors related to the illness itself.6 Ensuring uninterrupted delivery of an antipsychotic to a patient’s brain is as important to maintaining remission in schizophrenia as uninterrupted insulin treatment is for an individual with diabetes. The only way to guarantee ongoing daily pharmacotherapy in schizophrenia and avoid a longer DUP and more brain damage is to use long-acting injectable (LAI) formulations of antipsychotic medications, which are infrequently used despite making eminent sense to protect patients from the tragic consequences of psychotic relapse.7
Continue to: Start very early use of LAIs
2. Start very early use of LAIs
There is no doubt that switching from an oral to an LAI antipsychotic immediately after hospital discharge for the FEP is the single most important medical decision psychiatrists can make for patients with schizophrenia.8 This is because disability in schizophrenia begins after the second episode, not the first.9-11 Therefore, psychiatrists must behave like cardiologists,12 who strive to prevent a second destructive myocardial infarction. Regrettably, 99.9% of psychiatric practitioners never start an LAI after the FEP, and usually wait until the patient experiences multiple relapses, after extensive gray matter atrophy and white matter disintegration have occurred due to the neuroinflammation and oxidative stress (free radicals) that occur with every psychotic episode.13,14 This clearly does not make clinical sense, but remains the standard current practice.
In oncology, chemotherapy is far more effective in Stage 1 cancer, immediately after the diagnosis is made, rather than in Stage 4, when the prognosis is very poor. Similarly, LAIs are best used in Stage 1 schizophrenia, which is the first episode (schizophrenia researchers now regard the illness as having stages).15 Unfortunately, it is now rare for patients with schizophrenia to be switched to LAI pharmacotherapy right after recovery from the FEP. Instead, LAIs are more commonly used in Stage 3 or Stage 4, when the brains of patients with chronic schizophrenia have been already structurally damaged, and functional disability had set in. Bending the cure of outcome in schizophrenia is only possible when LAIs are used very early to prevent the second episode.
The prevention of relapse by using LAIs in FEP is truly remarkable. Subotnik et al16 reported that only 5% of FEP patients who received an LAI antipsychotic relapsed, compared to 33% of those who received an oral formulation of the same antipsychotic (a 650% difference). It is frankly inexplicable why psychiatrists do not exploit the relapse-preventing properties of LAIs at the time of discharge after the FEP, and instead continue to perpetuate the use of prescribing oral tablets to patients who are incapable of full adherence and doomed to “self-destruct.” This was the practice model in the previous century, when there was total ignorance about the brain-damaging effects of psychosis, and no sense of urgency about preventing psychotic relapses and DUP. Psychiatrists regarded LAIs as a last resort instead of a life-saving first resort.
In addition to relapse prevention,17 the benefits of second-generation LAIs include neuroprotection18 and lower all-cause mortality,19 a remarkable triad of benefits for patients with schizophrenia.20
3. Implement comprehensive psychosocial treatment
Most patients with schizophrenia do not have access to the array of psychosocial treatments that have been shown to be vital for rehabilitation following the FEP, just as physical rehabilitation is indispensable after the first stroke. Studies such as RAISE,21 which was funded by the National Institute of Mental Health, have demonstrated the value of psychosocial therapies (Table21-23). Collaborative care with primary care physicians is also essential due to the high prevalence of metabolic disorders (obesity, diabetics, dyslipidemia, hypertension), which tend to be undertreated in patients with schizophrenia.24
Finally, when patients continue to experience delusions and hallucinations despite full adherence (with LAIs), clozapine must be used. Like LAIs, clozapine is woefully underutilized25 despite having been shown to restore mental health and full recovery to many (but not all) patients written off as hopeless due to persistent and refractory psychotic symptoms.26
If clinicians who treat schizophrenia implement these 3 steps in their FEP patients, they will be gratified to witness a more benign trajectory of schizophrenia, which I have personally seen. The curve can indeed be bent in favor of better outcomes. By using the 3 evidence-based steps described here, clinicians will realize that schizophrenia does not have to carry the label of “the worst disease affecting mankind,” as an editorial in a top-tier journal pessimistically stated over 3 decades ago.27
1. Cahn W, Hulshoff Pol HE, Lems EB, et al. Brain volume changes in first-episode schizophrenia: a 1-year follow-up study. Arch Gen Psychiatry. 2002;59(11):1002-1010.
2. Howes OD, Whitehurst T, Shatalina E, et al. The clinical significance of duration of untreated psychosis: an umbrella review and random-effects meta-analysis. World Psychiatry. 2021;20(1):75-95.
3. Oliver D, Davies C, Crossland G, et al. Can we reduce the duration of untreated psychosis? A systematic review and meta-analysis of controlled interventional studies. Schizophr Bull. 2018;44(6):1362-1372.
4. Srihari VH, Ferrara M, Li F, et al. Reducing the duration of untreated psychosis (DUP) in a US community: a quasi-experimental trial. Schizophr Bull Open. 2022;3(1):sgab057. doi:10.1093/schizbullopen/sgab057
5. Nasrallah HA, Roque A. FAST and RAPID: acronyms to prevent brain damage in stroke and psychosis. Current Psychiatry. 2018;17(8):6-8.
6. Lieslehto J, Tiihonen J, Lähteenvuo M, et al. Primary nonadherence to antipsychotic treatment among persons with schizophrenia. Schizophr Bull. 2022;48(3):665-663.
7. Nasrallah HA. 10 devastating consequences of psychotic relapses. Current Psychiatry. 2021;20(5):9-12.
8. Emsley R, Oosthuizen P, Koen L, et al. Remission in patients with first-episode schizophrenia receiving assured antipsychotic medication: a study with risperidone long-acting injection. Int Clin Psychopharmacol. 2008;23(6):325-331.
9. Alvarez-Jiménez M, Parker AG, Hetrick SE, et al. Preventing the second episode: a systematic review and meta-analysis of psychosocial and pharmacological trials in first-episode psychosis. Schizophr Bull. 2011;37(3):619-630.
10. Taipale H, Tanskanen A, Correll CU, et al. Real-world effectiveness of antipsychotic doses for relapse prevention in patients with first-episode schizophrenia in Finland: a nationwide, register-based cohort study. Lancet Psychiatry. 2022;9(4):271-279.
11. Gardner KN, Nasrallah HA. Managing first-episode psychosis: rationale and evidence for nonstandard first-line treatments for schizophrenia. Current Psychiatry. 2015;14(7):38-45,e3.
12. Nasrallah HA. For first-episode psychosis, psychiatrists should behave like cardiologists. Current Psychiatry. 2017;16(8):4-7.
13. Feigenson KA, Kusnecov AW, Silverstein SM. Inflammation and the two-hit hypothesis of schizophrenia. Neurosci Biobehav Rev. 2014;38:72-93.
14. Flatow J, Buckley P, Miller BJ. Meta-analysis of oxidative stress in schizophrenia. Biol Psychiatry. 2013;74(6):400-409.
15. Lavoie S, Polari AR, Goldstone S, et al. Staging model in psychiatry: review of the evolution of electroencephalography abnormalities in major psychiatric disorders. Early Interv Psychiatry. 2019;13(6):1319-1328.
16. Subotnik KL, Casaus LR, Ventura J, et al. Long-acting injectable risperidone for relapse prevention and control of breakthrough symptoms after a recent first episode of schizophrenia. A randomized clinical trial. JAMA Psychiatry. 2015;72(8):822-829.
17. Lin YH, Wu CS, Liu CC, et al. Comparative effectiveness of antipsychotics in preventing readmission for first-admission schizophrenia patients in national cohorts from 2001 to 2017 in Taiwan. Schizophr Bull. 2022;sbac046. doi:10.1093/schbul/sbac046
18. Chen AT, Nasrallah HA. Neuroprotective effects of the second generation antipsychotics. Schizophr Res. 2019;208:1-7.
19. Taipale H, Mittendorfer-Rutz E, Alexanderson K, et al. Antipsychotics and mortality in a nationwide cohort of 29,823 patients with schizophrenia. Schizophr Res. 2018;197:274-280.
20. Nasrallah HA. Triple advantages of injectable long acting second generation antipsychotics: relapse prevention, neuroprotection, and lower mortality. Schizophr Res. 2018;197:69-70.
21. Kane JM, Robinson DG, Schooler NR, et al. Comprehensive versus usual community care for first-episode psychosis: 2-year outcomes from the NIMH RAISE Early Treatment Program. Am J Psychiatry. 2016;173(4):362-372.
22. Keshavan MS, Ongur D, Srihari VH. Toward an expanded and personalized approach to coordinated specialty care in early course psychoses. Schizophr Res. 2022;241:119-121.
23. Srihari VH, Keshavan MS. Early intervention services for schizophrenia: looking back and looking ahead. Schizophr Bull. 2022;48(3):544-550.
24. Nasrallah HA, Meyer JM, Goff DC, et al. Low rates of treatment for hypertension, dyslipidemia and diabetes in schizophrenia: data from the CATIE schizophrenia trial sample at baseline. Schizophr Res. 2006;86(1-3):15-22.
25. Nasrallah HA. Clozapine is a vastly underutilized, unique agent with multiple applications. Current Psychiatry. 2014;13(10):21,24-25.
26. CureSZ Foundation. Clozapine success stories. Accessed June 1, 2022. https://curesz.org/clozapine-success-stories/
27. Where next with psychiatric illness? Nature. 1988;336(6195):95-96.
Schizophrenia is arguably the most serious psychiatric brain syndrome. It disables teens and young adults and robs them of their potential and life dreams. It is widely regarded as a hopeless illness.
But it does not have to be. The reason most patients with schizophrenia do not return to their baseline is because obsolete clinical management approaches, a carryover from the last century, continue to be used.
Approximately 20 years ago, psychiatric researchers made a major discovery: psychosis is a neurotoxic state, and each psychotic episode is associated with significant brain damage in both gray and white matter.1 Based on that discovery, a more rational management of schizophrenia has emerged, focused on protecting patients from experiencing psychotic recurrence after the first-episode psychosis (FEP). In the past century, this strategy did not exist because psychiatrists were in a state of scientific ignorance, completely unaware that the malignant component of schizophrenia that leads to disability is psychotic relapses, the primary cause of which is very poor medication adherence after hospital discharge following the FEP.
Based on the emerging scientific evidence, here are 3 essential principles to halt the deterioration and bend the curve of outcomes in schizophrenia:
1. Minimize the duration of untreated psychosis (DUP)
Numerous studies have shown that the longer the DUP, the worse the outcome in schizophrenia.2,3 It is therefore vital to shorten the DUP spanning the emergence of psychotic symptoms at home, prior to the first hospital admission.4 The DUP is often prolonged from weeks to months by a combination of anosognosia by the patient, who fails to recognize how pathological their hallucinations and delusions are, plus the stigma of mental illness, which leads parents to delay bringing their son or daughter for psychiatric evaluation and treatment.
Another reason for a prolonged DUP is the legal system’s governing of the initiation of antipsychotic medications for an acutely psychotic patient who does not believe he/she is sick, and who adamantly refuses to receive medications. Laws passed decades ago have not kept up with scientific advances about brain damage during the DUP. Instead of delegating the rapid administration of an antipsychotic medication to the psychiatric physician who evaluated and diagnosed a patient with acute psychosis, the legal system further prolongs the DUP by requiring the psychiatrist to go to court and have a judge order the administration of antipsychotic medications. Such a legal requirement that delays urgently needed treatment has never been imposed on neurologists when administering medication to an obtunded stroke patient. Yet psychosis damages brain tissue and must be treated as urgently as stroke.5
Perhaps the most common reason for a long DUP is the recurrent relapses of psychosis, almost always caused by the high nonadherence rate among patients with schizophrenia due to multiple factors related to the illness itself.6 Ensuring uninterrupted delivery of an antipsychotic to a patient’s brain is as important to maintaining remission in schizophrenia as uninterrupted insulin treatment is for an individual with diabetes. The only way to guarantee ongoing daily pharmacotherapy in schizophrenia and avoid a longer DUP and more brain damage is to use long-acting injectable (LAI) formulations of antipsychotic medications, which are infrequently used despite making eminent sense to protect patients from the tragic consequences of psychotic relapse.7
Continue to: Start very early use of LAIs
2. Start very early use of LAIs
There is no doubt that switching from an oral to an LAI antipsychotic immediately after hospital discharge for the FEP is the single most important medical decision psychiatrists can make for patients with schizophrenia.8 This is because disability in schizophrenia begins after the second episode, not the first.9-11 Therefore, psychiatrists must behave like cardiologists,12 who strive to prevent a second destructive myocardial infarction. Regrettably, 99.9% of psychiatric practitioners never start an LAI after the FEP, and usually wait until the patient experiences multiple relapses, after extensive gray matter atrophy and white matter disintegration have occurred due to the neuroinflammation and oxidative stress (free radicals) that occur with every psychotic episode.13,14 This clearly does not make clinical sense, but remains the standard current practice.
In oncology, chemotherapy is far more effective in Stage 1 cancer, immediately after the diagnosis is made, rather than in Stage 4, when the prognosis is very poor. Similarly, LAIs are best used in Stage 1 schizophrenia, which is the first episode (schizophrenia researchers now regard the illness as having stages).15 Unfortunately, it is now rare for patients with schizophrenia to be switched to LAI pharmacotherapy right after recovery from the FEP. Instead, LAIs are more commonly used in Stage 3 or Stage 4, when the brains of patients with chronic schizophrenia have been already structurally damaged, and functional disability had set in. Bending the cure of outcome in schizophrenia is only possible when LAIs are used very early to prevent the second episode.
The prevention of relapse by using LAIs in FEP is truly remarkable. Subotnik et al16 reported that only 5% of FEP patients who received an LAI antipsychotic relapsed, compared to 33% of those who received an oral formulation of the same antipsychotic (a 650% difference). It is frankly inexplicable why psychiatrists do not exploit the relapse-preventing properties of LAIs at the time of discharge after the FEP, and instead continue to perpetuate the use of prescribing oral tablets to patients who are incapable of full adherence and doomed to “self-destruct.” This was the practice model in the previous century, when there was total ignorance about the brain-damaging effects of psychosis, and no sense of urgency about preventing psychotic relapses and DUP. Psychiatrists regarded LAIs as a last resort instead of a life-saving first resort.
In addition to relapse prevention,17 the benefits of second-generation LAIs include neuroprotection18 and lower all-cause mortality,19 a remarkable triad of benefits for patients with schizophrenia.20
3. Implement comprehensive psychosocial treatment
Most patients with schizophrenia do not have access to the array of psychosocial treatments that have been shown to be vital for rehabilitation following the FEP, just as physical rehabilitation is indispensable after the first stroke. Studies such as RAISE,21 which was funded by the National Institute of Mental Health, have demonstrated the value of psychosocial therapies (Table21-23). Collaborative care with primary care physicians is also essential due to the high prevalence of metabolic disorders (obesity, diabetics, dyslipidemia, hypertension), which tend to be undertreated in patients with schizophrenia.24
Finally, when patients continue to experience delusions and hallucinations despite full adherence (with LAIs), clozapine must be used. Like LAIs, clozapine is woefully underutilized25 despite having been shown to restore mental health and full recovery to many (but not all) patients written off as hopeless due to persistent and refractory psychotic symptoms.26
If clinicians who treat schizophrenia implement these 3 steps in their FEP patients, they will be gratified to witness a more benign trajectory of schizophrenia, which I have personally seen. The curve can indeed be bent in favor of better outcomes. By using the 3 evidence-based steps described here, clinicians will realize that schizophrenia does not have to carry the label of “the worst disease affecting mankind,” as an editorial in a top-tier journal pessimistically stated over 3 decades ago.27
Schizophrenia is arguably the most serious psychiatric brain syndrome. It disables teens and young adults and robs them of their potential and life dreams. It is widely regarded as a hopeless illness.
But it does not have to be. The reason most patients with schizophrenia do not return to their baseline is because obsolete clinical management approaches, a carryover from the last century, continue to be used.
Approximately 20 years ago, psychiatric researchers made a major discovery: psychosis is a neurotoxic state, and each psychotic episode is associated with significant brain damage in both gray and white matter.1 Based on that discovery, a more rational management of schizophrenia has emerged, focused on protecting patients from experiencing psychotic recurrence after the first-episode psychosis (FEP). In the past century, this strategy did not exist because psychiatrists were in a state of scientific ignorance, completely unaware that the malignant component of schizophrenia that leads to disability is psychotic relapses, the primary cause of which is very poor medication adherence after hospital discharge following the FEP.
Based on the emerging scientific evidence, here are 3 essential principles to halt the deterioration and bend the curve of outcomes in schizophrenia:
1. Minimize the duration of untreated psychosis (DUP)
Numerous studies have shown that the longer the DUP, the worse the outcome in schizophrenia.2,3 It is therefore vital to shorten the DUP spanning the emergence of psychotic symptoms at home, prior to the first hospital admission.4 The DUP is often prolonged from weeks to months by a combination of anosognosia by the patient, who fails to recognize how pathological their hallucinations and delusions are, plus the stigma of mental illness, which leads parents to delay bringing their son or daughter for psychiatric evaluation and treatment.
Another reason for a prolonged DUP is the legal system’s governing of the initiation of antipsychotic medications for an acutely psychotic patient who does not believe he/she is sick, and who adamantly refuses to receive medications. Laws passed decades ago have not kept up with scientific advances about brain damage during the DUP. Instead of delegating the rapid administration of an antipsychotic medication to the psychiatric physician who evaluated and diagnosed a patient with acute psychosis, the legal system further prolongs the DUP by requiring the psychiatrist to go to court and have a judge order the administration of antipsychotic medications. Such a legal requirement that delays urgently needed treatment has never been imposed on neurologists when administering medication to an obtunded stroke patient. Yet psychosis damages brain tissue and must be treated as urgently as stroke.5
Perhaps the most common reason for a long DUP is the recurrent relapses of psychosis, almost always caused by the high nonadherence rate among patients with schizophrenia due to multiple factors related to the illness itself.6 Ensuring uninterrupted delivery of an antipsychotic to a patient’s brain is as important to maintaining remission in schizophrenia as uninterrupted insulin treatment is for an individual with diabetes. The only way to guarantee ongoing daily pharmacotherapy in schizophrenia and avoid a longer DUP and more brain damage is to use long-acting injectable (LAI) formulations of antipsychotic medications, which are infrequently used despite making eminent sense to protect patients from the tragic consequences of psychotic relapse.7
Continue to: Start very early use of LAIs
2. Start very early use of LAIs
There is no doubt that switching from an oral to an LAI antipsychotic immediately after hospital discharge for the FEP is the single most important medical decision psychiatrists can make for patients with schizophrenia.8 This is because disability in schizophrenia begins after the second episode, not the first.9-11 Therefore, psychiatrists must behave like cardiologists,12 who strive to prevent a second destructive myocardial infarction. Regrettably, 99.9% of psychiatric practitioners never start an LAI after the FEP, and usually wait until the patient experiences multiple relapses, after extensive gray matter atrophy and white matter disintegration have occurred due to the neuroinflammation and oxidative stress (free radicals) that occur with every psychotic episode.13,14 This clearly does not make clinical sense, but remains the standard current practice.
In oncology, chemotherapy is far more effective in Stage 1 cancer, immediately after the diagnosis is made, rather than in Stage 4, when the prognosis is very poor. Similarly, LAIs are best used in Stage 1 schizophrenia, which is the first episode (schizophrenia researchers now regard the illness as having stages).15 Unfortunately, it is now rare for patients with schizophrenia to be switched to LAI pharmacotherapy right after recovery from the FEP. Instead, LAIs are more commonly used in Stage 3 or Stage 4, when the brains of patients with chronic schizophrenia have been already structurally damaged, and functional disability had set in. Bending the cure of outcome in schizophrenia is only possible when LAIs are used very early to prevent the second episode.
The prevention of relapse by using LAIs in FEP is truly remarkable. Subotnik et al16 reported that only 5% of FEP patients who received an LAI antipsychotic relapsed, compared to 33% of those who received an oral formulation of the same antipsychotic (a 650% difference). It is frankly inexplicable why psychiatrists do not exploit the relapse-preventing properties of LAIs at the time of discharge after the FEP, and instead continue to perpetuate the use of prescribing oral tablets to patients who are incapable of full adherence and doomed to “self-destruct.” This was the practice model in the previous century, when there was total ignorance about the brain-damaging effects of psychosis, and no sense of urgency about preventing psychotic relapses and DUP. Psychiatrists regarded LAIs as a last resort instead of a life-saving first resort.
In addition to relapse prevention,17 the benefits of second-generation LAIs include neuroprotection18 and lower all-cause mortality,19 a remarkable triad of benefits for patients with schizophrenia.20
3. Implement comprehensive psychosocial treatment
Most patients with schizophrenia do not have access to the array of psychosocial treatments that have been shown to be vital for rehabilitation following the FEP, just as physical rehabilitation is indispensable after the first stroke. Studies such as RAISE,21 which was funded by the National Institute of Mental Health, have demonstrated the value of psychosocial therapies (Table21-23). Collaborative care with primary care physicians is also essential due to the high prevalence of metabolic disorders (obesity, diabetics, dyslipidemia, hypertension), which tend to be undertreated in patients with schizophrenia.24
Finally, when patients continue to experience delusions and hallucinations despite full adherence (with LAIs), clozapine must be used. Like LAIs, clozapine is woefully underutilized25 despite having been shown to restore mental health and full recovery to many (but not all) patients written off as hopeless due to persistent and refractory psychotic symptoms.26
If clinicians who treat schizophrenia implement these 3 steps in their FEP patients, they will be gratified to witness a more benign trajectory of schizophrenia, which I have personally seen. The curve can indeed be bent in favor of better outcomes. By using the 3 evidence-based steps described here, clinicians will realize that schizophrenia does not have to carry the label of “the worst disease affecting mankind,” as an editorial in a top-tier journal pessimistically stated over 3 decades ago.27
1. Cahn W, Hulshoff Pol HE, Lems EB, et al. Brain volume changes in first-episode schizophrenia: a 1-year follow-up study. Arch Gen Psychiatry. 2002;59(11):1002-1010.
2. Howes OD, Whitehurst T, Shatalina E, et al. The clinical significance of duration of untreated psychosis: an umbrella review and random-effects meta-analysis. World Psychiatry. 2021;20(1):75-95.
3. Oliver D, Davies C, Crossland G, et al. Can we reduce the duration of untreated psychosis? A systematic review and meta-analysis of controlled interventional studies. Schizophr Bull. 2018;44(6):1362-1372.
4. Srihari VH, Ferrara M, Li F, et al. Reducing the duration of untreated psychosis (DUP) in a US community: a quasi-experimental trial. Schizophr Bull Open. 2022;3(1):sgab057. doi:10.1093/schizbullopen/sgab057
5. Nasrallah HA, Roque A. FAST and RAPID: acronyms to prevent brain damage in stroke and psychosis. Current Psychiatry. 2018;17(8):6-8.
6. Lieslehto J, Tiihonen J, Lähteenvuo M, et al. Primary nonadherence to antipsychotic treatment among persons with schizophrenia. Schizophr Bull. 2022;48(3):665-663.
7. Nasrallah HA. 10 devastating consequences of psychotic relapses. Current Psychiatry. 2021;20(5):9-12.
8. Emsley R, Oosthuizen P, Koen L, et al. Remission in patients with first-episode schizophrenia receiving assured antipsychotic medication: a study with risperidone long-acting injection. Int Clin Psychopharmacol. 2008;23(6):325-331.
9. Alvarez-Jiménez M, Parker AG, Hetrick SE, et al. Preventing the second episode: a systematic review and meta-analysis of psychosocial and pharmacological trials in first-episode psychosis. Schizophr Bull. 2011;37(3):619-630.
10. Taipale H, Tanskanen A, Correll CU, et al. Real-world effectiveness of antipsychotic doses for relapse prevention in patients with first-episode schizophrenia in Finland: a nationwide, register-based cohort study. Lancet Psychiatry. 2022;9(4):271-279.
11. Gardner KN, Nasrallah HA. Managing first-episode psychosis: rationale and evidence for nonstandard first-line treatments for schizophrenia. Current Psychiatry. 2015;14(7):38-45,e3.
12. Nasrallah HA. For first-episode psychosis, psychiatrists should behave like cardiologists. Current Psychiatry. 2017;16(8):4-7.
13. Feigenson KA, Kusnecov AW, Silverstein SM. Inflammation and the two-hit hypothesis of schizophrenia. Neurosci Biobehav Rev. 2014;38:72-93.
14. Flatow J, Buckley P, Miller BJ. Meta-analysis of oxidative stress in schizophrenia. Biol Psychiatry. 2013;74(6):400-409.
15. Lavoie S, Polari AR, Goldstone S, et al. Staging model in psychiatry: review of the evolution of electroencephalography abnormalities in major psychiatric disorders. Early Interv Psychiatry. 2019;13(6):1319-1328.
16. Subotnik KL, Casaus LR, Ventura J, et al. Long-acting injectable risperidone for relapse prevention and control of breakthrough symptoms after a recent first episode of schizophrenia. A randomized clinical trial. JAMA Psychiatry. 2015;72(8):822-829.
17. Lin YH, Wu CS, Liu CC, et al. Comparative effectiveness of antipsychotics in preventing readmission for first-admission schizophrenia patients in national cohorts from 2001 to 2017 in Taiwan. Schizophr Bull. 2022;sbac046. doi:10.1093/schbul/sbac046
18. Chen AT, Nasrallah HA. Neuroprotective effects of the second generation antipsychotics. Schizophr Res. 2019;208:1-7.
19. Taipale H, Mittendorfer-Rutz E, Alexanderson K, et al. Antipsychotics and mortality in a nationwide cohort of 29,823 patients with schizophrenia. Schizophr Res. 2018;197:274-280.
20. Nasrallah HA. Triple advantages of injectable long acting second generation antipsychotics: relapse prevention, neuroprotection, and lower mortality. Schizophr Res. 2018;197:69-70.
21. Kane JM, Robinson DG, Schooler NR, et al. Comprehensive versus usual community care for first-episode psychosis: 2-year outcomes from the NIMH RAISE Early Treatment Program. Am J Psychiatry. 2016;173(4):362-372.
22. Keshavan MS, Ongur D, Srihari VH. Toward an expanded and personalized approach to coordinated specialty care in early course psychoses. Schizophr Res. 2022;241:119-121.
23. Srihari VH, Keshavan MS. Early intervention services for schizophrenia: looking back and looking ahead. Schizophr Bull. 2022;48(3):544-550.
24. Nasrallah HA, Meyer JM, Goff DC, et al. Low rates of treatment for hypertension, dyslipidemia and diabetes in schizophrenia: data from the CATIE schizophrenia trial sample at baseline. Schizophr Res. 2006;86(1-3):15-22.
25. Nasrallah HA. Clozapine is a vastly underutilized, unique agent with multiple applications. Current Psychiatry. 2014;13(10):21,24-25.
26. CureSZ Foundation. Clozapine success stories. Accessed June 1, 2022. https://curesz.org/clozapine-success-stories/
27. Where next with psychiatric illness? Nature. 1988;336(6195):95-96.
1. Cahn W, Hulshoff Pol HE, Lems EB, et al. Brain volume changes in first-episode schizophrenia: a 1-year follow-up study. Arch Gen Psychiatry. 2002;59(11):1002-1010.
2. Howes OD, Whitehurst T, Shatalina E, et al. The clinical significance of duration of untreated psychosis: an umbrella review and random-effects meta-analysis. World Psychiatry. 2021;20(1):75-95.
3. Oliver D, Davies C, Crossland G, et al. Can we reduce the duration of untreated psychosis? A systematic review and meta-analysis of controlled interventional studies. Schizophr Bull. 2018;44(6):1362-1372.
4. Srihari VH, Ferrara M, Li F, et al. Reducing the duration of untreated psychosis (DUP) in a US community: a quasi-experimental trial. Schizophr Bull Open. 2022;3(1):sgab057. doi:10.1093/schizbullopen/sgab057
5. Nasrallah HA, Roque A. FAST and RAPID: acronyms to prevent brain damage in stroke and psychosis. Current Psychiatry. 2018;17(8):6-8.
6. Lieslehto J, Tiihonen J, Lähteenvuo M, et al. Primary nonadherence to antipsychotic treatment among persons with schizophrenia. Schizophr Bull. 2022;48(3):665-663.
7. Nasrallah HA. 10 devastating consequences of psychotic relapses. Current Psychiatry. 2021;20(5):9-12.
8. Emsley R, Oosthuizen P, Koen L, et al. Remission in patients with first-episode schizophrenia receiving assured antipsychotic medication: a study with risperidone long-acting injection. Int Clin Psychopharmacol. 2008;23(6):325-331.
9. Alvarez-Jiménez M, Parker AG, Hetrick SE, et al. Preventing the second episode: a systematic review and meta-analysis of psychosocial and pharmacological trials in first-episode psychosis. Schizophr Bull. 2011;37(3):619-630.
10. Taipale H, Tanskanen A, Correll CU, et al. Real-world effectiveness of antipsychotic doses for relapse prevention in patients with first-episode schizophrenia in Finland: a nationwide, register-based cohort study. Lancet Psychiatry. 2022;9(4):271-279.
11. Gardner KN, Nasrallah HA. Managing first-episode psychosis: rationale and evidence for nonstandard first-line treatments for schizophrenia. Current Psychiatry. 2015;14(7):38-45,e3.
12. Nasrallah HA. For first-episode psychosis, psychiatrists should behave like cardiologists. Current Psychiatry. 2017;16(8):4-7.
13. Feigenson KA, Kusnecov AW, Silverstein SM. Inflammation and the two-hit hypothesis of schizophrenia. Neurosci Biobehav Rev. 2014;38:72-93.
14. Flatow J, Buckley P, Miller BJ. Meta-analysis of oxidative stress in schizophrenia. Biol Psychiatry. 2013;74(6):400-409.
15. Lavoie S, Polari AR, Goldstone S, et al. Staging model in psychiatry: review of the evolution of electroencephalography abnormalities in major psychiatric disorders. Early Interv Psychiatry. 2019;13(6):1319-1328.
16. Subotnik KL, Casaus LR, Ventura J, et al. Long-acting injectable risperidone for relapse prevention and control of breakthrough symptoms after a recent first episode of schizophrenia. A randomized clinical trial. JAMA Psychiatry. 2015;72(8):822-829.
17. Lin YH, Wu CS, Liu CC, et al. Comparative effectiveness of antipsychotics in preventing readmission for first-admission schizophrenia patients in national cohorts from 2001 to 2017 in Taiwan. Schizophr Bull. 2022;sbac046. doi:10.1093/schbul/sbac046
18. Chen AT, Nasrallah HA. Neuroprotective effects of the second generation antipsychotics. Schizophr Res. 2019;208:1-7.
19. Taipale H, Mittendorfer-Rutz E, Alexanderson K, et al. Antipsychotics and mortality in a nationwide cohort of 29,823 patients with schizophrenia. Schizophr Res. 2018;197:274-280.
20. Nasrallah HA. Triple advantages of injectable long acting second generation antipsychotics: relapse prevention, neuroprotection, and lower mortality. Schizophr Res. 2018;197:69-70.
21. Kane JM, Robinson DG, Schooler NR, et al. Comprehensive versus usual community care for first-episode psychosis: 2-year outcomes from the NIMH RAISE Early Treatment Program. Am J Psychiatry. 2016;173(4):362-372.
22. Keshavan MS, Ongur D, Srihari VH. Toward an expanded and personalized approach to coordinated specialty care in early course psychoses. Schizophr Res. 2022;241:119-121.
23. Srihari VH, Keshavan MS. Early intervention services for schizophrenia: looking back and looking ahead. Schizophr Bull. 2022;48(3):544-550.
24. Nasrallah HA, Meyer JM, Goff DC, et al. Low rates of treatment for hypertension, dyslipidemia and diabetes in schizophrenia: data from the CATIE schizophrenia trial sample at baseline. Schizophr Res. 2006;86(1-3):15-22.
25. Nasrallah HA. Clozapine is a vastly underutilized, unique agent with multiple applications. Current Psychiatry. 2014;13(10):21,24-25.
26. CureSZ Foundation. Clozapine success stories. Accessed June 1, 2022. https://curesz.org/clozapine-success-stories/
27. Where next with psychiatric illness? Nature. 1988;336(6195):95-96.