Commentary

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

Whatever type of parenting a woman chooses, you can be sure that she, not the father, will be held accountable. 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 [email protected].

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

Whatever type of parenting a woman chooses, you can be sure that she, not the father, will be held accountable. 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 [email protected].

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

Whatever type of parenting a woman chooses, you can be sure that she, not the father, will be held accountable. 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 [email protected].

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 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.

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.

This week, we celebrate our nation’s birth in a national and individual display of our patriotic attachment to this country. To understand how that patriotic attachment arises, we need to step back and look at the ways in which our brains change and define how each of us develops a sense of Self — 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. To understand how that patriotic attachment arises, we need to step back and look at the ways in which our brains change and define how each of us develops a sense of Self — 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. To understand how that patriotic attachment arises, we need to step back and look at the ways in which our brains change and define how each of us develops a sense of Self — 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.

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 (Current Psychiatry, May 2022) looked into serotonin- and dopamine-associated symptoms. In Part 2 (Current Psychiatry, June 2022), we presented cases related to endorphin and norepinephrine dysfunction. We conclude the series by exploring gamma aminobutyric acid (GABA)- and glutamate-based clinical symptoms. Table 1 outlines medical and psychiatric symptoms that likely reflect GABA excess^1-9 and deficiency,^1-4,6,9-17 and Table 2 lists symptoms that likely reflect glutamate excess^9,18-31 and deficiency.^9,32-38 It is essential to note that both the quantity of neurotransmitters as well as the quality of the transmission (as in receptors, cellular pumps, and distribution mechanisms) are important.

GABA excess (Table 1^1-9)

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 vision^1,5,6,9 and problems with gait and balance,^5,6,9 as well as tremors.^1,4-7 She experienced enuresis well into adulthood^1,5,6,9 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 1^1-4,6,9-17)

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 high^1,9,11 and he feels stiff.^6,9 Mr. N’s pupils are narrow^1,9; he is hyper-reflexive^1,9,11 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 occasions^4,12,15 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 noise^1,9 and complains of palpitations^1,3,4,6,9 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 dysregulation^9,10 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

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 headache^28-30 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-D-aspartate receptor antagonists such as memantine and dextromethorphan and alpha-blockers (eg, clonidine and tizanidine) may be considered. Avoiding addictive substances would be prudent, though the use of ketamine seems rational. Anticonvulsants are recommended, along with sedating antidepressants. Serotonin-norepinephrine reuptake inhibitors may not be the best choice because norepinephrine potentiates glutamate function. Dopamine inhibits glutamate, so stimulants, bupropion, and amantadine³¹ may be paradoxically applied to treatment of both cognitive and physical symptoms (including pain) in a patient with glutamate hyperactivity.

Glutamate deficiency (Table 2^9,32-38)

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 outbursts^37,38 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 (Current Psychiatry, May 2022) looked into serotonin- and dopamine-associated symptoms. In Part 2 (Current Psychiatry, June 2022), we presented cases related to endorphin and norepinephrine dysfunction. We conclude the series by exploring gamma aminobutyric acid (GABA)- and glutamate-based clinical symptoms. Table 1 outlines medical and psychiatric symptoms that likely reflect GABA excess^1-9 and deficiency,^1-4,6,9-17 and Table 2 lists symptoms that likely reflect glutamate excess^9,18-31 and deficiency.^9,32-38 It is essential to note that both the quantity of neurotransmitters as well as the quality of the transmission (as in receptors, cellular pumps, and distribution mechanisms) are important.

GABA excess (Table 1^1-9)

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 vision^1,5,6,9 and problems with gait and balance,^5,6,9 as well as tremors.^1,4-7 She experienced enuresis well into adulthood^1,5,6,9 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 1^1-4,6,9-17)

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 high^1,9,11 and he feels stiff.^6,9 Mr. N’s pupils are narrow^1,9; he is hyper-reflexive^1,9,11 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 occasions^4,12,15 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 noise^1,9 and complains of palpitations^1,3,4,6,9 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 dysregulation^9,10 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

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 headache^28-30 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-D-aspartate receptor antagonists such as memantine and dextromethorphan and alpha-blockers (eg, clonidine and tizanidine) may be considered. Avoiding addictive substances would be prudent, though the use of ketamine seems rational. Anticonvulsants are recommended, along with sedating antidepressants. Serotonin-norepinephrine reuptake inhibitors may not be the best choice because norepinephrine potentiates glutamate function. Dopamine inhibits glutamate, so stimulants, bupropion, and amantadine³¹ may be paradoxically applied to treatment of both cognitive and physical symptoms (including pain) in a patient with glutamate hyperactivity.

Glutamate deficiency (Table 2^9,32-38)

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 outbursts^37,38 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 (Current Psychiatry, May 2022) looked into serotonin- and dopamine-associated symptoms. In Part 2 (Current Psychiatry, June 2022), we presented cases related to endorphin and norepinephrine dysfunction. We conclude the series by exploring gamma aminobutyric acid (GABA)- and glutamate-based clinical symptoms. Table 1 outlines medical and psychiatric symptoms that likely reflect GABA excess^1-9 and deficiency,^1-4,6,9-17 and Table 2 lists symptoms that likely reflect glutamate excess^9,18-31 and deficiency.^9,32-38 It is essential to note that both the quantity of neurotransmitters as well as the quality of the transmission (as in receptors, cellular pumps, and distribution mechanisms) are important.

GABA excess (Table 1^1-9)

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 vision^1,5,6,9 and problems with gait and balance,^5,6,9 as well as tremors.^1,4-7 She experienced enuresis well into adulthood^1,5,6,9 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 1^1-4,6,9-17)

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 high^1,9,11 and he feels stiff.^6,9 Mr. N’s pupils are narrow^1,9; he is hyper-reflexive^1,9,11 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 occasions^4,12,15 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 noise^1,9 and complains of palpitations^1,3,4,6,9 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 dysregulation^9,10 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

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 headache^28-30 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-D-aspartate receptor antagonists such as memantine and dextromethorphan and alpha-blockers (eg, clonidine and tizanidine) may be considered. Avoiding addictive substances would be prudent, though the use of ketamine seems rational. Anticonvulsants are recommended, along with sedating antidepressants. Serotonin-norepinephrine reuptake inhibitors may not be the best choice because norepinephrine potentiates glutamate function. Dopamine inhibits glutamate, so stimulants, bupropion, and amantadine³¹ may be paradoxically applied to treatment of both cognitive and physical symptoms (including pain) in a patient with glutamate hyperactivity.

Glutamate deficiency (Table 2^9,32-38)

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 outbursts^37,38 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

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 (Table^21-23). 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 (Table^21-23). 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 (Table^21-23). 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

In patients with attention-deficit/hyperactivity disorder (ADHD), stimulants reduce impulsivity and improve attention and focus. In individuals who do not have this disorder, stimulants are believed to enhance cognition, attention, and physical performance. In this article, I describe how a patient whose intermittent use of stimulants for motivation and cognitive enhancement shaped my approach to the diagnosis of ADHD.

Instant gratification and quick solutions

When I joined my psychiatry residency program, I expected to primarily treat patients who had depression, bipolar disorder, or psychosis. However, as I transitioned to my second year of residency, most patients I was assigned to had been diagnosed with ADHD. One of them was a 30-year-old in his fourth year of dental school. On his first visit, he requested a refill of dextroamphetamine and amphetamine 10 mg twice a day. He had been diagnosed with ADHD 5 years ago. He explained that he only needed this medication when preparing for his board examinations to motivate him and boost his focus and retention before studying. His study schedule included the exact doses and times he planned to take his stimulant.

I asked him questions to confirm the diagnosis, but he rushed to reassure me that he had already been diagnosed with ADHD and had been doing well on dextroamphetamine and amphetamine for many years. I was inclined to question his diagnosis of ADHD after learning of his “as-needed” use of stimulants as brain enhancers. His medical record reflecting the diagnosis of ADHD dated back to when he was a first-year dental student. The diagnosis was based on the patient’s report of procrastination for as long as he could remember. It also hinged on difficulties learning a second language and math being a challenging subject for him. Despite this, he managed to do well in school and earn an undergraduate degree, well enough to later pursue dentistry at a reputable university.

I thought, “Isn’t it normal to lose motivation and have doubts when preparing for a high-stakes exam like the boards? Aren’t these negative thoughts distracting enough to render sustained focus impossible? Doesn’t everyone struggle with procrastination, especially when they need to study? If learning a new language requires devotion, consistency, and sacrifice, isn’t it inherently challenging? Doesn’t good performance in math depend on multiple factors (ie, a strong foundation, cumulative learning, frequent practice), and thus leaves many students struggling?”

This interaction and many similar ones made me scrutinize the diagnosis of ADHD in patients I encounter in clinical settings. We live in a society where instant gratification is cherished, and quick fixes are pursued with little contemplation of pitfalls. Students use stimulants to cram for exams, high-functioning professionals use them to meet deadlines, and athletes use them to enhance performance and improve reaction times. Psychiatry seems to be drawn into the demands of society and may be fueling the “quick-fix” mentality by prescribing stimulants to healthy individuals who want to improve their focus, and then diagnosing them with ADHD to align the prescription with an appropriate diagnosis. Research on the adverse effects of stimulant use in adults is not convincing nor conclusive enough to sway prescribers from denying the average adult patient a stimulant to enhance cognitive function before a high-stakes exam or a critical, career-shaping project if they present with some ADHD traits, which the patient might even hyperbolize to secure the desired prescription. All of this may contribute to the perceived rising prevalence of ADHD among adults.

As for my 30-year-old dental student, I reasoned that continuing his medication, for now, would help me establish rapport and trust. This would allow me to counsel him on the long-term adverse effects of stimulants, and develop a plan to optimize his sleep, focus, and time management skills, eventually improving his cognition and attention naturally. Unfortunately, he did not show up to future appointments after I sent him the refill.

In patients with attention-deficit/hyperactivity disorder (ADHD), stimulants reduce impulsivity and improve attention and focus. In individuals who do not have this disorder, stimulants are believed to enhance cognition, attention, and physical performance. In this article, I describe how a patient whose intermittent use of stimulants for motivation and cognitive enhancement shaped my approach to the diagnosis of ADHD.

Instant gratification and quick solutions

When I joined my psychiatry residency program, I expected to primarily treat patients who had depression, bipolar disorder, or psychosis. However, as I transitioned to my second year of residency, most patients I was assigned to had been diagnosed with ADHD. One of them was a 30-year-old in his fourth year of dental school. On his first visit, he requested a refill of dextroamphetamine and amphetamine 10 mg twice a day. He had been diagnosed with ADHD 5 years ago. He explained that he only needed this medication when preparing for his board examinations to motivate him and boost his focus and retention before studying. His study schedule included the exact doses and times he planned to take his stimulant.

I asked him questions to confirm the diagnosis, but he rushed to reassure me that he had already been diagnosed with ADHD and had been doing well on dextroamphetamine and amphetamine for many years. I was inclined to question his diagnosis of ADHD after learning of his “as-needed” use of stimulants as brain enhancers. His medical record reflecting the diagnosis of ADHD dated back to when he was a first-year dental student. The diagnosis was based on the patient’s report of procrastination for as long as he could remember. It also hinged on difficulties learning a second language and math being a challenging subject for him. Despite this, he managed to do well in school and earn an undergraduate degree, well enough to later pursue dentistry at a reputable university.

I thought, “Isn’t it normal to lose motivation and have doubts when preparing for a high-stakes exam like the boards? Aren’t these negative thoughts distracting enough to render sustained focus impossible? Doesn’t everyone struggle with procrastination, especially when they need to study? If learning a new language requires devotion, consistency, and sacrifice, isn’t it inherently challenging? Doesn’t good performance in math depend on multiple factors (ie, a strong foundation, cumulative learning, frequent practice), and thus leaves many students struggling?”

This interaction and many similar ones made me scrutinize the diagnosis of ADHD in patients I encounter in clinical settings. We live in a society where instant gratification is cherished, and quick fixes are pursued with little contemplation of pitfalls. Students use stimulants to cram for exams, high-functioning professionals use them to meet deadlines, and athletes use them to enhance performance and improve reaction times. Psychiatry seems to be drawn into the demands of society and may be fueling the “quick-fix” mentality by prescribing stimulants to healthy individuals who want to improve their focus, and then diagnosing them with ADHD to align the prescription with an appropriate diagnosis. Research on the adverse effects of stimulant use in adults is not convincing nor conclusive enough to sway prescribers from denying the average adult patient a stimulant to enhance cognitive function before a high-stakes exam or a critical, career-shaping project if they present with some ADHD traits, which the patient might even hyperbolize to secure the desired prescription. All of this may contribute to the perceived rising prevalence of ADHD among adults.

As for my 30-year-old dental student, I reasoned that continuing his medication, for now, would help me establish rapport and trust. This would allow me to counsel him on the long-term adverse effects of stimulants, and develop a plan to optimize his sleep, focus, and time management skills, eventually improving his cognition and attention naturally. Unfortunately, he did not show up to future appointments after I sent him the refill.

In patients with attention-deficit/hyperactivity disorder (ADHD), stimulants reduce impulsivity and improve attention and focus. In individuals who do not have this disorder, stimulants are believed to enhance cognition, attention, and physical performance. In this article, I describe how a patient whose intermittent use of stimulants for motivation and cognitive enhancement shaped my approach to the diagnosis of ADHD.

Instant gratification and quick solutions

When I joined my psychiatry residency program, I expected to primarily treat patients who had depression, bipolar disorder, or psychosis. However, as I transitioned to my second year of residency, most patients I was assigned to had been diagnosed with ADHD. One of them was a 30-year-old in his fourth year of dental school. On his first visit, he requested a refill of dextroamphetamine and amphetamine 10 mg twice a day. He had been diagnosed with ADHD 5 years ago. He explained that he only needed this medication when preparing for his board examinations to motivate him and boost his focus and retention before studying. His study schedule included the exact doses and times he planned to take his stimulant.

I asked him questions to confirm the diagnosis, but he rushed to reassure me that he had already been diagnosed with ADHD and had been doing well on dextroamphetamine and amphetamine for many years. I was inclined to question his diagnosis of ADHD after learning of his “as-needed” use of stimulants as brain enhancers. His medical record reflecting the diagnosis of ADHD dated back to when he was a first-year dental student. The diagnosis was based on the patient’s report of procrastination for as long as he could remember. It also hinged on difficulties learning a second language and math being a challenging subject for him. Despite this, he managed to do well in school and earn an undergraduate degree, well enough to later pursue dentistry at a reputable university.

I thought, “Isn’t it normal to lose motivation and have doubts when preparing for a high-stakes exam like the boards? Aren’t these negative thoughts distracting enough to render sustained focus impossible? Doesn’t everyone struggle with procrastination, especially when they need to study? If learning a new language requires devotion, consistency, and sacrifice, isn’t it inherently challenging? Doesn’t good performance in math depend on multiple factors (ie, a strong foundation, cumulative learning, frequent practice), and thus leaves many students struggling?”

This interaction and many similar ones made me scrutinize the diagnosis of ADHD in patients I encounter in clinical settings. We live in a society where instant gratification is cherished, and quick fixes are pursued with little contemplation of pitfalls. Students use stimulants to cram for exams, high-functioning professionals use them to meet deadlines, and athletes use them to enhance performance and improve reaction times. Psychiatry seems to be drawn into the demands of society and may be fueling the “quick-fix” mentality by prescribing stimulants to healthy individuals who want to improve their focus, and then diagnosing them with ADHD to align the prescription with an appropriate diagnosis. Research on the adverse effects of stimulant use in adults is not convincing nor conclusive enough to sway prescribers from denying the average adult patient a stimulant to enhance cognitive function before a high-stakes exam or a critical, career-shaping project if they present with some ADHD traits, which the patient might even hyperbolize to secure the desired prescription. All of this may contribute to the perceived rising prevalence of ADHD among adults.

As for my 30-year-old dental student, I reasoned that continuing his medication, for now, would help me establish rapport and trust. This would allow me to counsel him on the long-term adverse effects of stimulants, and develop a plan to optimize his sleep, focus, and time management skills, eventually improving his cognition and attention naturally. Unfortunately, he did not show up to future appointments after I sent him the refill.

Physician stress – indeed, the stress level for all medical personnel – has reached new heights.

As if it weren’t enough that doctors work in a profession where it’s almost more a question of when they’ll be sued than if they’ll be sued – where COVID, staff shortages, long hours, and patients frustrated over canceled procedures have caused unrelenting fatigue and stress – they now have to worry that an unhappy patient is going to buy a gun, walk into their office, and kill them.

That’s exactly what happened in Tulsa, Okla., where a patient complaining of pain after back surgery murdered his doctor and several others who happened to be in the wrong place at the wrong time. 

The temptation in the aftermath of such tragedies is to think about preventive measures: Make medical facilities “hardened” targets, like schools have become, with armed guards, metal detectors, automatically locking doors, physical barriers within, security cameras, and buzzers for entry – although hardening a large medical center where members of the community routinely come and go would be challenging.

What about the enormous stress on doctors, nurses, and others in the medical workplace? Physicians who have been sued for malpractice often describe how it changes the way they interact with patients: They now size patients up and make judgments about their potential litigiousness. Will the physicians now look over their patients’ shoulders at the video feed from a security camera when they’re taking a history? Will medical professionals be forced to make snap judgments about patients’ psychological state before deciding whether to treat them?

Remember, there was a time when school shootings were unimaginable. Once one person crosses that line, others inevitably follow.

It could be a drug-seeking patient complaining of ongoing pain, angry because he can’t get a new prescription. It could be a patient whose unpaid bill was turned over to a collection agency, angry because he’s now getting calls from collectors. It could be someone who blames a physician for the loss of a loved one. It could be someone who would otherwise have filed a lawsuit, who now thinks he has a more effective option for exacting retribution.

Most of us would find it unbearable to live and work under the kind of stress faced by medical professionals today. And unfortunately, there is no short-term, systemic relief on the horizon. But there are methods of relieving at least some of the psychological burden being carried by these dedicated individuals.

For starters, the government should provide funds to improve safety and security at medical facilities. It’s sad but it’s a fact of life. The physical structure of schools, along with emergency procedures, have been changed since Columbine and Sandy Hook, and our children and their teachers undergo active shooter drills. Health care facilities will need to adopt similar strategies.

But if we don’t also support the individuals who work in health care, we’ll no longer have even partially staffed health care facilities. Hospitals and medical groups need to be conscious of the effects stress may have on them. Medical staff and administrators need to recognize changes in their colleagues’ behavior and refer those cohorts to professional stress coaches who can get them back on track.

Medical personnel should be picking up on warning signs, like irritability, depression, sudden weight gain or loss, lack of motivation and job satisfaction, obsessiveness, unusual levels of fatigue, alcohol or drug use, and, of course, avoidable medical errors.

In addition, colleagues in the medical workplace need to know each other well. They are usually the first ones to notice if something is off and may be in the best position to refer coworkers for help. Also, medical malpractice insurance carriers should consider encouraging and covering coaching sessions, because helping physicians cope with this heightened stress will prevent medical errors and the lawsuits that inevitably accompany mistakes.

This needn’t be a long-term process like ongoing psychotherapy; a few sessions with a well-trained coach may help psychologically challenged peers restore their focus and perspective. It won’t eliminate the threat any more than litigation stress coaching eliminates the threat of being sued, but it can prevent that stress from leading to avoidable errors. It also can prevent physicians’ personal lives and relationships from going off the rails and driving them out of the medical profession.

None of us can afford to ignore the impacts that these new stressors are having and simply act as if it’s business as usual. The people in the trenches need our help.

Ms. Fiore is President of Winning Focus in Murrysville, Pa. She has disclosed no relevant financial relationships.

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

Physician stress – indeed, the stress level for all medical personnel – has reached new heights.

As if it weren’t enough that doctors work in a profession where it’s almost more a question of when they’ll be sued than if they’ll be sued – where COVID, staff shortages, long hours, and patients frustrated over canceled procedures have caused unrelenting fatigue and stress – they now have to worry that an unhappy patient is going to buy a gun, walk into their office, and kill them.

That’s exactly what happened in Tulsa, Okla., where a patient complaining of pain after back surgery murdered his doctor and several others who happened to be in the wrong place at the wrong time. 

The temptation in the aftermath of such tragedies is to think about preventive measures: Make medical facilities “hardened” targets, like schools have become, with armed guards, metal detectors, automatically locking doors, physical barriers within, security cameras, and buzzers for entry – although hardening a large medical center where members of the community routinely come and go would be challenging.

What about the enormous stress on doctors, nurses, and others in the medical workplace? Physicians who have been sued for malpractice often describe how it changes the way they interact with patients: They now size patients up and make judgments about their potential litigiousness. Will the physicians now look over their patients’ shoulders at the video feed from a security camera when they’re taking a history? Will medical professionals be forced to make snap judgments about patients’ psychological state before deciding whether to treat them?

Remember, there was a time when school shootings were unimaginable. Once one person crosses that line, others inevitably follow.

It could be a drug-seeking patient complaining of ongoing pain, angry because he can’t get a new prescription. It could be a patient whose unpaid bill was turned over to a collection agency, angry because he’s now getting calls from collectors. It could be someone who blames a physician for the loss of a loved one. It could be someone who would otherwise have filed a lawsuit, who now thinks he has a more effective option for exacting retribution.

Most of us would find it unbearable to live and work under the kind of stress faced by medical professionals today. And unfortunately, there is no short-term, systemic relief on the horizon. But there are methods of relieving at least some of the psychological burden being carried by these dedicated individuals.

For starters, the government should provide funds to improve safety and security at medical facilities. It’s sad but it’s a fact of life. The physical structure of schools, along with emergency procedures, have been changed since Columbine and Sandy Hook, and our children and their teachers undergo active shooter drills. Health care facilities will need to adopt similar strategies.

But if we don’t also support the individuals who work in health care, we’ll no longer have even partially staffed health care facilities. Hospitals and medical groups need to be conscious of the effects stress may have on them. Medical staff and administrators need to recognize changes in their colleagues’ behavior and refer those cohorts to professional stress coaches who can get them back on track.

Medical personnel should be picking up on warning signs, like irritability, depression, sudden weight gain or loss, lack of motivation and job satisfaction, obsessiveness, unusual levels of fatigue, alcohol or drug use, and, of course, avoidable medical errors.

In addition, colleagues in the medical workplace need to know each other well. They are usually the first ones to notice if something is off and may be in the best position to refer coworkers for help. Also, medical malpractice insurance carriers should consider encouraging and covering coaching sessions, because helping physicians cope with this heightened stress will prevent medical errors and the lawsuits that inevitably accompany mistakes.

This needn’t be a long-term process like ongoing psychotherapy; a few sessions with a well-trained coach may help psychologically challenged peers restore their focus and perspective. It won’t eliminate the threat any more than litigation stress coaching eliminates the threat of being sued, but it can prevent that stress from leading to avoidable errors. It also can prevent physicians’ personal lives and relationships from going off the rails and driving them out of the medical profession.

None of us can afford to ignore the impacts that these new stressors are having and simply act as if it’s business as usual. The people in the trenches need our help.

Ms. Fiore is President of Winning Focus in Murrysville, Pa. She has disclosed no relevant financial relationships.

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

Physician stress – indeed, the stress level for all medical personnel – has reached new heights.

As if it weren’t enough that doctors work in a profession where it’s almost more a question of when they’ll be sued than if they’ll be sued – where COVID, staff shortages, long hours, and patients frustrated over canceled procedures have caused unrelenting fatigue and stress – they now have to worry that an unhappy patient is going to buy a gun, walk into their office, and kill them.

That’s exactly what happened in Tulsa, Okla., where a patient complaining of pain after back surgery murdered his doctor and several others who happened to be in the wrong place at the wrong time. 

The temptation in the aftermath of such tragedies is to think about preventive measures: Make medical facilities “hardened” targets, like schools have become, with armed guards, metal detectors, automatically locking doors, physical barriers within, security cameras, and buzzers for entry – although hardening a large medical center where members of the community routinely come and go would be challenging.

What about the enormous stress on doctors, nurses, and others in the medical workplace? Physicians who have been sued for malpractice often describe how it changes the way they interact with patients: They now size patients up and make judgments about their potential litigiousness. Will the physicians now look over their patients’ shoulders at the video feed from a security camera when they’re taking a history? Will medical professionals be forced to make snap judgments about patients’ psychological state before deciding whether to treat them?

Remember, there was a time when school shootings were unimaginable. Once one person crosses that line, others inevitably follow.

It could be a drug-seeking patient complaining of ongoing pain, angry because he can’t get a new prescription. It could be a patient whose unpaid bill was turned over to a collection agency, angry because he’s now getting calls from collectors. It could be someone who blames a physician for the loss of a loved one. It could be someone who would otherwise have filed a lawsuit, who now thinks he has a more effective option for exacting retribution.

Most of us would find it unbearable to live and work under the kind of stress faced by medical professionals today. And unfortunately, there is no short-term, systemic relief on the horizon. But there are methods of relieving at least some of the psychological burden being carried by these dedicated individuals.

For starters, the government should provide funds to improve safety and security at medical facilities. It’s sad but it’s a fact of life. The physical structure of schools, along with emergency procedures, have been changed since Columbine and Sandy Hook, and our children and their teachers undergo active shooter drills. Health care facilities will need to adopt similar strategies.

But if we don’t also support the individuals who work in health care, we’ll no longer have even partially staffed health care facilities. Hospitals and medical groups need to be conscious of the effects stress may have on them. Medical staff and administrators need to recognize changes in their colleagues’ behavior and refer those cohorts to professional stress coaches who can get them back on track.

Medical personnel should be picking up on warning signs, like irritability, depression, sudden weight gain or loss, lack of motivation and job satisfaction, obsessiveness, unusual levels of fatigue, alcohol or drug use, and, of course, avoidable medical errors.

In addition, colleagues in the medical workplace need to know each other well. They are usually the first ones to notice if something is off and may be in the best position to refer coworkers for help. Also, medical malpractice insurance carriers should consider encouraging and covering coaching sessions, because helping physicians cope with this heightened stress will prevent medical errors and the lawsuits that inevitably accompany mistakes.

This needn’t be a long-term process like ongoing psychotherapy; a few sessions with a well-trained coach may help psychologically challenged peers restore their focus and perspective. It won’t eliminate the threat any more than litigation stress coaching eliminates the threat of being sued, but it can prevent that stress from leading to avoidable errors. It also can prevent physicians’ personal lives and relationships from going off the rails and driving them out of the medical profession.

None of us can afford to ignore the impacts that these new stressors are having and simply act as if it’s business as usual. The people in the trenches need our help.

Ms. Fiore is President of Winning Focus in Murrysville, Pa. She has disclosed no relevant financial relationships.

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

More on T. gondii

We reviewed the article by Dr. Torrey on Toxoplasma gondii (T. gondii) and schizophrenia (“Cats, toxoplasmosis, and psychosis: Understanding the risks,” Current Psychiatry, May 2022, p. 14-19) with interest. Understanding infections in utero, during the perinatal period, and at other critical developmental stages may offer ways to prevent neurodevelopmental disorders. There appear to be good reasons to explore infectious and immune disruption of normal brain development. In a meta-analysis of 7 studies, Nayeri et al¹ found evidence to suggest T. gondii is a risk factor for autism spectrum disorder (ASD). Given the enormous loss of human potential and suffering resulting from schizophrenia and ASD, further exploration of toxoplasmosis and other infections may be valuable as we try to reduce the severe impact of these diseases.

The natural history of toxoplasmosis is an extraordinary example of nature’s complexity. The life cycle of this parasite uses the nervous system of the mouse to increase its transmission. Behavior changes ranging from reduced cat urine avoidance and increased risk-taking are observed in mice infected with T. gondii.² Chronic toxoplasmosis may also affect human behavior.³

Cats are fascinating, complex creatures. Of note, they produce a protein structurally like the secretion of the slow loris.⁴ The loris uses this brachial gland protein secretion as part of a defense strategy.⁵ Consideration of a possible toxic, neuroimmune role of these small mammal proteins in psychiatric disorders may open other avenues to explore.⁶

Our relationship to domesticated animals has been connected to serious diseases throughout human history.⁷ Severe acute respiratory syndrome and COVID-19 appear to be linked to animal reservoirs, mammals of the small animal trade, and the fur industry.^8,9 The rapid development of vaccines for COVID-19 is commendable. In conditions with multifactorial causation, managing an infectious component is worthy of consideration.

With mounting evidence suggesting a link between T. gondii and schizophrenia, ASD, and other diseases, further epidemiological studies and pilot interventions offer value. Interventions, including encouraging keeping cats indoors only, cat immunization, and human treatment, could be implemented in high-risk families. Efficacy requires data collection. While not easy, collaborative work by psychiatrists, developmental pediatricians, veterinarians, and epidemiologists is encouraged.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Michelle Douglass, PA-S2
Duke University Physician Assistant Program
Durham, North Carolina

References

1. Nayeri T, Sarvi S, Moosazadeh M, et al. Relationship between toxoplasmosis and autism: a systematic review and meta-analysis. Microb Pathog. 2020;147:104434. doi:10.1016/j.micpath.2020.104434
2. Kochanowsky JA, Koshy AA. Toxoplasma gondii. Curr Biol. 2018;28(14):R770-R771. doi:10.1016/j.cub.2018.05.035
3. Letcher S. Parasite mind control: how a single celled parasite carried in the cat intestine may be quietly tweaking our behavior. Scientific Kenyon: The Neuroscience Edition. 2018;22(1):4-11.
4. Scheib H, Nekaris KA, Rode-Margono J, et al. The toxicological intersection between allergen and toxin: a structural comparison of the cat dander allergenic protein Fel d1 and the slow loris brachial gland secretion protein. Toxins (Basel). 2020;12(2):86. doi:10.3390/toxins12020086
5. Nekaris KA, Moore RS, Rode EJ, et al. Mad, bad and dangerous to know: the biochemistry, ecology and evolution of slow loris venom. J Venom Anim Toxins Incl Trop Dis. 2013;19(1):21. doi:10.1186/1678-9199-19-21
6. Ligabue-Braun R. Hello, kitty: could cat allergy be a form of intoxication? J Venom Anim Toxins Incl Trop Dis. 2020;26:e20200051. doi:10.1590/1678-9199-JVATITD-2020-0051
7. Pearce-Duvet JM. The origin of human pathogens: evaluating the role of agriculture and domestic animals in the evolution of human disease. Biol Rev Camb Philos Soc. 2006;81(3):369-382. doi:10.1017/S1464793106007020
8. Jo WK, de Oliveira-Filho EF, Rasche A, et al. Potential zoonotic sources of SARS-CoV-2 infections. Transbound Emerg Dis. 2021;68(4):1824-1834. doi:10.1111/tbed.13872
9. Bell D, Roberton S, Hunter PR. Animal origins of SARS coronavirus: possible links with the international trade in small carnivores. Philos Trans R Soc Lond B Biol Sci. 2004;359(1447):1107-1114. doi:10.1098/rstb.2004.1492

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

Continue to: Pramipexole for MDD

I appreciate Dr. Espejo’s recommendations for treating patients who experience limited response from initial antidepressant therapy (“Treating major depressive disorder after limited response to an initial agent,” Current Psychiatry, October 2021, p. 51-53). I would like to add that pramipexole, a dopamine receptor agonist, can also alleviate depression. A meta-analysis concluded that patients receiving monotherapy or augmentation with pramipexole (mean maximum dose 1.62 mg/d) achieved response or remission of depression.¹ In an observational study of 116 patients with unipolar or bipolar depression, nearly 75% experienced response and 66% achieved remission with pramipexole augmentation (median maximum dose 1.05 mg/d).² Pramipexole is usually well-tolerated, although patients may experience nausea, somnolence, headache, and constipation, and they should be cautioned about the risk for compulsive behaviors and psychosis.

Jonathan R. Scarff, MD
Lexington VA Health Care System
Lexington, Kentucky

References

1. Tundo A, de Filippis R, De Crescenzo F. Pramipexole in the treatment of unipolar and bipolar depression. A systematic review and meta-analysis. Acta Psychiatr Scand. 2019;140(2):116-125.
2. Tundo A, Betrò S, Iommi M, et al. Efficacy and safety of 24-week pramipexole augmentation in patients with treatment resistant depression. A retrospective cohort study. Prog Neuropsychopharmacol Biol Psychiatry. 2022;112:110425. doi:10.1016/j.pnpbp.2021.110425

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

More on T. gondii

We reviewed the article by Dr. Torrey on Toxoplasma gondii (T. gondii) and schizophrenia (“Cats, toxoplasmosis, and psychosis: Understanding the risks,” Current Psychiatry, May 2022, p. 14-19) with interest. Understanding infections in utero, during the perinatal period, and at other critical developmental stages may offer ways to prevent neurodevelopmental disorders. There appear to be good reasons to explore infectious and immune disruption of normal brain development. In a meta-analysis of 7 studies, Nayeri et al¹ found evidence to suggest T. gondii is a risk factor for autism spectrum disorder (ASD). Given the enormous loss of human potential and suffering resulting from schizophrenia and ASD, further exploration of toxoplasmosis and other infections may be valuable as we try to reduce the severe impact of these diseases.

The natural history of toxoplasmosis is an extraordinary example of nature’s complexity. The life cycle of this parasite uses the nervous system of the mouse to increase its transmission. Behavior changes ranging from reduced cat urine avoidance and increased risk-taking are observed in mice infected with T. gondii.² Chronic toxoplasmosis may also affect human behavior.³

Cats are fascinating, complex creatures. Of note, they produce a protein structurally like the secretion of the slow loris.⁴ The loris uses this brachial gland protein secretion as part of a defense strategy.⁵ Consideration of a possible toxic, neuroimmune role of these small mammal proteins in psychiatric disorders may open other avenues to explore.⁶

Our relationship to domesticated animals has been connected to serious diseases throughout human history.⁷ Severe acute respiratory syndrome and COVID-19 appear to be linked to animal reservoirs, mammals of the small animal trade, and the fur industry.^8,9 The rapid development of vaccines for COVID-19 is commendable. In conditions with multifactorial causation, managing an infectious component is worthy of consideration.

With mounting evidence suggesting a link between T. gondii and schizophrenia, ASD, and other diseases, further epidemiological studies and pilot interventions offer value. Interventions, including encouraging keeping cats indoors only, cat immunization, and human treatment, could be implemented in high-risk families. Efficacy requires data collection. While not easy, collaborative work by psychiatrists, developmental pediatricians, veterinarians, and epidemiologists is encouraged.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Michelle Douglass, PA-S2
Duke University Physician Assistant Program
Durham, North Carolina

References

1. Nayeri T, Sarvi S, Moosazadeh M, et al. Relationship between toxoplasmosis and autism: a systematic review and meta-analysis. Microb Pathog. 2020;147:104434. doi:10.1016/j.micpath.2020.104434
2. Kochanowsky JA, Koshy AA. Toxoplasma gondii. Curr Biol. 2018;28(14):R770-R771. doi:10.1016/j.cub.2018.05.035
3. Letcher S. Parasite mind control: how a single celled parasite carried in the cat intestine may be quietly tweaking our behavior. Scientific Kenyon: The Neuroscience Edition. 2018;22(1):4-11.
4. Scheib H, Nekaris KA, Rode-Margono J, et al. The toxicological intersection between allergen and toxin: a structural comparison of the cat dander allergenic protein Fel d1 and the slow loris brachial gland secretion protein. Toxins (Basel). 2020;12(2):86. doi:10.3390/toxins12020086
5. Nekaris KA, Moore RS, Rode EJ, et al. Mad, bad and dangerous to know: the biochemistry, ecology and evolution of slow loris venom. J Venom Anim Toxins Incl Trop Dis. 2013;19(1):21. doi:10.1186/1678-9199-19-21
6. Ligabue-Braun R. Hello, kitty: could cat allergy be a form of intoxication? J Venom Anim Toxins Incl Trop Dis. 2020;26:e20200051. doi:10.1590/1678-9199-JVATITD-2020-0051
7. Pearce-Duvet JM. The origin of human pathogens: evaluating the role of agriculture and domestic animals in the evolution of human disease. Biol Rev Camb Philos Soc. 2006;81(3):369-382. doi:10.1017/S1464793106007020
8. Jo WK, de Oliveira-Filho EF, Rasche A, et al. Potential zoonotic sources of SARS-CoV-2 infections. Transbound Emerg Dis. 2021;68(4):1824-1834. doi:10.1111/tbed.13872
9. Bell D, Roberton S, Hunter PR. Animal origins of SARS coronavirus: possible links with the international trade in small carnivores. Philos Trans R Soc Lond B Biol Sci. 2004;359(1447):1107-1114. doi:10.1098/rstb.2004.1492

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

Continue to: Pramipexole for MDD

I appreciate Dr. Espejo’s recommendations for treating patients who experience limited response from initial antidepressant therapy (“Treating major depressive disorder after limited response to an initial agent,” Current Psychiatry, October 2021, p. 51-53). I would like to add that pramipexole, a dopamine receptor agonist, can also alleviate depression. A meta-analysis concluded that patients receiving monotherapy or augmentation with pramipexole (mean maximum dose 1.62 mg/d) achieved response or remission of depression.¹ In an observational study of 116 patients with unipolar or bipolar depression, nearly 75% experienced response and 66% achieved remission with pramipexole augmentation (median maximum dose 1.05 mg/d).² Pramipexole is usually well-tolerated, although patients may experience nausea, somnolence, headache, and constipation, and they should be cautioned about the risk for compulsive behaviors and psychosis.

Jonathan R. Scarff, MD
Lexington VA Health Care System
Lexington, Kentucky

References

1. Tundo A, de Filippis R, De Crescenzo F. Pramipexole in the treatment of unipolar and bipolar depression. A systematic review and meta-analysis. Acta Psychiatr Scand. 2019;140(2):116-125.
2. Tundo A, Betrò S, Iommi M, et al. Efficacy and safety of 24-week pramipexole augmentation in patients with treatment resistant depression. A retrospective cohort study. Prog Neuropsychopharmacol Biol Psychiatry. 2022;112:110425. doi:10.1016/j.pnpbp.2021.110425

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

More on T. gondii

We reviewed the article by Dr. Torrey on Toxoplasma gondii (T. gondii) and schizophrenia (“Cats, toxoplasmosis, and psychosis: Understanding the risks,” Current Psychiatry, May 2022, p. 14-19) with interest. Understanding infections in utero, during the perinatal period, and at other critical developmental stages may offer ways to prevent neurodevelopmental disorders. There appear to be good reasons to explore infectious and immune disruption of normal brain development. In a meta-analysis of 7 studies, Nayeri et al¹ found evidence to suggest T. gondii is a risk factor for autism spectrum disorder (ASD). Given the enormous loss of human potential and suffering resulting from schizophrenia and ASD, further exploration of toxoplasmosis and other infections may be valuable as we try to reduce the severe impact of these diseases.

The natural history of toxoplasmosis is an extraordinary example of nature’s complexity. The life cycle of this parasite uses the nervous system of the mouse to increase its transmission. Behavior changes ranging from reduced cat urine avoidance and increased risk-taking are observed in mice infected with T. gondii.² Chronic toxoplasmosis may also affect human behavior.³

Cats are fascinating, complex creatures. Of note, they produce a protein structurally like the secretion of the slow loris.⁴ The loris uses this brachial gland protein secretion as part of a defense strategy.⁵ Consideration of a possible toxic, neuroimmune role of these small mammal proteins in psychiatric disorders may open other avenues to explore.⁶

Our relationship to domesticated animals has been connected to serious diseases throughout human history.⁷ Severe acute respiratory syndrome and COVID-19 appear to be linked to animal reservoirs, mammals of the small animal trade, and the fur industry.^8,9 The rapid development of vaccines for COVID-19 is commendable. In conditions with multifactorial causation, managing an infectious component is worthy of consideration.

With mounting evidence suggesting a link between T. gondii and schizophrenia, ASD, and other diseases, further epidemiological studies and pilot interventions offer value. Interventions, including encouraging keeping cats indoors only, cat immunization, and human treatment, could be implemented in high-risk families. Efficacy requires data collection. While not easy, collaborative work by psychiatrists, developmental pediatricians, veterinarians, and epidemiologists is encouraged.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Michelle Douglass, PA-S2
Duke University Physician Assistant Program
Durham, North Carolina

References

1. Nayeri T, Sarvi S, Moosazadeh M, et al. Relationship between toxoplasmosis and autism: a systematic review and meta-analysis. Microb Pathog. 2020;147:104434. doi:10.1016/j.micpath.2020.104434
2. Kochanowsky JA, Koshy AA. Toxoplasma gondii. Curr Biol. 2018;28(14):R770-R771. doi:10.1016/j.cub.2018.05.035
3. Letcher S. Parasite mind control: how a single celled parasite carried in the cat intestine may be quietly tweaking our behavior. Scientific Kenyon: The Neuroscience Edition. 2018;22(1):4-11.
4. Scheib H, Nekaris KA, Rode-Margono J, et al. The toxicological intersection between allergen and toxin: a structural comparison of the cat dander allergenic protein Fel d1 and the slow loris brachial gland secretion protein. Toxins (Basel). 2020;12(2):86. doi:10.3390/toxins12020086
5. Nekaris KA, Moore RS, Rode EJ, et al. Mad, bad and dangerous to know: the biochemistry, ecology and evolution of slow loris venom. J Venom Anim Toxins Incl Trop Dis. 2013;19(1):21. doi:10.1186/1678-9199-19-21
6. Ligabue-Braun R. Hello, kitty: could cat allergy be a form of intoxication? J Venom Anim Toxins Incl Trop Dis. 2020;26:e20200051. doi:10.1590/1678-9199-JVATITD-2020-0051
7. Pearce-Duvet JM. The origin of human pathogens: evaluating the role of agriculture and domestic animals in the evolution of human disease. Biol Rev Camb Philos Soc. 2006;81(3):369-382. doi:10.1017/S1464793106007020
8. Jo WK, de Oliveira-Filho EF, Rasche A, et al. Potential zoonotic sources of SARS-CoV-2 infections. Transbound Emerg Dis. 2021;68(4):1824-1834. doi:10.1111/tbed.13872
9. Bell D, Roberton S, Hunter PR. Animal origins of SARS coronavirus: possible links with the international trade in small carnivores. Philos Trans R Soc Lond B Biol Sci. 2004;359(1447):1107-1114. doi:10.1098/rstb.2004.1492

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

Continue to: Pramipexole for MDD

I appreciate Dr. Espejo’s recommendations for treating patients who experience limited response from initial antidepressant therapy (“Treating major depressive disorder after limited response to an initial agent,” Current Psychiatry, October 2021, p. 51-53). I would like to add that pramipexole, a dopamine receptor agonist, can also alleviate depression. A meta-analysis concluded that patients receiving monotherapy or augmentation with pramipexole (mean maximum dose 1.62 mg/d) achieved response or remission of depression.¹ In an observational study of 116 patients with unipolar or bipolar depression, nearly 75% experienced response and 66% achieved remission with pramipexole augmentation (median maximum dose 1.05 mg/d).² Pramipexole is usually well-tolerated, although patients may experience nausea, somnolence, headache, and constipation, and they should be cautioned about the risk for compulsive behaviors and psychosis.

Jonathan R. Scarff, MD
Lexington VA Health Care System
Lexington, Kentucky

References

1. Tundo A, de Filippis R, De Crescenzo F. Pramipexole in the treatment of unipolar and bipolar depression. A systematic review and meta-analysis. Acta Psychiatr Scand. 2019;140(2):116-125.
2. Tundo A, Betrò S, Iommi M, et al. Efficacy and safety of 24-week pramipexole augmentation in patients with treatment resistant depression. A retrospective cohort study. Prog Neuropsychopharmacol Biol Psychiatry. 2022;112:110425. doi:10.1016/j.pnpbp.2021.110425

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

I can dimly recall watching Queen Elizabeth’s coronation on a very small black and white television screen. Even in monochrome it was a riveting event. Recently, the Queen celebrated her Platinum Jubilee, marking her 70-year reign. Apparently it was a multiday event with all the trappings, floating above an undercurrent of scandal and intrigue. I had better things to do than I did as a 7-year-old entranced by the novelty of a neighbor’s television set.

But, it turns out that I had missed the opportunity to see live and in color a royal meltdown starring the Queen’s great-grandson, 4-year-old Prince Louis. Not to worry. It remains on video archives for our education and pleasure ad infinitum. His performance was no more dramatic than what you have seen numerous times in the checkout line of the grocery store. However, this meltdown was on the world stage in the front row of the royal box and performed in various venues on each day of a 4-day event.

As long as you weren’t his parents, Kate Middleton and Prince William, the meltdown had its moments of hilarity. Louis made full use of his youthful and plastic face, creating a wide variety of taunts and responses to his mother’s praiseworthy and understated attempts at regaining control. Of course, the British press and every armchair parent with a Twitter account had a field day contributing their explanations and advice.

For example, here’s the headline on an international news website that caught my eye: “Royal reveals why Prince Louis was so ‘mischievous’ during the Jubilee”. In the article, a fellow royal and former rugby star who was sitting directly behind the little Prince during one of his performances chalked up the 4-year-old’s behavior to a “sugar high” resulting from the ample supply of sweets available behind the royal box.

Nowhere in the article is there a question of whether the “sugar high” is a science-based phenomenon. In fact, the reporter assumes we all know it exists and writes that “parents across the globe can probably [read: definitely] relate.”

I’m curious: How do you respond when a parent in the office explains the child’s behavior as the result of a “sugar high”? Or when you’re at a cookout and someone makes a comment that makes it obvious that they believe that “sugar highs” are real? Do you immediately pause the conversation and launch into a short but tasteful observation that you know of no scientific studies that sugar can cause a high? Or, figuring that in the face of an overwhelming burden of old wives’ tales it’s not worth mounting a rebuttal, do you pretend you didn’t hear the comment?

Or am I completely off base because your experience has left you convinced that despite the lack of supporting studies the “sugar high” phenomenon exists? Maybe you even include it on your list of explanations and remedies for pediatric misbehaviors. I am ready to listen, but it will take some heavy lifting to convince me.

I suspect your response to offhand comments about “sugar highs” is similar to mine. It depends on the situation. If I think there are obvious and correctable causes for the child’s misbehavior such as sleep deprivation or a mismatch between parental expectation and the child’s tolerance for a stimulating environment I will include in my parenting advice the comment, “Sugar highs probably don’t exist.”

On the other hand, if I’m tired and think my observation will fall on deaf ears I let the conversation drift. I worry that my silence will be interpreted as a confirmation of an old wives’ tale. What I really don’t want to do is perpetuate a myth that may prevent some children from getting the care they need.

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 [email protected].

I can dimly recall watching Queen Elizabeth’s coronation on a very small black and white television screen. Even in monochrome it was a riveting event. Recently, the Queen celebrated her Platinum Jubilee, marking her 70-year reign. Apparently it was a multiday event with all the trappings, floating above an undercurrent of scandal and intrigue. I had better things to do than I did as a 7-year-old entranced by the novelty of a neighbor’s television set.

But, it turns out that I had missed the opportunity to see live and in color a royal meltdown starring the Queen’s great-grandson, 4-year-old Prince Louis. Not to worry. It remains on video archives for our education and pleasure ad infinitum. His performance was no more dramatic than what you have seen numerous times in the checkout line of the grocery store. However, this meltdown was on the world stage in the front row of the royal box and performed in various venues on each day of a 4-day event.

As long as you weren’t his parents, Kate Middleton and Prince William, the meltdown had its moments of hilarity. Louis made full use of his youthful and plastic face, creating a wide variety of taunts and responses to his mother’s praiseworthy and understated attempts at regaining control. Of course, the British press and every armchair parent with a Twitter account had a field day contributing their explanations and advice.

For example, here’s the headline on an international news website that caught my eye: “Royal reveals why Prince Louis was so ‘mischievous’ during the Jubilee”. In the article, a fellow royal and former rugby star who was sitting directly behind the little Prince during one of his performances chalked up the 4-year-old’s behavior to a “sugar high” resulting from the ample supply of sweets available behind the royal box.

Nowhere in the article is there a question of whether the “sugar high” is a science-based phenomenon. In fact, the reporter assumes we all know it exists and writes that “parents across the globe can probably [read: definitely] relate.”

I’m curious: How do you respond when a parent in the office explains the child’s behavior as the result of a “sugar high”? Or when you’re at a cookout and someone makes a comment that makes it obvious that they believe that “sugar highs” are real? Do you immediately pause the conversation and launch into a short but tasteful observation that you know of no scientific studies that sugar can cause a high? Or, figuring that in the face of an overwhelming burden of old wives’ tales it’s not worth mounting a rebuttal, do you pretend you didn’t hear the comment?

Or am I completely off base because your experience has left you convinced that despite the lack of supporting studies the “sugar high” phenomenon exists? Maybe you even include it on your list of explanations and remedies for pediatric misbehaviors. I am ready to listen, but it will take some heavy lifting to convince me.

I suspect your response to offhand comments about “sugar highs” is similar to mine. It depends on the situation. If I think there are obvious and correctable causes for the child’s misbehavior such as sleep deprivation or a mismatch between parental expectation and the child’s tolerance for a stimulating environment I will include in my parenting advice the comment, “Sugar highs probably don’t exist.”

On the other hand, if I’m tired and think my observation will fall on deaf ears I let the conversation drift. I worry that my silence will be interpreted as a confirmation of an old wives’ tale. What I really don’t want to do is perpetuate a myth that may prevent some children from getting the care they need.

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 [email protected].

I can dimly recall watching Queen Elizabeth’s coronation on a very small black and white television screen. Even in monochrome it was a riveting event. Recently, the Queen celebrated her Platinum Jubilee, marking her 70-year reign. Apparently it was a multiday event with all the trappings, floating above an undercurrent of scandal and intrigue. I had better things to do than I did as a 7-year-old entranced by the novelty of a neighbor’s television set.

But, it turns out that I had missed the opportunity to see live and in color a royal meltdown starring the Queen’s great-grandson, 4-year-old Prince Louis. Not to worry. It remains on video archives for our education and pleasure ad infinitum. His performance was no more dramatic than what you have seen numerous times in the checkout line of the grocery store. However, this meltdown was on the world stage in the front row of the royal box and performed in various venues on each day of a 4-day event.

As long as you weren’t his parents, Kate Middleton and Prince William, the meltdown had its moments of hilarity. Louis made full use of his youthful and plastic face, creating a wide variety of taunts and responses to his mother’s praiseworthy and understated attempts at regaining control. Of course, the British press and every armchair parent with a Twitter account had a field day contributing their explanations and advice.

For example, here’s the headline on an international news website that caught my eye: “Royal reveals why Prince Louis was so ‘mischievous’ during the Jubilee”. In the article, a fellow royal and former rugby star who was sitting directly behind the little Prince during one of his performances chalked up the 4-year-old’s behavior to a “sugar high” resulting from the ample supply of sweets available behind the royal box.

Nowhere in the article is there a question of whether the “sugar high” is a science-based phenomenon. In fact, the reporter assumes we all know it exists and writes that “parents across the globe can probably [read: definitely] relate.”

I’m curious: How do you respond when a parent in the office explains the child’s behavior as the result of a “sugar high”? Or when you’re at a cookout and someone makes a comment that makes it obvious that they believe that “sugar highs” are real? Do you immediately pause the conversation and launch into a short but tasteful observation that you know of no scientific studies that sugar can cause a high? Or, figuring that in the face of an overwhelming burden of old wives’ tales it’s not worth mounting a rebuttal, do you pretend you didn’t hear the comment?

Or am I completely off base because your experience has left you convinced that despite the lack of supporting studies the “sugar high” phenomenon exists? Maybe you even include it on your list of explanations and remedies for pediatric misbehaviors. I am ready to listen, but it will take some heavy lifting to convince me.

I suspect your response to offhand comments about “sugar highs” is similar to mine. It depends on the situation. If I think there are obvious and correctable causes for the child’s misbehavior such as sleep deprivation or a mismatch between parental expectation and the child’s tolerance for a stimulating environment I will include in my parenting advice the comment, “Sugar highs probably don’t exist.”

On the other hand, if I’m tired and think my observation will fall on deaf ears I let the conversation drift. I worry that my silence will be interpreted as a confirmation of an old wives’ tale. What I really don’t want to do is perpetuate a myth that may prevent some children from getting the care they need.

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 [email protected].