Commentary

I have become obsessed with the reality that the unprecedented national shortage of formula is keeping some families from adequately feeding their infants and young children. I am deeply concerned, both as a family medicine physician and a new mother, about the heartbreaking stories that I’ve heard from parents of all socioeconomic backgrounds. New mothers, unable to breastfeed for a multitude of reasons, find themselves standing in front of empty store shelves, in tears.

In recent months, many health care providers have had patients disclose that they are diluting ready-to-feed formula or mixing powdered formula with more water than instructed to make it go further. Some parents are giving cow’s milk to their children at too young an age because they can’t find formula. Others are foregoing milk altogether and feeding their children beverages such as juice or soda. All of these practices can threaten a child’s life, growth, and development.
 

When breastfeeding isn’t possible

We all know that human milk is the optimal, most nutritionally complete food source for newborn babies and infants. It can improve dental health and neurodevelopmental outcomes, as well as reduce the risk for asthma, eczema, diabetes, and obesity. An added benefit during the COVID-19 pandemic has been providing newborn infants with a boost of immunity before they are able to be vaccinated against SARS-CoV-2 infection.

But lactation and breastfeeding aren’t possible for everyone. Earlier this year, when my daughter was born more than a month prematurely, I worried that I would be unable to breastfeed her. The complications of prematurity can interfere with establishing lactation, and my daughter spent some time in the neonatal intensive care unit (NICU), requiring frequent feedings to treat hypoglycemia. She also lacked the muscle strength or coordination to latch on to the breast, so she was fed my colostrum and donor breast milk by bottle.

Not knowing when my mature milk would come in, my family scoured the retail stores for formula while I was still recovering from delivery. My daughter needed a specific type of high-calorie formula for premature infants. Eventually, my mother found one can of this powdered formula. The hospital also sent us home with 16 oz of ready-to-feed samples and enough donor breastmilk to last 24 hours at home. We considered ourselves lucky. The fear and anxiety about being able to feed my baby still stands out in my mind.
 

Pumping and sharing

Over the next few months, out of necessity, I became an “exclusively pumping” mother. My daughter, unable to latch, drank my pumped milk from a bottle. My body started to produce more milk than she needed in a day. In an effort to pay it forward and to put my extra milk to use, I became a human-milk donor. I underwent rigorous screening, including testing for infectious diseases such as HIV and hepatitis C. I was approved to donate to our local hospital’s milk bank, helping other families in the NICU feed their babies. Through informal connections on the internet, I also provide expressed milk to another mother in the community who is unable to lactate. To date, I’ve donated more than 1,500 oz of human milk (and counting).

The practice of human-milk donation dates back millennia with wet-nursing, when children were breastfed by someone other than their biological mothers: relatives, friends, or even strangers. The first milk bank in the United States opened in Boston in the early 20th century. In 1980, the World Health Organization and the United Nations Children’s Fund released a joint statement supporting the use of human-donor milk as the first alternative if the biological mother is unable to breastfeed. Donor milk is a safe option for families who cannot provide their own human milk to their children.
 

Human-milk banks

More than 30 nonprofit milk banks now operate in the United States. Because their mission is primarily to meet the needs of sick and hospitalized children rather than the general public, these milk banks are an impractical solution to the national formula shortage. Although families with healthy children can purchase donor milk with a prescription, supplies are scarce, and insurance doesn’t cover the cost.

Milk provided by formal human-milk banks is considered safe. Certain infections such as HIV and hepatitis can be transmitted through human milk. However, milk banks screen their donors and safely pasteurize and store donated breastmilk, following standard protocols. The risk of contracting an illness from banked donor milk is very low. The American Academy of Pediatrics recommends accepting donor milk only from a milk bank.
 

Informal human-milk donation

An increasingly popular alternative to formal human-milk banks is informal human-milk sharing. But many people, including health care professionals, hold misconceptions about how informal milk donation works. Today’s informal milk donation looks very different from age-old wet-nursing: Moms in support groups, often via social media, are requesting pumped milk from one another. (Note that this definition of “informal human-milk donation” does not include selling or purchasing human milk.)

Although the safety of sharing pumped human milk this way cannot be guaranteed, a harm-reduction approach is warranted, especially in view of the current formula scarcity.

I believe that medical professionals have a responsibility to raise awareness and dispel myths about donor breast milk. Many physicians acknowledge that informal milk sharing is common but rarely recommend it to patients. Whether they are donors or recipients, families who choose to participate need to be educated about how to go about the process as safely as possible.

Patients who are considering accepting informally donated human milk should ask key questions of the donor to gauge the risk of pathogens or other harmful substances being passed to their babies:

• What medications do you take?
• What supplements do you take?
• What recreational drugs do you take?
• Any recent travel?
• Any tattoos and if so, how recent?
• How much alcohol do you drink and how often?
• Have you been diagnosed with any infections?
• Any recent illness?
• How do you pump your breast milk?
• How do you store your breast milk?
• When was the available milk pumped?

We can help families by offering our medical expertise, allowing them to make an informed decision about whether to accept donated human milk. Clinicians can encourage patients and their families to use resources like the Infant Risk Center, which provides evidence-based information about medication safety and breast milk.

If your lactating patient is considering donating milk through informal channels to a family in need, encourage them to be open and honest about their medical history and lifestyle habits. If they cannot be transparent, they should not donate. A mutual level of respect and honesty can ensure the safety of those they hope to help. It is also important to counsel prospective milk donors to notify their milk recipients of any new illnesses, substance use, medications, travel, tattoos, or changes to their medical history.

Finally, encourage lactating patients who are able to do so to donate their extra milk to local nonprofit milk banks to increase the availability of screened, pasteurized breast milk in the community.

As a physician and mother, I hope that U.S. families will be less vulnerable to future formula shortages. Human milk is an ideal food source, but not everyone can lactate. Though not perfect, human milk donated outside of formal milk banks offers a safer alternative to diluting formula or feeding other unsuitable beverages to infants and children. As health care professionals, we need to counsel our patients about how to engage in this practice safely.

Dr. Mieses Malchuk is assistant professor in the department of family medicine at the University of North Carolina at Chapel Hill and a board-certified family physician and attending physician at UNC Health in Chapel Hill. She has disclosed no relevant financial relationships.

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

I have become obsessed with the reality that the unprecedented national shortage of formula is keeping some families from adequately feeding their infants and young children. I am deeply concerned, both as a family medicine physician and a new mother, about the heartbreaking stories that I’ve heard from parents of all socioeconomic backgrounds. New mothers, unable to breastfeed for a multitude of reasons, find themselves standing in front of empty store shelves, in tears.

In recent months, many health care providers have had patients disclose that they are diluting ready-to-feed formula or mixing powdered formula with more water than instructed to make it go further. Some parents are giving cow’s milk to their children at too young an age because they can’t find formula. Others are foregoing milk altogether and feeding their children beverages such as juice or soda. All of these practices can threaten a child’s life, growth, and development.
 

When breastfeeding isn’t possible

We all know that human milk is the optimal, most nutritionally complete food source for newborn babies and infants. It can improve dental health and neurodevelopmental outcomes, as well as reduce the risk for asthma, eczema, diabetes, and obesity. An added benefit during the COVID-19 pandemic has been providing newborn infants with a boost of immunity before they are able to be vaccinated against SARS-CoV-2 infection.

But lactation and breastfeeding aren’t possible for everyone. Earlier this year, when my daughter was born more than a month prematurely, I worried that I would be unable to breastfeed her. The complications of prematurity can interfere with establishing lactation, and my daughter spent some time in the neonatal intensive care unit (NICU), requiring frequent feedings to treat hypoglycemia. She also lacked the muscle strength or coordination to latch on to the breast, so she was fed my colostrum and donor breast milk by bottle.

Not knowing when my mature milk would come in, my family scoured the retail stores for formula while I was still recovering from delivery. My daughter needed a specific type of high-calorie formula for premature infants. Eventually, my mother found one can of this powdered formula. The hospital also sent us home with 16 oz of ready-to-feed samples and enough donor breastmilk to last 24 hours at home. We considered ourselves lucky. The fear and anxiety about being able to feed my baby still stands out in my mind.
 

Pumping and sharing

Over the next few months, out of necessity, I became an “exclusively pumping” mother. My daughter, unable to latch, drank my pumped milk from a bottle. My body started to produce more milk than she needed in a day. In an effort to pay it forward and to put my extra milk to use, I became a human-milk donor. I underwent rigorous screening, including testing for infectious diseases such as HIV and hepatitis C. I was approved to donate to our local hospital’s milk bank, helping other families in the NICU feed their babies. Through informal connections on the internet, I also provide expressed milk to another mother in the community who is unable to lactate. To date, I’ve donated more than 1,500 oz of human milk (and counting).

The practice of human-milk donation dates back millennia with wet-nursing, when children were breastfed by someone other than their biological mothers: relatives, friends, or even strangers. The first milk bank in the United States opened in Boston in the early 20th century. In 1980, the World Health Organization and the United Nations Children’s Fund released a joint statement supporting the use of human-donor milk as the first alternative if the biological mother is unable to breastfeed. Donor milk is a safe option for families who cannot provide their own human milk to their children.
 

Human-milk banks

More than 30 nonprofit milk banks now operate in the United States. Because their mission is primarily to meet the needs of sick and hospitalized children rather than the general public, these milk banks are an impractical solution to the national formula shortage. Although families with healthy children can purchase donor milk with a prescription, supplies are scarce, and insurance doesn’t cover the cost.

Milk provided by formal human-milk banks is considered safe. Certain infections such as HIV and hepatitis can be transmitted through human milk. However, milk banks screen their donors and safely pasteurize and store donated breastmilk, following standard protocols. The risk of contracting an illness from banked donor milk is very low. The American Academy of Pediatrics recommends accepting donor milk only from a milk bank.
 

Informal human-milk donation

An increasingly popular alternative to formal human-milk banks is informal human-milk sharing. But many people, including health care professionals, hold misconceptions about how informal milk donation works. Today’s informal milk donation looks very different from age-old wet-nursing: Moms in support groups, often via social media, are requesting pumped milk from one another. (Note that this definition of “informal human-milk donation” does not include selling or purchasing human milk.)

Although the safety of sharing pumped human milk this way cannot be guaranteed, a harm-reduction approach is warranted, especially in view of the current formula scarcity.

I believe that medical professionals have a responsibility to raise awareness and dispel myths about donor breast milk. Many physicians acknowledge that informal milk sharing is common but rarely recommend it to patients. Whether they are donors or recipients, families who choose to participate need to be educated about how to go about the process as safely as possible.

Patients who are considering accepting informally donated human milk should ask key questions of the donor to gauge the risk of pathogens or other harmful substances being passed to their babies:

• What medications do you take?
• What supplements do you take?
• What recreational drugs do you take?
• Any recent travel?
• Any tattoos and if so, how recent?
• How much alcohol do you drink and how often?
• Have you been diagnosed with any infections?
• Any recent illness?
• How do you pump your breast milk?
• How do you store your breast milk?
• When was the available milk pumped?

We can help families by offering our medical expertise, allowing them to make an informed decision about whether to accept donated human milk. Clinicians can encourage patients and their families to use resources like the Infant Risk Center, which provides evidence-based information about medication safety and breast milk.

If your lactating patient is considering donating milk through informal channels to a family in need, encourage them to be open and honest about their medical history and lifestyle habits. If they cannot be transparent, they should not donate. A mutual level of respect and honesty can ensure the safety of those they hope to help. It is also important to counsel prospective milk donors to notify their milk recipients of any new illnesses, substance use, medications, travel, tattoos, or changes to their medical history.

Finally, encourage lactating patients who are able to do so to donate their extra milk to local nonprofit milk banks to increase the availability of screened, pasteurized breast milk in the community.

As a physician and mother, I hope that U.S. families will be less vulnerable to future formula shortages. Human milk is an ideal food source, but not everyone can lactate. Though not perfect, human milk donated outside of formal milk banks offers a safer alternative to diluting formula or feeding other unsuitable beverages to infants and children. As health care professionals, we need to counsel our patients about how to engage in this practice safely.

Dr. Mieses Malchuk is assistant professor in the department of family medicine at the University of North Carolina at Chapel Hill and a board-certified family physician and attending physician at UNC Health in Chapel Hill. She has disclosed no relevant financial relationships.

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

I have become obsessed with the reality that the unprecedented national shortage of formula is keeping some families from adequately feeding their infants and young children. I am deeply concerned, both as a family medicine physician and a new mother, about the heartbreaking stories that I’ve heard from parents of all socioeconomic backgrounds. New mothers, unable to breastfeed for a multitude of reasons, find themselves standing in front of empty store shelves, in tears.

In recent months, many health care providers have had patients disclose that they are diluting ready-to-feed formula or mixing powdered formula with more water than instructed to make it go further. Some parents are giving cow’s milk to their children at too young an age because they can’t find formula. Others are foregoing milk altogether and feeding their children beverages such as juice or soda. All of these practices can threaten a child’s life, growth, and development.
 

When breastfeeding isn’t possible

We all know that human milk is the optimal, most nutritionally complete food source for newborn babies and infants. It can improve dental health and neurodevelopmental outcomes, as well as reduce the risk for asthma, eczema, diabetes, and obesity. An added benefit during the COVID-19 pandemic has been providing newborn infants with a boost of immunity before they are able to be vaccinated against SARS-CoV-2 infection.

But lactation and breastfeeding aren’t possible for everyone. Earlier this year, when my daughter was born more than a month prematurely, I worried that I would be unable to breastfeed her. The complications of prematurity can interfere with establishing lactation, and my daughter spent some time in the neonatal intensive care unit (NICU), requiring frequent feedings to treat hypoglycemia. She also lacked the muscle strength or coordination to latch on to the breast, so she was fed my colostrum and donor breast milk by bottle.

Not knowing when my mature milk would come in, my family scoured the retail stores for formula while I was still recovering from delivery. My daughter needed a specific type of high-calorie formula for premature infants. Eventually, my mother found one can of this powdered formula. The hospital also sent us home with 16 oz of ready-to-feed samples and enough donor breastmilk to last 24 hours at home. We considered ourselves lucky. The fear and anxiety about being able to feed my baby still stands out in my mind.
 

Pumping and sharing

Over the next few months, out of necessity, I became an “exclusively pumping” mother. My daughter, unable to latch, drank my pumped milk from a bottle. My body started to produce more milk than she needed in a day. In an effort to pay it forward and to put my extra milk to use, I became a human-milk donor. I underwent rigorous screening, including testing for infectious diseases such as HIV and hepatitis C. I was approved to donate to our local hospital’s milk bank, helping other families in the NICU feed their babies. Through informal connections on the internet, I also provide expressed milk to another mother in the community who is unable to lactate. To date, I’ve donated more than 1,500 oz of human milk (and counting).

The practice of human-milk donation dates back millennia with wet-nursing, when children were breastfed by someone other than their biological mothers: relatives, friends, or even strangers. The first milk bank in the United States opened in Boston in the early 20th century. In 1980, the World Health Organization and the United Nations Children’s Fund released a joint statement supporting the use of human-donor milk as the first alternative if the biological mother is unable to breastfeed. Donor milk is a safe option for families who cannot provide their own human milk to their children.
 

Human-milk banks

More than 30 nonprofit milk banks now operate in the United States. Because their mission is primarily to meet the needs of sick and hospitalized children rather than the general public, these milk banks are an impractical solution to the national formula shortage. Although families with healthy children can purchase donor milk with a prescription, supplies are scarce, and insurance doesn’t cover the cost.

Milk provided by formal human-milk banks is considered safe. Certain infections such as HIV and hepatitis can be transmitted through human milk. However, milk banks screen their donors and safely pasteurize and store donated breastmilk, following standard protocols. The risk of contracting an illness from banked donor milk is very low. The American Academy of Pediatrics recommends accepting donor milk only from a milk bank.
 

Informal human-milk donation

An increasingly popular alternative to formal human-milk banks is informal human-milk sharing. But many people, including health care professionals, hold misconceptions about how informal milk donation works. Today’s informal milk donation looks very different from age-old wet-nursing: Moms in support groups, often via social media, are requesting pumped milk from one another. (Note that this definition of “informal human-milk donation” does not include selling or purchasing human milk.)

Although the safety of sharing pumped human milk this way cannot be guaranteed, a harm-reduction approach is warranted, especially in view of the current formula scarcity.

I believe that medical professionals have a responsibility to raise awareness and dispel myths about donor breast milk. Many physicians acknowledge that informal milk sharing is common but rarely recommend it to patients. Whether they are donors or recipients, families who choose to participate need to be educated about how to go about the process as safely as possible.

Patients who are considering accepting informally donated human milk should ask key questions of the donor to gauge the risk of pathogens or other harmful substances being passed to their babies:

• What medications do you take?
• What supplements do you take?
• What recreational drugs do you take?
• Any recent travel?
• Any tattoos and if so, how recent?
• How much alcohol do you drink and how often?
• Have you been diagnosed with any infections?
• Any recent illness?
• How do you pump your breast milk?
• How do you store your breast milk?
• When was the available milk pumped?

We can help families by offering our medical expertise, allowing them to make an informed decision about whether to accept donated human milk. Clinicians can encourage patients and their families to use resources like the Infant Risk Center, which provides evidence-based information about medication safety and breast milk.

If your lactating patient is considering donating milk through informal channels to a family in need, encourage them to be open and honest about their medical history and lifestyle habits. If they cannot be transparent, they should not donate. A mutual level of respect and honesty can ensure the safety of those they hope to help. It is also important to counsel prospective milk donors to notify their milk recipients of any new illnesses, substance use, medications, travel, tattoos, or changes to their medical history.

Finally, encourage lactating patients who are able to do so to donate their extra milk to local nonprofit milk banks to increase the availability of screened, pasteurized breast milk in the community.

As a physician and mother, I hope that U.S. families will be less vulnerable to future formula shortages. Human milk is an ideal food source, but not everyone can lactate. Though not perfect, human milk donated outside of formal milk banks offers a safer alternative to diluting formula or feeding other unsuitable beverages to infants and children. As health care professionals, we need to counsel our patients about how to engage in this practice safely.

Dr. Mieses Malchuk is assistant professor in the department of family medicine at the University of North Carolina at Chapel Hill and a board-certified family physician and attending physician at UNC Health in Chapel Hill. She has disclosed no relevant financial relationships.

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

The 2022 Pediatric Academic Societies meeting included an excellent session on the acute and delayed effects of COVID-19 on children’s hearts. Data on the risk for cardiac injury during acute COVID-19, return-to-play guidelines after COVID-19–related heart injury, and post–vaccine-associated myocarditis were reviewed.

COVID-induced cardiac injury

The risk for COVID-induced cardiac injury is directly associated with age. Recent Centers for Disease Control and Prevention data revealed a “myocarditis or pericarditis” rate in the range of 12-17 cases per 100,000 SARS-CoV-2 infections among male children aged 5-11 years (lower rates for females); the rate jumps to 50-65 cases per 100,000 infections among male children aged 12-17 years. So cardiac injury caused by acute COVID-19 appears rare, but the risk is clearly associated with male sex and adolescent age.

Return to play after COVID-19

Clinicians may be pressed by patients and parents for advice on return to play after illness with COVID-19. In July 2020, the American College of Cardiology published an algorithm that has been adjusted over time, most recently in 2022 by the American Academy of Pediatrics. These algorithms stratify recommendations by degree of illness. One rule of thumb: Patients with severe COVID-19 (ICU care or multisystem inflammatory syndrome in children [MIS-C]) have only one box on the algorithm, and that is to rest for 3-6 months and only return to usual activity after cardiac clearance. Moderate disease (defined as ≥ 4 days of fever > 100.4 °F; ≥ 1 week of myalgia, chills, lethargy, or any non-ICU hospital stay; and no evidence of MIS-C) require undergoing an ECG to look for cardiac dysfunction, followed by at least 10 days of rest if the ECG is negative or referral for cardiac evaluation if either ECG or exam by a pediatric cardiologist is abnormal.

Clinicians can perhaps be more permissible with patients who are younger or who have had less severe disease. For example, if a patient aged younger than 12 years is asymptomatic with routine activity at the time of evaluation, an ECG is not indicated. For patients aged 12-15 years who are asymptomatic at the time of evaluation but participate in a high-intensity sport, clinicians might consider obtaining an ECG. As few as 3 days of rest might be enough for select patients who are asymptomatic at presentation. For other patients, clinicians should work with parents to introduce activity gradually and make it clear to parents that any activity intolerance requires quick reevaluation. On existing athlete registries, no deaths that are attributable to post–COVID-19 cardiac effects have been confirmed in children; however, all data presented during the session were from prior to the Omicron variant surge in early 2022, so more information may be forthcoming.
 

Considerations for MIS-C

Among children experiencing MIS-C, 35% had ECG changes, 40% exhibited left ventricular systolic or diastolic dysfunction, and 30% had mitral regurgitation, meaning that a large percentage of patients with MIS-C show some degree of cardiac dysfunction. Unfortunately, we are still in the data-gathering phase for long-term outcomes. Functional parameters tend to improve within a week, and most patients will return to normal cardiac function by 3-4 months.

Return to play after MIS-C is quite different from that for acute COVID-19. Patients with MIS-C should be treated much like other patients with myocarditis with an expected return to play in 3-6 months and only after cardiac follow-up. Another good-to-remember recommendation is to delay COVID-19 vaccination for at least 90 days after an episode of MIS-C.
 

Vaccine-related myocarditis

Once again, older age appears to be a risk factor because most patients with postvaccine myocarditis have been in their mid-teens to early 20s, with events more likely after the second vaccine dose and also more likely in male children (4:1 ratio to female children). No deaths have occurred from postvaccination myocarditis in patients younger than 30 years. Still, many individuals have exhibited residual MRI enhancement in the cardiac tissue for some time after experiencing postvaccination myocarditis; it’s currently unclear whether that has clinical implications. By comparison, CDC data demonstrates convincingly that the risk for cardiac effects is much greater after acute COVID-19 than after COVID-19 vaccination, with risk ratios often higher than 20, depending on age and condition (for example, myocarditis vs. pericarditis). Data are still insufficient to determine whether clinicians should recommend or avoid COVID-19 vaccination in children with congenital heart disease.

In summary, administering COVID-19 vaccines requires a great deal of shared decision-making with parents, and the clinician’s role is to educate parents about all potential risks related to both the vaccine and COVID-19 illness. Research has consistently shown that acute COVID-19 myocarditis and myocarditis associated with MIS-C are much more likely to occur in unvaccinated youth and more likely than postvaccination myocarditis, regardless of age.

William T. Basco, Jr., MD, MS, is a professor of pediatrics at the Medical University of South Carolina, Charleston, and director of the division of general pediatrics. He is an active health services researcher and has published more than 60 manuscripts in the peer-reviewed literature.

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

The 2022 Pediatric Academic Societies meeting included an excellent session on the acute and delayed effects of COVID-19 on children’s hearts. Data on the risk for cardiac injury during acute COVID-19, return-to-play guidelines after COVID-19–related heart injury, and post–vaccine-associated myocarditis were reviewed.

COVID-induced cardiac injury

The risk for COVID-induced cardiac injury is directly associated with age. Recent Centers for Disease Control and Prevention data revealed a “myocarditis or pericarditis” rate in the range of 12-17 cases per 100,000 SARS-CoV-2 infections among male children aged 5-11 years (lower rates for females); the rate jumps to 50-65 cases per 100,000 infections among male children aged 12-17 years. So cardiac injury caused by acute COVID-19 appears rare, but the risk is clearly associated with male sex and adolescent age.

Return to play after COVID-19

Clinicians may be pressed by patients and parents for advice on return to play after illness with COVID-19. In July 2020, the American College of Cardiology published an algorithm that has been adjusted over time, most recently in 2022 by the American Academy of Pediatrics. These algorithms stratify recommendations by degree of illness. One rule of thumb: Patients with severe COVID-19 (ICU care or multisystem inflammatory syndrome in children [MIS-C]) have only one box on the algorithm, and that is to rest for 3-6 months and only return to usual activity after cardiac clearance. Moderate disease (defined as ≥ 4 days of fever > 100.4 °F; ≥ 1 week of myalgia, chills, lethargy, or any non-ICU hospital stay; and no evidence of MIS-C) require undergoing an ECG to look for cardiac dysfunction, followed by at least 10 days of rest if the ECG is negative or referral for cardiac evaluation if either ECG or exam by a pediatric cardiologist is abnormal.

Clinicians can perhaps be more permissible with patients who are younger or who have had less severe disease. For example, if a patient aged younger than 12 years is asymptomatic with routine activity at the time of evaluation, an ECG is not indicated. For patients aged 12-15 years who are asymptomatic at the time of evaluation but participate in a high-intensity sport, clinicians might consider obtaining an ECG. As few as 3 days of rest might be enough for select patients who are asymptomatic at presentation. For other patients, clinicians should work with parents to introduce activity gradually and make it clear to parents that any activity intolerance requires quick reevaluation. On existing athlete registries, no deaths that are attributable to post–COVID-19 cardiac effects have been confirmed in children; however, all data presented during the session were from prior to the Omicron variant surge in early 2022, so more information may be forthcoming.
 

Considerations for MIS-C

Among children experiencing MIS-C, 35% had ECG changes, 40% exhibited left ventricular systolic or diastolic dysfunction, and 30% had mitral regurgitation, meaning that a large percentage of patients with MIS-C show some degree of cardiac dysfunction. Unfortunately, we are still in the data-gathering phase for long-term outcomes. Functional parameters tend to improve within a week, and most patients will return to normal cardiac function by 3-4 months.

Return to play after MIS-C is quite different from that for acute COVID-19. Patients with MIS-C should be treated much like other patients with myocarditis with an expected return to play in 3-6 months and only after cardiac follow-up. Another good-to-remember recommendation is to delay COVID-19 vaccination for at least 90 days after an episode of MIS-C.
 

Vaccine-related myocarditis

Once again, older age appears to be a risk factor because most patients with postvaccine myocarditis have been in their mid-teens to early 20s, with events more likely after the second vaccine dose and also more likely in male children (4:1 ratio to female children). No deaths have occurred from postvaccination myocarditis in patients younger than 30 years. Still, many individuals have exhibited residual MRI enhancement in the cardiac tissue for some time after experiencing postvaccination myocarditis; it’s currently unclear whether that has clinical implications. By comparison, CDC data demonstrates convincingly that the risk for cardiac effects is much greater after acute COVID-19 than after COVID-19 vaccination, with risk ratios often higher than 20, depending on age and condition (for example, myocarditis vs. pericarditis). Data are still insufficient to determine whether clinicians should recommend or avoid COVID-19 vaccination in children with congenital heart disease.

In summary, administering COVID-19 vaccines requires a great deal of shared decision-making with parents, and the clinician’s role is to educate parents about all potential risks related to both the vaccine and COVID-19 illness. Research has consistently shown that acute COVID-19 myocarditis and myocarditis associated with MIS-C are much more likely to occur in unvaccinated youth and more likely than postvaccination myocarditis, regardless of age.

William T. Basco, Jr., MD, MS, is a professor of pediatrics at the Medical University of South Carolina, Charleston, and director of the division of general pediatrics. He is an active health services researcher and has published more than 60 manuscripts in the peer-reviewed literature.

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

The 2022 Pediatric Academic Societies meeting included an excellent session on the acute and delayed effects of COVID-19 on children’s hearts. Data on the risk for cardiac injury during acute COVID-19, return-to-play guidelines after COVID-19–related heart injury, and post–vaccine-associated myocarditis were reviewed.

COVID-induced cardiac injury

The risk for COVID-induced cardiac injury is directly associated with age. Recent Centers for Disease Control and Prevention data revealed a “myocarditis or pericarditis” rate in the range of 12-17 cases per 100,000 SARS-CoV-2 infections among male children aged 5-11 years (lower rates for females); the rate jumps to 50-65 cases per 100,000 infections among male children aged 12-17 years. So cardiac injury caused by acute COVID-19 appears rare, but the risk is clearly associated with male sex and adolescent age.

Return to play after COVID-19

Clinicians may be pressed by patients and parents for advice on return to play after illness with COVID-19. In July 2020, the American College of Cardiology published an algorithm that has been adjusted over time, most recently in 2022 by the American Academy of Pediatrics. These algorithms stratify recommendations by degree of illness. One rule of thumb: Patients with severe COVID-19 (ICU care or multisystem inflammatory syndrome in children [MIS-C]) have only one box on the algorithm, and that is to rest for 3-6 months and only return to usual activity after cardiac clearance. Moderate disease (defined as ≥ 4 days of fever > 100.4 °F; ≥ 1 week of myalgia, chills, lethargy, or any non-ICU hospital stay; and no evidence of MIS-C) require undergoing an ECG to look for cardiac dysfunction, followed by at least 10 days of rest if the ECG is negative or referral for cardiac evaluation if either ECG or exam by a pediatric cardiologist is abnormal.

Clinicians can perhaps be more permissible with patients who are younger or who have had less severe disease. For example, if a patient aged younger than 12 years is asymptomatic with routine activity at the time of evaluation, an ECG is not indicated. For patients aged 12-15 years who are asymptomatic at the time of evaluation but participate in a high-intensity sport, clinicians might consider obtaining an ECG. As few as 3 days of rest might be enough for select patients who are asymptomatic at presentation. For other patients, clinicians should work with parents to introduce activity gradually and make it clear to parents that any activity intolerance requires quick reevaluation. On existing athlete registries, no deaths that are attributable to post–COVID-19 cardiac effects have been confirmed in children; however, all data presented during the session were from prior to the Omicron variant surge in early 2022, so more information may be forthcoming.
 

Considerations for MIS-C

Among children experiencing MIS-C, 35% had ECG changes, 40% exhibited left ventricular systolic or diastolic dysfunction, and 30% had mitral regurgitation, meaning that a large percentage of patients with MIS-C show some degree of cardiac dysfunction. Unfortunately, we are still in the data-gathering phase for long-term outcomes. Functional parameters tend to improve within a week, and most patients will return to normal cardiac function by 3-4 months.

Return to play after MIS-C is quite different from that for acute COVID-19. Patients with MIS-C should be treated much like other patients with myocarditis with an expected return to play in 3-6 months and only after cardiac follow-up. Another good-to-remember recommendation is to delay COVID-19 vaccination for at least 90 days after an episode of MIS-C.
 

Vaccine-related myocarditis

Once again, older age appears to be a risk factor because most patients with postvaccine myocarditis have been in their mid-teens to early 20s, with events more likely after the second vaccine dose and also more likely in male children (4:1 ratio to female children). No deaths have occurred from postvaccination myocarditis in patients younger than 30 years. Still, many individuals have exhibited residual MRI enhancement in the cardiac tissue for some time after experiencing postvaccination myocarditis; it’s currently unclear whether that has clinical implications. By comparison, CDC data demonstrates convincingly that the risk for cardiac effects is much greater after acute COVID-19 than after COVID-19 vaccination, with risk ratios often higher than 20, depending on age and condition (for example, myocarditis vs. pericarditis). Data are still insufficient to determine whether clinicians should recommend or avoid COVID-19 vaccination in children with congenital heart disease.

In summary, administering COVID-19 vaccines requires a great deal of shared decision-making with parents, and the clinician’s role is to educate parents about all potential risks related to both the vaccine and COVID-19 illness. Research has consistently shown that acute COVID-19 myocarditis and myocarditis associated with MIS-C are much more likely to occur in unvaccinated youth and more likely than postvaccination myocarditis, regardless of age.

William T. Basco, Jr., MD, MS, is a professor of pediatrics at the Medical University of South Carolina, Charleston, and director of the division of general pediatrics. He is an active health services researcher and has published more than 60 manuscripts in the peer-reviewed literature.

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

I had an early attraction to newspapers. As a child growing up in Jersey City, N.J., I delivered them door-to-door. I was editor-in-chief of my high school newspaper and worked as a copy boy and sports reporter on the daily Jersey Journal. At Princeton, I joined the University Press Club, working as a string reporter for the New York Herald Tribune, Philadelphia Inquirer, and Associated Press.

I thought I might become a journalist, but medicine was too strong a calling. During my GI elective as a senior medical resident at New York Hospital, I was able to work with some of the first commercial fiberoptic instruments, which presaged my academic career in endoscopic innovation. I was editor-in-chief of Gastrointestinal Endoscopy from 1988 to 1996, and have been the consulting editor for GI Endoscopy Clinics of North America since 1997.

As the first editor-in-chief of GI & Hepatology News, I had the opportunity to combine a background in peer review with my early newspaper experience. My vision for the new publication was to provide information curated and vetted by experts, in contrast to the torrent pouring down from the Internet that was (pertinent to our specialty) “indigestible.” I put in much effort selecting stories provided by Elsevier Global Medical News, especially in constructing the front page. AGA Institute provided strong support, allowing me to choose an editorial board covering all subspecialties. I wanted to highlight the excitement of researchers balanced by expert review and commentary. The digital version added search features, and I tried to promote the “browse factor” that would also encourage advertising, critical to the success of any newspaper. At the end of my term, I felt I had laid a strong foundation, and have been delighted to see the publication continue to thrive.
 

Charles Lightdale, MD, is professor of medicine at Columbia University Medical Center in New York. He disclosed having no conflicts of interest.

I had an early attraction to newspapers. As a child growing up in Jersey City, N.J., I delivered them door-to-door. I was editor-in-chief of my high school newspaper and worked as a copy boy and sports reporter on the daily Jersey Journal. At Princeton, I joined the University Press Club, working as a string reporter for the New York Herald Tribune, Philadelphia Inquirer, and Associated Press.

I thought I might become a journalist, but medicine was too strong a calling. During my GI elective as a senior medical resident at New York Hospital, I was able to work with some of the first commercial fiberoptic instruments, which presaged my academic career in endoscopic innovation. I was editor-in-chief of Gastrointestinal Endoscopy from 1988 to 1996, and have been the consulting editor for GI Endoscopy Clinics of North America since 1997.

As the first editor-in-chief of GI & Hepatology News, I had the opportunity to combine a background in peer review with my early newspaper experience. My vision for the new publication was to provide information curated and vetted by experts, in contrast to the torrent pouring down from the Internet that was (pertinent to our specialty) “indigestible.” I put in much effort selecting stories provided by Elsevier Global Medical News, especially in constructing the front page. AGA Institute provided strong support, allowing me to choose an editorial board covering all subspecialties. I wanted to highlight the excitement of researchers balanced by expert review and commentary. The digital version added search features, and I tried to promote the “browse factor” that would also encourage advertising, critical to the success of any newspaper. At the end of my term, I felt I had laid a strong foundation, and have been delighted to see the publication continue to thrive.
 

Charles Lightdale, MD, is professor of medicine at Columbia University Medical Center in New York. He disclosed having no conflicts of interest.

I had an early attraction to newspapers. As a child growing up in Jersey City, N.J., I delivered them door-to-door. I was editor-in-chief of my high school newspaper and worked as a copy boy and sports reporter on the daily Jersey Journal. At Princeton, I joined the University Press Club, working as a string reporter for the New York Herald Tribune, Philadelphia Inquirer, and Associated Press.

I thought I might become a journalist, but medicine was too strong a calling. During my GI elective as a senior medical resident at New York Hospital, I was able to work with some of the first commercial fiberoptic instruments, which presaged my academic career in endoscopic innovation. I was editor-in-chief of Gastrointestinal Endoscopy from 1988 to 1996, and have been the consulting editor for GI Endoscopy Clinics of North America since 1997.

As the first editor-in-chief of GI & Hepatology News, I had the opportunity to combine a background in peer review with my early newspaper experience. My vision for the new publication was to provide information curated and vetted by experts, in contrast to the torrent pouring down from the Internet that was (pertinent to our specialty) “indigestible.” I put in much effort selecting stories provided by Elsevier Global Medical News, especially in constructing the front page. AGA Institute provided strong support, allowing me to choose an editorial board covering all subspecialties. I wanted to highlight the excitement of researchers balanced by expert review and commentary. The digital version added search features, and I tried to promote the “browse factor” that would also encourage advertising, critical to the success of any newspaper. At the end of my term, I felt I had laid a strong foundation, and have been delighted to see the publication continue to thrive.
 

Charles Lightdale, MD, is professor of medicine at Columbia University Medical Center in New York. He disclosed having no conflicts of interest.

There is a need to connect mental and physical symptoms in the diagnosis and treatment of psychiatric disorders. Obviously, we are not yet equipped to clearly recognize which neurotransmitters cause which symptoms. The science of defining the underlying mechanisms is lagging behind the clinical needs. However, in this article, we present a few hypothetical clinical cases to emphasize a possible way of analyzing symptoms in order to identify underlying pathology and guide more effective treatment. Our descriptions do not reflect the entire set of symptoms caused by these neurotransmitters; we created them based on what is presently known (or suspected). Additional research is needed to confirm or disprove the hypotheses we present.

In Part 1 (Current Psychiatry, May 2022), we argued that for depression, anxiety, psychosis, and bipolar disorder, development and approval of medications is currently based on descriptive diagnoses, with disregard to the various underlying causes of those conditions. Similar to how the many types of pneumonia are treated differently based on the specific infective agent, we suggested there are various types of depression or chronic pain based on the underlying neuro­transmitter pathology. Such an approach may be extrapolated to anxiety, psychosis, or bipolar disorder, although those conditions are outside the scope of this article. In Part 1, we described serotonin- and dopamine-associated mental and physical symptoms that suggest distinctly different types of depression or chronic pain, and we suggested specific ways of treating those described conditions. Part 2 reflects on pathology that is possibly connected to endorphin and norepinephrine dysfunction. Table 1 outlines medical and psychiatric symptoms that likely reflect endorphin excess^1-16 and deficiency,^1,16-24 and Table 2 lists symptoms that likely reflect norepinephrine excess^16,25-30and deficiency.^16,26,31-39 It is worth noting that both the quantity of neurotransmitters as well as the quality of the transmission (as in receptors, cellular pumps, and distribution mechanisms) are important.

Endorphin excess (Table 1^1-16)

Ms. R is a frustrated chronic pain patient who bitterly complains that despite having seen more than 20 physicians, she does not have an answer to what causes her “all over” pain and headache.^4,5,11 She does not believe that all her laboratory test are normal, and insists that “something is missing.” She aches all over but says she can actually tolerate more pain than others and experiences only a little discomfort during an electromyogram or dental interventions. Though Ms. R is not very susceptible to acute pain,^4,5,9,16 pain all over without an identifiable cause is part of her life.^4,5,11 She says that listening to music and social interactions help decrease her pain.^4,5,10 Ms. R states that opioid medications do not help her pain, though she has a history of opioid overuse and opioid-induced hyperalgesia.^6,11,16

Ms. R tends to overdo pleasureful activities to achieve satisfaction.² She says exercise is particularly satisfying, to the point that she experiences euphoria and a loss of time.⁹ She is angry that her neurologist suggested she see a psychiatrist. Her depression bothers her more than her anxiety.^2,5,7

Ms. R clearly has a self-image problem, alternating between high and low self-esteem. She has a low appetite^1,12,14-16 and sleeps excessively.^2,4,7,9,10 Her mother privately tells you that Ms. R has a history of childhood sexual abuse and lagged in life due to a lack of motivation. Ms. R used to self-mutilate “to feel normal.”¹² Her primary care physician chronically addresses Ms. R’s poorly explained cholestasis and pruritus⁸ as well as dysregulation of blood pressure and heart rate, both of which tend to be low.^12,13,16

Impression. Ms. R shows multiple symptoms associated with endorphin excess. A trial of an opioid antagonist may be reasonable. Dopamine blockade helps with endorphin suppression and also may be used for this patient. Using a low starting dose and a slow titration of such medications would be beneficial due to frequent intolerance issues, especially nausea. Gamma aminobutyric acid-ergic medications modulate the opioid system and may be considered. A serotonin-norepinephrine reuptake inhibitor (SNRI) or mirtazapine may help patients such as Ms. R to control mood and pain through norepinephrine’s influence on endorphins.

Endorphin deficiency (Table 1^1,16-24)

Mr. J complains of low back pain, diffuse body pain, depression, and moodiness.^19,20,24 He is sluggish and plagued by psychomotor retardation.²⁴ All his life, a heightened perception of pain has caused him problems,^19,20 but has not stopped him from engaging in self-mutilation.²⁴ His “unexplained” pain and general body aches seem to be associated with objectively verifiable pain generators (such as bruises and surgical procedures) but this pain is in excess of what would generally be expected. Mr. J describes his low back pain as mild degenerative disc disease and is eager to explain that his wife’s spine is more diseased, yet she has no back pain.

Continue to: Mr. J responds to treatment...

Mr. J responds to treatment with opioids^16,20 but comments that his mood, and not necessarily his pain, improves when he takes these medications.²⁰ He tends to overuse his pain medications, and had run into trouble with his previous pain management physician. Nitrous oxide is remarkably effective during dental procedures.¹⁹ Acupuncture helps to control his pain and mood.¹⁷ Exercise is also rewarding.¹⁸

Mr. J has difficulty achieving orgasm, a decreased sexual drive, and emotional sensitivity.²⁴ He is impulsive.^19,20,24 His baseline mood is low-grade; anxiety bothers him more than depression.^23,24 Mr. J is thin, has a poor appetite,^1,16 and sleeps poorly.²⁴ His primary care physician struggles to help Mr. J to control dysregulation of his heart rate, blood pressure,²¹ and urinary retention,^16,22 as well as episodes of hypoglycemia.^1,16 He reluctantly admits to abusing alcohol, but explains that it helps with his mood and pain better than his prescribed medications.^18,23

Impression. Mr. J exhibits multiple symptoms associated with endorphin deficiency. Short-term use of opioids is warranted, but he should avoid long-term opioid use, and he and his physician should work together to establish strict control of their intake. Buprenorphine would be the opioid of choice for such a patient. Psychiatric treatment, including for alcohol use disorder, should be a mandatory part of his treatment regimen. Behavioral therapy with a focus on finding healthy ways to achieve gratification would be effective. Alternative treatments such as acupuncture may be of value.

Norepinephrine excess (Table 2^16,25-30)

Mr. G comes to the office irritable and angry^28,30 because no one can help him with his intractable headaches.^16,25 He is pale, his breathing is noisy, and he licks his dry lips while sweating.^16,25 His wife is shy and seems to be afraid of her husband, who is easily irritated and edgy.^28,30 His heart rate and blood pressure are high; he has a history of palpitations and chest pain.^16,25 When unhappy, he gets pale, sweaty, tremulous, and nauseous.^16,25 He masks his anxiety with aggression and has impaired concentration, restless sleep, muscle tension, muscle cramps, and abdominal cramps.^27,28,30 Mr. G suffers from frequent nausea.^16,25 His neck is stiff and pupils are dilated; he clenches his teeth and uses a mouth guard for correction of temporomandibular joint disorder.^16,25 His sleep apnea is poorly controlled because he feels entrapped when he uses a continuous positive airway pressure machine.²⁹ He blames his wife for his premature ejaculation and says that she gives him goosebumps.²⁵ His hypervigilance and hyperarousal are torturous to his wife.^27,30 Despite his overall angry state, Mr. G is also constantly fearful.^28,30 He is almost never hungry, does not like crowds, hates your waiting area, and is vocal about his dislike of doctors being late “all the time.”^26,28,30

Comment. Norepinephrine and dopamine functions are connected through common neuronal and glial uptake mechanisms. This is a foundation of norepinephrine excess symptoms crossing over with symptoms of dopamine deficiency.

Continue to: Impression

Impression. Mr. G shows multiple symptoms associated with norepinephrine excess. It is important to avoid caffeine intake in patients with clinical signs of excessive norepinephrine. Beta-blockers and alpha-2 agonists work well in patients such as Mr. G. Benzodiazepines indirectly decrease norepinephrine activity, but need to be used carefully due to the potential for misuse and addiction. In particular, short-acting benzodiazepines such as alprazolam and lorazepam must be avoided due to the induction of CNS instability with rapidly changing medication blood levels. Chlordiazepoxide may be a good choice for a patient such as Mr. G because it has the fewest adverse effects and the lowest abuse potential compared with other benzodiazepines. Avoid SNRIs in such a patient. Using mood-stabilizing antipsychotic medications may be especially warranted in treating Mr. G’s depression and pain.

Norepinephrine deficiency (Table 2^16,26,31-39)

Two years ago, Ms. A was diagnosed with chronic fatigue³¹ and fibromyalgia. She also had been diagnosed with depression and attention-deficit/hyperactivity disorder (ADHD). She presents with concerns of “brain fog,” no energy, low sex drive, and daytime sleepiness.^33,35 Allodynia is widespread.^16,36,37 Ms. A suffers from bulimia; she eats once a day but is still overweight.²⁶ She has orthostatic hypotension in addition to baseline low blood pressure and bradycardia.^16,38,39 Her pupils are almost pinpoint, even when she does not take opioid medications.¹⁶ Her skin is dry and her hair is brittle; deep tendon reflexes are weakened, and her muscle tone is decreased.¹⁶ Ms. A’s constant low mood drives her to drink excessive amounts of caffeine, which she says “helps with daytime sleepiness but does not last”^32,33 and causes heart rhythm problems³⁸ and dyspepsia.¹⁶ She sees that her headaches and body pain are associated with her caffeine intake, but refuses to stop taking caffeine. Her low interest in life and general passivity have caused her many problems, though the problems themselves do not make her feel much.^31,32,39 She is rather indifferent to pleasurable activities, including sex.³¹ Her response to exciting experiences is blunted,³² but she is still frequently tearful.³⁴ Ms. A’s mood does not improve with selective serotonin reuptake inhibitors; she has tried many. She says that she would not come to see a physician, but “my mom told me to.” She resents that her family thinks she is lazy^31,32,39 and blames her ADHD for underperformance in life.^32,33 Ms. A has a family history of chronic pain and Alzheimer disease, and the longer she experiences pain, the worse her memory.³⁵

Comment. As mentioned earlier, because of the norepinephrine/dopamine relationship, symptoms of excess dopamine overlap with symptoms of norepinephrine deficiency.

Impression. Ms. A shows multiple symptoms associated with norepinephrine deficiency. The use of noradrenergic antidepressants (such as SNRIs and mirtazapine)²⁶ and stimulants may be warranted. Physical exercise, participating in social activities, massage, acupuncture, and family support may help with Ms. A’s pain as well as her depression, as might vasopressors.

In Part 3, we will address gamma aminobutyric acid and glutamate.

Bottom Line

Both high and low levels of endorphins and norepinephrine 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

Drug Brand Names

Alprazolam • Xanax
Chlordiazepoxide • Librium
Lorazepam • Ativan
Mirtazapine • Remeron

There is a need to connect mental and physical symptoms in the diagnosis and treatment of psychiatric disorders. Obviously, we are not yet equipped to clearly recognize which neurotransmitters cause which symptoms. The science of defining the underlying mechanisms is lagging behind the clinical needs. However, in this article, we present a few hypothetical clinical cases to emphasize a possible way of analyzing symptoms in order to identify underlying pathology and guide more effective treatment. Our descriptions do not reflect the entire set of symptoms caused by these neurotransmitters; we created them based on what is presently known (or suspected). Additional research is needed to confirm or disprove the hypotheses we present.

In Part 1 (Current Psychiatry, May 2022), we argued that for depression, anxiety, psychosis, and bipolar disorder, development and approval of medications is currently based on descriptive diagnoses, with disregard to the various underlying causes of those conditions. Similar to how the many types of pneumonia are treated differently based on the specific infective agent, we suggested there are various types of depression or chronic pain based on the underlying neuro­transmitter pathology. Such an approach may be extrapolated to anxiety, psychosis, or bipolar disorder, although those conditions are outside the scope of this article. In Part 1, we described serotonin- and dopamine-associated mental and physical symptoms that suggest distinctly different types of depression or chronic pain, and we suggested specific ways of treating those described conditions. Part 2 reflects on pathology that is possibly connected to endorphin and norepinephrine dysfunction. Table 1 outlines medical and psychiatric symptoms that likely reflect endorphin excess^1-16 and deficiency,^1,16-24 and Table 2 lists symptoms that likely reflect norepinephrine excess^16,25-30and deficiency.^16,26,31-39 It is worth noting that both the quantity of neurotransmitters as well as the quality of the transmission (as in receptors, cellular pumps, and distribution mechanisms) are important.

Endorphin excess (Table 1^1-16)

Ms. R is a frustrated chronic pain patient who bitterly complains that despite having seen more than 20 physicians, she does not have an answer to what causes her “all over” pain and headache.^4,5,11 She does not believe that all her laboratory test are normal, and insists that “something is missing.” She aches all over but says she can actually tolerate more pain than others and experiences only a little discomfort during an electromyogram or dental interventions. Though Ms. R is not very susceptible to acute pain,^4,5,9,16 pain all over without an identifiable cause is part of her life.^4,5,11 She says that listening to music and social interactions help decrease her pain.^4,5,10 Ms. R states that opioid medications do not help her pain, though she has a history of opioid overuse and opioid-induced hyperalgesia.^6,11,16

Ms. R tends to overdo pleasureful activities to achieve satisfaction.² She says exercise is particularly satisfying, to the point that she experiences euphoria and a loss of time.⁹ She is angry that her neurologist suggested she see a psychiatrist. Her depression bothers her more than her anxiety.^2,5,7

Ms. R clearly has a self-image problem, alternating between high and low self-esteem. She has a low appetite^1,12,14-16 and sleeps excessively.^2,4,7,9,10 Her mother privately tells you that Ms. R has a history of childhood sexual abuse and lagged in life due to a lack of motivation. Ms. R used to self-mutilate “to feel normal.”¹² Her primary care physician chronically addresses Ms. R’s poorly explained cholestasis and pruritus⁸ as well as dysregulation of blood pressure and heart rate, both of which tend to be low.^12,13,16

Impression. Ms. R shows multiple symptoms associated with endorphin excess. A trial of an opioid antagonist may be reasonable. Dopamine blockade helps with endorphin suppression and also may be used for this patient. Using a low starting dose and a slow titration of such medications would be beneficial due to frequent intolerance issues, especially nausea. Gamma aminobutyric acid-ergic medications modulate the opioid system and may be considered. A serotonin-norepinephrine reuptake inhibitor (SNRI) or mirtazapine may help patients such as Ms. R to control mood and pain through norepinephrine’s influence on endorphins.

Endorphin deficiency (Table 1^1,16-24)

Mr. J complains of low back pain, diffuse body pain, depression, and moodiness.^19,20,24 He is sluggish and plagued by psychomotor retardation.²⁴ All his life, a heightened perception of pain has caused him problems,^19,20 but has not stopped him from engaging in self-mutilation.²⁴ His “unexplained” pain and general body aches seem to be associated with objectively verifiable pain generators (such as bruises and surgical procedures) but this pain is in excess of what would generally be expected. Mr. J describes his low back pain as mild degenerative disc disease and is eager to explain that his wife’s spine is more diseased, yet she has no back pain.

Continue to: Mr. J responds to treatment...

Mr. J responds to treatment with opioids^16,20 but comments that his mood, and not necessarily his pain, improves when he takes these medications.²⁰ He tends to overuse his pain medications, and had run into trouble with his previous pain management physician. Nitrous oxide is remarkably effective during dental procedures.¹⁹ Acupuncture helps to control his pain and mood.¹⁷ Exercise is also rewarding.¹⁸

Mr. J has difficulty achieving orgasm, a decreased sexual drive, and emotional sensitivity.²⁴ He is impulsive.^19,20,24 His baseline mood is low-grade; anxiety bothers him more than depression.^23,24 Mr. J is thin, has a poor appetite,^1,16 and sleeps poorly.²⁴ His primary care physician struggles to help Mr. J to control dysregulation of his heart rate, blood pressure,²¹ and urinary retention,^16,22 as well as episodes of hypoglycemia.^1,16 He reluctantly admits to abusing alcohol, but explains that it helps with his mood and pain better than his prescribed medications.^18,23

Impression. Mr. J exhibits multiple symptoms associated with endorphin deficiency. Short-term use of opioids is warranted, but he should avoid long-term opioid use, and he and his physician should work together to establish strict control of their intake. Buprenorphine would be the opioid of choice for such a patient. Psychiatric treatment, including for alcohol use disorder, should be a mandatory part of his treatment regimen. Behavioral therapy with a focus on finding healthy ways to achieve gratification would be effective. Alternative treatments such as acupuncture may be of value.

Norepinephrine excess (Table 2^16,25-30)

Mr. G comes to the office irritable and angry^28,30 because no one can help him with his intractable headaches.^16,25 He is pale, his breathing is noisy, and he licks his dry lips while sweating.^16,25 His wife is shy and seems to be afraid of her husband, who is easily irritated and edgy.^28,30 His heart rate and blood pressure are high; he has a history of palpitations and chest pain.^16,25 When unhappy, he gets pale, sweaty, tremulous, and nauseous.^16,25 He masks his anxiety with aggression and has impaired concentration, restless sleep, muscle tension, muscle cramps, and abdominal cramps.^27,28,30 Mr. G suffers from frequent nausea.^16,25 His neck is stiff and pupils are dilated; he clenches his teeth and uses a mouth guard for correction of temporomandibular joint disorder.^16,25 His sleep apnea is poorly controlled because he feels entrapped when he uses a continuous positive airway pressure machine.²⁹ He blames his wife for his premature ejaculation and says that she gives him goosebumps.²⁵ His hypervigilance and hyperarousal are torturous to his wife.^27,30 Despite his overall angry state, Mr. G is also constantly fearful.^28,30 He is almost never hungry, does not like crowds, hates your waiting area, and is vocal about his dislike of doctors being late “all the time.”^26,28,30

Comment. Norepinephrine and dopamine functions are connected through common neuronal and glial uptake mechanisms. This is a foundation of norepinephrine excess symptoms crossing over with symptoms of dopamine deficiency.

Continue to: Impression

Impression. Mr. G shows multiple symptoms associated with norepinephrine excess. It is important to avoid caffeine intake in patients with clinical signs of excessive norepinephrine. Beta-blockers and alpha-2 agonists work well in patients such as Mr. G. Benzodiazepines indirectly decrease norepinephrine activity, but need to be used carefully due to the potential for misuse and addiction. In particular, short-acting benzodiazepines such as alprazolam and lorazepam must be avoided due to the induction of CNS instability with rapidly changing medication blood levels. Chlordiazepoxide may be a good choice for a patient such as Mr. G because it has the fewest adverse effects and the lowest abuse potential compared with other benzodiazepines. Avoid SNRIs in such a patient. Using mood-stabilizing antipsychotic medications may be especially warranted in treating Mr. G’s depression and pain.

Norepinephrine deficiency (Table 2^16,26,31-39)

Two years ago, Ms. A was diagnosed with chronic fatigue³¹ and fibromyalgia. She also had been diagnosed with depression and attention-deficit/hyperactivity disorder (ADHD). She presents with concerns of “brain fog,” no energy, low sex drive, and daytime sleepiness.^33,35 Allodynia is widespread.^16,36,37 Ms. A suffers from bulimia; she eats once a day but is still overweight.²⁶ She has orthostatic hypotension in addition to baseline low blood pressure and bradycardia.^16,38,39 Her pupils are almost pinpoint, even when she does not take opioid medications.¹⁶ Her skin is dry and her hair is brittle; deep tendon reflexes are weakened, and her muscle tone is decreased.¹⁶ Ms. A’s constant low mood drives her to drink excessive amounts of caffeine, which she says “helps with daytime sleepiness but does not last”^32,33 and causes heart rhythm problems³⁸ and dyspepsia.¹⁶ She sees that her headaches and body pain are associated with her caffeine intake, but refuses to stop taking caffeine. Her low interest in life and general passivity have caused her many problems, though the problems themselves do not make her feel much.^31,32,39 She is rather indifferent to pleasurable activities, including sex.³¹ Her response to exciting experiences is blunted,³² but she is still frequently tearful.³⁴ Ms. A’s mood does not improve with selective serotonin reuptake inhibitors; she has tried many. She says that she would not come to see a physician, but “my mom told me to.” She resents that her family thinks she is lazy^31,32,39 and blames her ADHD for underperformance in life.^32,33 Ms. A has a family history of chronic pain and Alzheimer disease, and the longer she experiences pain, the worse her memory.³⁵

Comment. As mentioned earlier, because of the norepinephrine/dopamine relationship, symptoms of excess dopamine overlap with symptoms of norepinephrine deficiency.

Impression. Ms. A shows multiple symptoms associated with norepinephrine deficiency. The use of noradrenergic antidepressants (such as SNRIs and mirtazapine)²⁶ and stimulants may be warranted. Physical exercise, participating in social activities, massage, acupuncture, and family support may help with Ms. A’s pain as well as her depression, as might vasopressors.

In Part 3, we will address gamma aminobutyric acid and glutamate.

Bottom Line

Both high and low levels of endorphins and norepinephrine 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

Drug Brand Names

Alprazolam • Xanax
Chlordiazepoxide • Librium
Lorazepam • Ativan
Mirtazapine • Remeron

There is a need to connect mental and physical symptoms in the diagnosis and treatment of psychiatric disorders. Obviously, we are not yet equipped to clearly recognize which neurotransmitters cause which symptoms. The science of defining the underlying mechanisms is lagging behind the clinical needs. However, in this article, we present a few hypothetical clinical cases to emphasize a possible way of analyzing symptoms in order to identify underlying pathology and guide more effective treatment. Our descriptions do not reflect the entire set of symptoms caused by these neurotransmitters; we created them based on what is presently known (or suspected). Additional research is needed to confirm or disprove the hypotheses we present.

In Part 1 (Current Psychiatry, May 2022), we argued that for depression, anxiety, psychosis, and bipolar disorder, development and approval of medications is currently based on descriptive diagnoses, with disregard to the various underlying causes of those conditions. Similar to how the many types of pneumonia are treated differently based on the specific infective agent, we suggested there are various types of depression or chronic pain based on the underlying neuro­transmitter pathology. Such an approach may be extrapolated to anxiety, psychosis, or bipolar disorder, although those conditions are outside the scope of this article. In Part 1, we described serotonin- and dopamine-associated mental and physical symptoms that suggest distinctly different types of depression or chronic pain, and we suggested specific ways of treating those described conditions. Part 2 reflects on pathology that is possibly connected to endorphin and norepinephrine dysfunction. Table 1 outlines medical and psychiatric symptoms that likely reflect endorphin excess^1-16 and deficiency,^1,16-24 and Table 2 lists symptoms that likely reflect norepinephrine excess^16,25-30and deficiency.^16,26,31-39 It is worth noting that both the quantity of neurotransmitters as well as the quality of the transmission (as in receptors, cellular pumps, and distribution mechanisms) are important.

Endorphin excess (Table 1^1-16)

Ms. R is a frustrated chronic pain patient who bitterly complains that despite having seen more than 20 physicians, she does not have an answer to what causes her “all over” pain and headache.^4,5,11 She does not believe that all her laboratory test are normal, and insists that “something is missing.” She aches all over but says she can actually tolerate more pain than others and experiences only a little discomfort during an electromyogram or dental interventions. Though Ms. R is not very susceptible to acute pain,^4,5,9,16 pain all over without an identifiable cause is part of her life.^4,5,11 She says that listening to music and social interactions help decrease her pain.^4,5,10 Ms. R states that opioid medications do not help her pain, though she has a history of opioid overuse and opioid-induced hyperalgesia.^6,11,16

Ms. R tends to overdo pleasureful activities to achieve satisfaction.² She says exercise is particularly satisfying, to the point that she experiences euphoria and a loss of time.⁹ She is angry that her neurologist suggested she see a psychiatrist. Her depression bothers her more than her anxiety.^2,5,7

Ms. R clearly has a self-image problem, alternating between high and low self-esteem. She has a low appetite^1,12,14-16 and sleeps excessively.^2,4,7,9,10 Her mother privately tells you that Ms. R has a history of childhood sexual abuse and lagged in life due to a lack of motivation. Ms. R used to self-mutilate “to feel normal.”¹² Her primary care physician chronically addresses Ms. R’s poorly explained cholestasis and pruritus⁸ as well as dysregulation of blood pressure and heart rate, both of which tend to be low.^12,13,16

Impression. Ms. R shows multiple symptoms associated with endorphin excess. A trial of an opioid antagonist may be reasonable. Dopamine blockade helps with endorphin suppression and also may be used for this patient. Using a low starting dose and a slow titration of such medications would be beneficial due to frequent intolerance issues, especially nausea. Gamma aminobutyric acid-ergic medications modulate the opioid system and may be considered. A serotonin-norepinephrine reuptake inhibitor (SNRI) or mirtazapine may help patients such as Ms. R to control mood and pain through norepinephrine’s influence on endorphins.

Endorphin deficiency (Table 1^1,16-24)

Mr. J complains of low back pain, diffuse body pain, depression, and moodiness.^19,20,24 He is sluggish and plagued by psychomotor retardation.²⁴ All his life, a heightened perception of pain has caused him problems,^19,20 but has not stopped him from engaging in self-mutilation.²⁴ His “unexplained” pain and general body aches seem to be associated with objectively verifiable pain generators (such as bruises and surgical procedures) but this pain is in excess of what would generally be expected. Mr. J describes his low back pain as mild degenerative disc disease and is eager to explain that his wife’s spine is more diseased, yet she has no back pain.

Continue to: Mr. J responds to treatment...

Mr. J responds to treatment with opioids^16,20 but comments that his mood, and not necessarily his pain, improves when he takes these medications.²⁰ He tends to overuse his pain medications, and had run into trouble with his previous pain management physician. Nitrous oxide is remarkably effective during dental procedures.¹⁹ Acupuncture helps to control his pain and mood.¹⁷ Exercise is also rewarding.¹⁸

Mr. J has difficulty achieving orgasm, a decreased sexual drive, and emotional sensitivity.²⁴ He is impulsive.^19,20,24 His baseline mood is low-grade; anxiety bothers him more than depression.^23,24 Mr. J is thin, has a poor appetite,^1,16 and sleeps poorly.²⁴ His primary care physician struggles to help Mr. J to control dysregulation of his heart rate, blood pressure,²¹ and urinary retention,^16,22 as well as episodes of hypoglycemia.^1,16 He reluctantly admits to abusing alcohol, but explains that it helps with his mood and pain better than his prescribed medications.^18,23

Impression. Mr. J exhibits multiple symptoms associated with endorphin deficiency. Short-term use of opioids is warranted, but he should avoid long-term opioid use, and he and his physician should work together to establish strict control of their intake. Buprenorphine would be the opioid of choice for such a patient. Psychiatric treatment, including for alcohol use disorder, should be a mandatory part of his treatment regimen. Behavioral therapy with a focus on finding healthy ways to achieve gratification would be effective. Alternative treatments such as acupuncture may be of value.

Norepinephrine excess (Table 2^16,25-30)

Mr. G comes to the office irritable and angry^28,30 because no one can help him with his intractable headaches.^16,25 He is pale, his breathing is noisy, and he licks his dry lips while sweating.^16,25 His wife is shy and seems to be afraid of her husband, who is easily irritated and edgy.^28,30 His heart rate and blood pressure are high; he has a history of palpitations and chest pain.^16,25 When unhappy, he gets pale, sweaty, tremulous, and nauseous.^16,25 He masks his anxiety with aggression and has impaired concentration, restless sleep, muscle tension, muscle cramps, and abdominal cramps.^27,28,30 Mr. G suffers from frequent nausea.^16,25 His neck is stiff and pupils are dilated; he clenches his teeth and uses a mouth guard for correction of temporomandibular joint disorder.^16,25 His sleep apnea is poorly controlled because he feels entrapped when he uses a continuous positive airway pressure machine.²⁹ He blames his wife for his premature ejaculation and says that she gives him goosebumps.²⁵ His hypervigilance and hyperarousal are torturous to his wife.^27,30 Despite his overall angry state, Mr. G is also constantly fearful.^28,30 He is almost never hungry, does not like crowds, hates your waiting area, and is vocal about his dislike of doctors being late “all the time.”^26,28,30

Comment. Norepinephrine and dopamine functions are connected through common neuronal and glial uptake mechanisms. This is a foundation of norepinephrine excess symptoms crossing over with symptoms of dopamine deficiency.

Continue to: Impression

Impression. Mr. G shows multiple symptoms associated with norepinephrine excess. It is important to avoid caffeine intake in patients with clinical signs of excessive norepinephrine. Beta-blockers and alpha-2 agonists work well in patients such as Mr. G. Benzodiazepines indirectly decrease norepinephrine activity, but need to be used carefully due to the potential for misuse and addiction. In particular, short-acting benzodiazepines such as alprazolam and lorazepam must be avoided due to the induction of CNS instability with rapidly changing medication blood levels. Chlordiazepoxide may be a good choice for a patient such as Mr. G because it has the fewest adverse effects and the lowest abuse potential compared with other benzodiazepines. Avoid SNRIs in such a patient. Using mood-stabilizing antipsychotic medications may be especially warranted in treating Mr. G’s depression and pain.

Norepinephrine deficiency (Table 2^16,26,31-39)

Two years ago, Ms. A was diagnosed with chronic fatigue³¹ and fibromyalgia. She also had been diagnosed with depression and attention-deficit/hyperactivity disorder (ADHD). She presents with concerns of “brain fog,” no energy, low sex drive, and daytime sleepiness.^33,35 Allodynia is widespread.^16,36,37 Ms. A suffers from bulimia; she eats once a day but is still overweight.²⁶ She has orthostatic hypotension in addition to baseline low blood pressure and bradycardia.^16,38,39 Her pupils are almost pinpoint, even when she does not take opioid medications.¹⁶ Her skin is dry and her hair is brittle; deep tendon reflexes are weakened, and her muscle tone is decreased.¹⁶ Ms. A’s constant low mood drives her to drink excessive amounts of caffeine, which she says “helps with daytime sleepiness but does not last”^32,33 and causes heart rhythm problems³⁸ and dyspepsia.¹⁶ She sees that her headaches and body pain are associated with her caffeine intake, but refuses to stop taking caffeine. Her low interest in life and general passivity have caused her many problems, though the problems themselves do not make her feel much.^31,32,39 She is rather indifferent to pleasurable activities, including sex.³¹ Her response to exciting experiences is blunted,³² but she is still frequently tearful.³⁴ Ms. A’s mood does not improve with selective serotonin reuptake inhibitors; she has tried many. She says that she would not come to see a physician, but “my mom told me to.” She resents that her family thinks she is lazy^31,32,39 and blames her ADHD for underperformance in life.^32,33 Ms. A has a family history of chronic pain and Alzheimer disease, and the longer she experiences pain, the worse her memory.³⁵

Comment. As mentioned earlier, because of the norepinephrine/dopamine relationship, symptoms of excess dopamine overlap with symptoms of norepinephrine deficiency.

Impression. Ms. A shows multiple symptoms associated with norepinephrine deficiency. The use of noradrenergic antidepressants (such as SNRIs and mirtazapine)²⁶ and stimulants may be warranted. Physical exercise, participating in social activities, massage, acupuncture, and family support may help with Ms. A’s pain as well as her depression, as might vasopressors.

In Part 3, we will address gamma aminobutyric acid and glutamate.

Bottom Line

Both high and low levels of endorphins and norepinephrine 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

Drug Brand Names

Alprazolam • Xanax
Chlordiazepoxide • Librium
Lorazepam • Ativan
Mirtazapine • Remeron

Having witnessed the devastating impact of stigma on patients with mental illness throughout my psychiatric career, I am fed up and disgusted with this malevolent scourge.

I regard the stigma that engulfs neuropsychiatric disorders as a malignancy that mutilates patients’ souls and hastens their mortality.

Stigma is hate speech

How would you feel if you had a serious medical illness, a disabling brain disorder such as schizophrenia, depression, or anxiety, and people refer to you with pejorative and insulting terms such as crazy, deranged, lunatic, unhinged, nutty, insane, wacky, berserk, cuckoo, bonkers, flaky, screwball, or unglued? This is hate speech generated by stigma against people with mental illness. Individuals with heart disease, cancer, or diabetes never get called such disgraceful and stigmatizing terms that shame, stain, besmirch, and scar them, which happens daily to persons with psychiatric brain disorders.

The damage and harm of the discriminatory stigma on our patients is multifaceted. It is painful, detrimental, pernicious, and deleterious. It is corrosive to their spirits, crippling to their self-image, and subversive to their self-confidence. Hate speech is not simply words, but a menacing weapon that assaults the core humanity of medically ill psychiatric patients.

Although hate speech is punishable by law, there are rarely any legal actions against those who hurl hate speech at psychiatric patients every day. Society has institutionalized the stigma of mental illness and takes it in stride instead of recognizing it as an illegal, harmful act.

Long before the stresses of the COVID-19 pandemic, 43% of the population had been shown to experience a diagnosable psychiatric disorder over the course of their life.¹ Thus, tens of millions of people are burdened by stigma and the hate speech associated with it. This is directly related to massive ignorance about mental illness being the result of a neurobiological condition due to either genetic or intrauterine adverse events that disrupt brain development. Delusions and hallucinations are symptoms of a malfunctioning brain, depression is not a sign of personal weakness, anxiety is the most prevalent mental disorder in the world, and obsessive-compulsive disorder (OCD) is not odd behavior but the result of dysfunction of neural circuits. Correcting public misperceptions about psychiatric brain disorders can mitigate stigma, but it has yet to happen.

Stigma is a hate crime

Stigma can accelerate physical death and premature mortality. Many studies have confirmed that persons with schizophrenia do not receive basic primary care treatments for the life-shortening medical conditions that often afflict them, such as diabetes, dyslipidemia, and hypertension.² Stigma is responsible for a significant disparity of medical^3-5 and intensive care⁶ among individuals with mental illness compared to the general population. It’s no wonder most psychiatric disorders are associated with accelerated mortality.⁷ A recent study during the pandemic by Balasuriya et al⁸ reported that patients with depression had poor access to care. Stigma interferes with or delays necessary medical care, leading to clinical deterioration and unnecessary, preventable death. Stigma shortens life and is a hate crime.

Continue to: The extremely high suicide rates...

The extremely high suicide rates among individuals with serious mental illness, who live under the oppressiveness of stigma, is another example of how stigma is a hate crime that can cause patients with psychiatric disorders to give up and end their lives. Zaheer et al⁹ found that young patients with schizophrenia had an astronomical suicide rate compared to the general population (1 in 52 in individuals with schizophrenia, compared to 12 in 100,000 in the general population, roughly a 200-fold increase!). This is clearly a consequence of stigma and discrimination,¹⁰ which leads to demoralization, shame, loneliness, distress, and hopelessness. Stigma can be fatal, and that makes it a hate crime.

Stigma also limits vocational opportunities for individuals with mental illness. They are either not hired, or quickly fired. Even highly educated professionals such as physicians, nurses, lawyers, or teachers can lose their jobs if they divulge a history of a psychiatric disorder or alcohol or substance abuse, regardless of whether they are receiving treatment and are medically in remission. Even highly qualified politicians have been deemed “ineligible” for higher office if they disclose a history of psychiatric treatment. Stigma is loaded with outrageous discrimination that deprives our patients of “the pursuit of happiness,” a fundamental constitutional right.

Stigma surrounding the mental health professions

Stigma also engulfs mental health professionals, simply because they deal with psychiatric patients every day. In a classic article titled “The Enigma of Stigma,”¹¹ Dr. Paul Fink, past president of the American Psychiatric Association (1988-1989), described how psychiatrists are perceived as “different” from other physicians by the public and by the media. He said psychiatrists are tarred by the same brush as their patients as “undesirables” in society. And movies such as Psycho and One Flew Over the Cuckoo’s Nest reinforce the stigma against both psychiatric patients and the psychiatrists and nurses who treat them. The health care system that carves out “behavioral health” from the umbrella of “medical care” further accentuates the stigma by portraying the “separateness” of psychiatry, a genuine medical specialty, from its fellow medical disciplines. This becomes fodder for the antipsychiatry movement at every turn and can even lead to questioning the existence of mental illness, as Thomas Szasz¹² did by declaring that mental illness is a myth and describing psychiatry as “the science of lies.” No other medical specialty endures abuse and insults like psychiatry, and that’s a direct result of stigma.

Extinguishing stigma is a societal imperative

So what can be done to squelch stigma and defeat it once and for all, so that psychiatric patients can be treated with dignity and compassion, like people with cancer, heart attacks, diabetes, or brain tumors? The pandemic, terrible as it has been for the entire world, did have the silver lining of raising awareness about the ubiquity of psychiatric symptoms, such as anxiety and depression, across all ages, genders, educational and religious backgrounds, and socioeconomic classes. But there should also be a robust legal battle against the damaging effects of stigma. There are laws to sanction and penalize hate speech and hate crimes that must be implemented when stigma is documented. There are also parity laws, but they have no teeth and have not ameliorated the insurance discrepancies and economic burden of psychiatric disorders. A bold step would be to reclassify serious psychiatric brain disorders (schizophrenia, bipolar disorder, major depressive disorder, OCD, attention-deficit/hyperactivity disorder, generalized anxiety disorder/panic attacks, and borderline personality disorder) as neurologic disorders, which would automatically give patients with these disorders broad access to medical care, which happened when autism was reclassified as a neurologic disorder. Finally, a much more intensive public education must be disseminated about the neurobiological etiologies, brain structure, and function in psychiatric disorders, and the psychiatric symptoms associated with all neurologic disorders. Regrettably, empathy can be difficult to teach.

Stigma is hate speech and a hate crime. It must be permanently eliminated by effective laws and by erasing the widespread ignorance about the medical and neurologic roots of mental disorders, and by emphasizing the fact that they are as treatable as other general medical conditions.

Having witnessed the devastating impact of stigma on patients with mental illness throughout my psychiatric career, I am fed up and disgusted with this malevolent scourge.

I regard the stigma that engulfs neuropsychiatric disorders as a malignancy that mutilates patients’ souls and hastens their mortality.

Stigma is hate speech

How would you feel if you had a serious medical illness, a disabling brain disorder such as schizophrenia, depression, or anxiety, and people refer to you with pejorative and insulting terms such as crazy, deranged, lunatic, unhinged, nutty, insane, wacky, berserk, cuckoo, bonkers, flaky, screwball, or unglued? This is hate speech generated by stigma against people with mental illness. Individuals with heart disease, cancer, or diabetes never get called such disgraceful and stigmatizing terms that shame, stain, besmirch, and scar them, which happens daily to persons with psychiatric brain disorders.

The damage and harm of the discriminatory stigma on our patients is multifaceted. It is painful, detrimental, pernicious, and deleterious. It is corrosive to their spirits, crippling to their self-image, and subversive to their self-confidence. Hate speech is not simply words, but a menacing weapon that assaults the core humanity of medically ill psychiatric patients.

Although hate speech is punishable by law, there are rarely any legal actions against those who hurl hate speech at psychiatric patients every day. Society has institutionalized the stigma of mental illness and takes it in stride instead of recognizing it as an illegal, harmful act.

Long before the stresses of the COVID-19 pandemic, 43% of the population had been shown to experience a diagnosable psychiatric disorder over the course of their life.¹ Thus, tens of millions of people are burdened by stigma and the hate speech associated with it. This is directly related to massive ignorance about mental illness being the result of a neurobiological condition due to either genetic or intrauterine adverse events that disrupt brain development. Delusions and hallucinations are symptoms of a malfunctioning brain, depression is not a sign of personal weakness, anxiety is the most prevalent mental disorder in the world, and obsessive-compulsive disorder (OCD) is not odd behavior but the result of dysfunction of neural circuits. Correcting public misperceptions about psychiatric brain disorders can mitigate stigma, but it has yet to happen.

Stigma is a hate crime

Stigma can accelerate physical death and premature mortality. Many studies have confirmed that persons with schizophrenia do not receive basic primary care treatments for the life-shortening medical conditions that often afflict them, such as diabetes, dyslipidemia, and hypertension.² Stigma is responsible for a significant disparity of medical^3-5 and intensive care⁶ among individuals with mental illness compared to the general population. It’s no wonder most psychiatric disorders are associated with accelerated mortality.⁷ A recent study during the pandemic by Balasuriya et al⁸ reported that patients with depression had poor access to care. Stigma interferes with or delays necessary medical care, leading to clinical deterioration and unnecessary, preventable death. Stigma shortens life and is a hate crime.

Continue to: The extremely high suicide rates...

The extremely high suicide rates among individuals with serious mental illness, who live under the oppressiveness of stigma, is another example of how stigma is a hate crime that can cause patients with psychiatric disorders to give up and end their lives. Zaheer et al⁹ found that young patients with schizophrenia had an astronomical suicide rate compared to the general population (1 in 52 in individuals with schizophrenia, compared to 12 in 100,000 in the general population, roughly a 200-fold increase!). This is clearly a consequence of stigma and discrimination,¹⁰ which leads to demoralization, shame, loneliness, distress, and hopelessness. Stigma can be fatal, and that makes it a hate crime.

Stigma also limits vocational opportunities for individuals with mental illness. They are either not hired, or quickly fired. Even highly educated professionals such as physicians, nurses, lawyers, or teachers can lose their jobs if they divulge a history of a psychiatric disorder or alcohol or substance abuse, regardless of whether they are receiving treatment and are medically in remission. Even highly qualified politicians have been deemed “ineligible” for higher office if they disclose a history of psychiatric treatment. Stigma is loaded with outrageous discrimination that deprives our patients of “the pursuit of happiness,” a fundamental constitutional right.

Stigma surrounding the mental health professions

Stigma also engulfs mental health professionals, simply because they deal with psychiatric patients every day. In a classic article titled “The Enigma of Stigma,”¹¹ Dr. Paul Fink, past president of the American Psychiatric Association (1988-1989), described how psychiatrists are perceived as “different” from other physicians by the public and by the media. He said psychiatrists are tarred by the same brush as their patients as “undesirables” in society. And movies such as Psycho and One Flew Over the Cuckoo’s Nest reinforce the stigma against both psychiatric patients and the psychiatrists and nurses who treat them. The health care system that carves out “behavioral health” from the umbrella of “medical care” further accentuates the stigma by portraying the “separateness” of psychiatry, a genuine medical specialty, from its fellow medical disciplines. This becomes fodder for the antipsychiatry movement at every turn and can even lead to questioning the existence of mental illness, as Thomas Szasz¹² did by declaring that mental illness is a myth and describing psychiatry as “the science of lies.” No other medical specialty endures abuse and insults like psychiatry, and that’s a direct result of stigma.

Extinguishing stigma is a societal imperative

So what can be done to squelch stigma and defeat it once and for all, so that psychiatric patients can be treated with dignity and compassion, like people with cancer, heart attacks, diabetes, or brain tumors? The pandemic, terrible as it has been for the entire world, did have the silver lining of raising awareness about the ubiquity of psychiatric symptoms, such as anxiety and depression, across all ages, genders, educational and religious backgrounds, and socioeconomic classes. But there should also be a robust legal battle against the damaging effects of stigma. There are laws to sanction and penalize hate speech and hate crimes that must be implemented when stigma is documented. There are also parity laws, but they have no teeth and have not ameliorated the insurance discrepancies and economic burden of psychiatric disorders. A bold step would be to reclassify serious psychiatric brain disorders (schizophrenia, bipolar disorder, major depressive disorder, OCD, attention-deficit/hyperactivity disorder, generalized anxiety disorder/panic attacks, and borderline personality disorder) as neurologic disorders, which would automatically give patients with these disorders broad access to medical care, which happened when autism was reclassified as a neurologic disorder. Finally, a much more intensive public education must be disseminated about the neurobiological etiologies, brain structure, and function in psychiatric disorders, and the psychiatric symptoms associated with all neurologic disorders. Regrettably, empathy can be difficult to teach.

Stigma is hate speech and a hate crime. It must be permanently eliminated by effective laws and by erasing the widespread ignorance about the medical and neurologic roots of mental disorders, and by emphasizing the fact that they are as treatable as other general medical conditions.

Having witnessed the devastating impact of stigma on patients with mental illness throughout my psychiatric career, I am fed up and disgusted with this malevolent scourge.

I regard the stigma that engulfs neuropsychiatric disorders as a malignancy that mutilates patients’ souls and hastens their mortality.

Stigma is hate speech

How would you feel if you had a serious medical illness, a disabling brain disorder such as schizophrenia, depression, or anxiety, and people refer to you with pejorative and insulting terms such as crazy, deranged, lunatic, unhinged, nutty, insane, wacky, berserk, cuckoo, bonkers, flaky, screwball, or unglued? This is hate speech generated by stigma against people with mental illness. Individuals with heart disease, cancer, or diabetes never get called such disgraceful and stigmatizing terms that shame, stain, besmirch, and scar them, which happens daily to persons with psychiatric brain disorders.

The damage and harm of the discriminatory stigma on our patients is multifaceted. It is painful, detrimental, pernicious, and deleterious. It is corrosive to their spirits, crippling to their self-image, and subversive to their self-confidence. Hate speech is not simply words, but a menacing weapon that assaults the core humanity of medically ill psychiatric patients.

Although hate speech is punishable by law, there are rarely any legal actions against those who hurl hate speech at psychiatric patients every day. Society has institutionalized the stigma of mental illness and takes it in stride instead of recognizing it as an illegal, harmful act.

Long before the stresses of the COVID-19 pandemic, 43% of the population had been shown to experience a diagnosable psychiatric disorder over the course of their life.¹ Thus, tens of millions of people are burdened by stigma and the hate speech associated with it. This is directly related to massive ignorance about mental illness being the result of a neurobiological condition due to either genetic or intrauterine adverse events that disrupt brain development. Delusions and hallucinations are symptoms of a malfunctioning brain, depression is not a sign of personal weakness, anxiety is the most prevalent mental disorder in the world, and obsessive-compulsive disorder (OCD) is not odd behavior but the result of dysfunction of neural circuits. Correcting public misperceptions about psychiatric brain disorders can mitigate stigma, but it has yet to happen.

Stigma is a hate crime

Stigma can accelerate physical death and premature mortality. Many studies have confirmed that persons with schizophrenia do not receive basic primary care treatments for the life-shortening medical conditions that often afflict them, such as diabetes, dyslipidemia, and hypertension.² Stigma is responsible for a significant disparity of medical^3-5 and intensive care⁶ among individuals with mental illness compared to the general population. It’s no wonder most psychiatric disorders are associated with accelerated mortality.⁷ A recent study during the pandemic by Balasuriya et al⁸ reported that patients with depression had poor access to care. Stigma interferes with or delays necessary medical care, leading to clinical deterioration and unnecessary, preventable death. Stigma shortens life and is a hate crime.

Continue to: The extremely high suicide rates...

The extremely high suicide rates among individuals with serious mental illness, who live under the oppressiveness of stigma, is another example of how stigma is a hate crime that can cause patients with psychiatric disorders to give up and end their lives. Zaheer et al⁹ found that young patients with schizophrenia had an astronomical suicide rate compared to the general population (1 in 52 in individuals with schizophrenia, compared to 12 in 100,000 in the general population, roughly a 200-fold increase!). This is clearly a consequence of stigma and discrimination,¹⁰ which leads to demoralization, shame, loneliness, distress, and hopelessness. Stigma can be fatal, and that makes it a hate crime.

Stigma also limits vocational opportunities for individuals with mental illness. They are either not hired, or quickly fired. Even highly educated professionals such as physicians, nurses, lawyers, or teachers can lose their jobs if they divulge a history of a psychiatric disorder or alcohol or substance abuse, regardless of whether they are receiving treatment and are medically in remission. Even highly qualified politicians have been deemed “ineligible” for higher office if they disclose a history of psychiatric treatment. Stigma is loaded with outrageous discrimination that deprives our patients of “the pursuit of happiness,” a fundamental constitutional right.

Stigma surrounding the mental health professions

Stigma also engulfs mental health professionals, simply because they deal with psychiatric patients every day. In a classic article titled “The Enigma of Stigma,”¹¹ Dr. Paul Fink, past president of the American Psychiatric Association (1988-1989), described how psychiatrists are perceived as “different” from other physicians by the public and by the media. He said psychiatrists are tarred by the same brush as their patients as “undesirables” in society. And movies such as Psycho and One Flew Over the Cuckoo’s Nest reinforce the stigma against both psychiatric patients and the psychiatrists and nurses who treat them. The health care system that carves out “behavioral health” from the umbrella of “medical care” further accentuates the stigma by portraying the “separateness” of psychiatry, a genuine medical specialty, from its fellow medical disciplines. This becomes fodder for the antipsychiatry movement at every turn and can even lead to questioning the existence of mental illness, as Thomas Szasz¹² did by declaring that mental illness is a myth and describing psychiatry as “the science of lies.” No other medical specialty endures abuse and insults like psychiatry, and that’s a direct result of stigma.

Extinguishing stigma is a societal imperative

So what can be done to squelch stigma and defeat it once and for all, so that psychiatric patients can be treated with dignity and compassion, like people with cancer, heart attacks, diabetes, or brain tumors? The pandemic, terrible as it has been for the entire world, did have the silver lining of raising awareness about the ubiquity of psychiatric symptoms, such as anxiety and depression, across all ages, genders, educational and religious backgrounds, and socioeconomic classes. But there should also be a robust legal battle against the damaging effects of stigma. There are laws to sanction and penalize hate speech and hate crimes that must be implemented when stigma is documented. There are also parity laws, but they have no teeth and have not ameliorated the insurance discrepancies and economic burden of psychiatric disorders. A bold step would be to reclassify serious psychiatric brain disorders (schizophrenia, bipolar disorder, major depressive disorder, OCD, attention-deficit/hyperactivity disorder, generalized anxiety disorder/panic attacks, and borderline personality disorder) as neurologic disorders, which would automatically give patients with these disorders broad access to medical care, which happened when autism was reclassified as a neurologic disorder. Finally, a much more intensive public education must be disseminated about the neurobiological etiologies, brain structure, and function in psychiatric disorders, and the psychiatric symptoms associated with all neurologic disorders. Regrettably, empathy can be difficult to teach.

Stigma is hate speech and a hate crime. It must be permanently eliminated by effective laws and by erasing the widespread ignorance about the medical and neurologic roots of mental disorders, and by emphasizing the fact that they are as treatable as other general medical conditions.

Ramadan is one of the obligatory pillars in Islam during which healthy Muslims are required to fast from dawn until sunset every day for 1 month. There are an estimated 3.45 million Muslims in the United States, and this population will continue to grow by 100,000 per year.¹ With the increased growth of the Muslim population, it is important for clinicians to be aware of how patients of Muslim faith are affected during Ramadan. In this article, we explore the potential risks, as well as the benefits, the month of Ramadan brings to patients. We will also explain how being religiously aware is necessary to provide optimal care for these individuals.

For some patients, fasting may pose risks

Similar to other communities in the United States, individuals who are Muslim experience mood disorders, anxiety disorders, posttraumatic stress disorder, obsessive-compulsive disorder, schizophrenia, substance use disorders, and other psychiatric illnesses.² During the month of Ramadan, Muslims are to abstain completely from eating and drinking from dawn until sunset. This includes medications as well as food and drink.

Due to these circumstances, patients will often change the timing, frequency, and dosing of their medications to allow them to fast. One study found 60% of Muslims made medication adjustments during Ramadan without seeking medical advice.³ It is possible that such alterations may be detrimental. During Ramadan, some Muslims wake up early in the morning to eat a pre-dawn meal, and often go back to sleep. This has been reported to cause a delay in sleep-wake times and to reduce rapid eye movement sleep.⁴ These circadian rhythm changes can be detrimental to patients with bipolar disorder. One study found higher rates of relapse to depression and mania in patients with bipolar disorder who were fasting during Ramadan.⁵ Circadian rhythm disturbances also may worsen depression.⁶ Another point of concern is patients with eating disorders. One small case series (N = 6) found that fasting during Ramadan exacerbated symptoms in patients with eating disorders.⁷

Another concern is that dehydration while fasting can lead to lithium toxicity. However, one study found lithium levels remained stable while fasting for 10 to 12 hours.⁵ Another showed that changing lithium dosing from twice a day to once a day allowed for easier administration without causing a subtherapeutic change in blood lithium levels.⁸

The practice also may have benefits for mental health

For many Muslims, Ramadan is the best time of the year, where they reconnect with their religion and experience the utmost spiritual growth. Studies have shown that the incidence of suicide is lowest during Ramadan compared to other months.⁹ A study of older men found that intermittent fasting and calorie restriction (not during Ramadan) resulted in decreases in tension, confusion, anger, and mood disturbance.¹⁰ Another study found that fasting during Ramadan had a positive impact on depression, anxiety, stress, and cognitive function.¹¹

Clinical considerations

To provide the best care for Muslim patients during Ramadan, clinicians should take a holistic approach and take all factors into consideration. It is common for circadian rhythm disruptions to exacerbate mood disorders, so encourage patients to maintain healthy sleep hygiene to their best ability during this month. Another important consideration is medication timing and dosing.¹² For patients prescribed a medication that typically is taken twice a day, determine if this dosing can be changed to once a day, or if both doses can be taken when it is permissible to eat (sunset to dawn). For medications that are absorbed with food, consider how these medications might be adjusted and maintained while a patient is fasting. Some medications may be sedating or activating, so the timing of administration may need to be adjusted to meet the patient’s needs. Lastly, keep in mind that certain medications can have withdrawal effects, and the likelihood of this occurring while a patient is fasting.

One vital point is that if a patient is at high risk of clinically decompensating due to fasting or medication adjustments or discontinuation, advise them to not fast. Muslims with physical or mental illnesses are excused from fasting. Bear in mind that because Ramadan is meant to be a month of heightened spirituality, many Muslims will prefer to fast.

Ramadan is one of the obligatory pillars in Islam during which healthy Muslims are required to fast from dawn until sunset every day for 1 month. There are an estimated 3.45 million Muslims in the United States, and this population will continue to grow by 100,000 per year.¹ With the increased growth of the Muslim population, it is important for clinicians to be aware of how patients of Muslim faith are affected during Ramadan. In this article, we explore the potential risks, as well as the benefits, the month of Ramadan brings to patients. We will also explain how being religiously aware is necessary to provide optimal care for these individuals.

For some patients, fasting may pose risks

Similar to other communities in the United States, individuals who are Muslim experience mood disorders, anxiety disorders, posttraumatic stress disorder, obsessive-compulsive disorder, schizophrenia, substance use disorders, and other psychiatric illnesses.² During the month of Ramadan, Muslims are to abstain completely from eating and drinking from dawn until sunset. This includes medications as well as food and drink.

Due to these circumstances, patients will often change the timing, frequency, and dosing of their medications to allow them to fast. One study found 60% of Muslims made medication adjustments during Ramadan without seeking medical advice.³ It is possible that such alterations may be detrimental. During Ramadan, some Muslims wake up early in the morning to eat a pre-dawn meal, and often go back to sleep. This has been reported to cause a delay in sleep-wake times and to reduce rapid eye movement sleep.⁴ These circadian rhythm changes can be detrimental to patients with bipolar disorder. One study found higher rates of relapse to depression and mania in patients with bipolar disorder who were fasting during Ramadan.⁵ Circadian rhythm disturbances also may worsen depression.⁶ Another point of concern is patients with eating disorders. One small case series (N = 6) found that fasting during Ramadan exacerbated symptoms in patients with eating disorders.⁷

Another concern is that dehydration while fasting can lead to lithium toxicity. However, one study found lithium levels remained stable while fasting for 10 to 12 hours.⁵ Another showed that changing lithium dosing from twice a day to once a day allowed for easier administration without causing a subtherapeutic change in blood lithium levels.⁸

The practice also may have benefits for mental health

For many Muslims, Ramadan is the best time of the year, where they reconnect with their religion and experience the utmost spiritual growth. Studies have shown that the incidence of suicide is lowest during Ramadan compared to other months.⁹ A study of older men found that intermittent fasting and calorie restriction (not during Ramadan) resulted in decreases in tension, confusion, anger, and mood disturbance.¹⁰ Another study found that fasting during Ramadan had a positive impact on depression, anxiety, stress, and cognitive function.¹¹

Clinical considerations

To provide the best care for Muslim patients during Ramadan, clinicians should take a holistic approach and take all factors into consideration. It is common for circadian rhythm disruptions to exacerbate mood disorders, so encourage patients to maintain healthy sleep hygiene to their best ability during this month. Another important consideration is medication timing and dosing.¹² For patients prescribed a medication that typically is taken twice a day, determine if this dosing can be changed to once a day, or if both doses can be taken when it is permissible to eat (sunset to dawn). For medications that are absorbed with food, consider how these medications might be adjusted and maintained while a patient is fasting. Some medications may be sedating or activating, so the timing of administration may need to be adjusted to meet the patient’s needs. Lastly, keep in mind that certain medications can have withdrawal effects, and the likelihood of this occurring while a patient is fasting.

One vital point is that if a patient is at high risk of clinically decompensating due to fasting or medication adjustments or discontinuation, advise them to not fast. Muslims with physical or mental illnesses are excused from fasting. Bear in mind that because Ramadan is meant to be a month of heightened spirituality, many Muslims will prefer to fast.

Ramadan is one of the obligatory pillars in Islam during which healthy Muslims are required to fast from dawn until sunset every day for 1 month. There are an estimated 3.45 million Muslims in the United States, and this population will continue to grow by 100,000 per year.¹ With the increased growth of the Muslim population, it is important for clinicians to be aware of how patients of Muslim faith are affected during Ramadan. In this article, we explore the potential risks, as well as the benefits, the month of Ramadan brings to patients. We will also explain how being religiously aware is necessary to provide optimal care for these individuals.

For some patients, fasting may pose risks

Similar to other communities in the United States, individuals who are Muslim experience mood disorders, anxiety disorders, posttraumatic stress disorder, obsessive-compulsive disorder, schizophrenia, substance use disorders, and other psychiatric illnesses.² During the month of Ramadan, Muslims are to abstain completely from eating and drinking from dawn until sunset. This includes medications as well as food and drink.

Due to these circumstances, patients will often change the timing, frequency, and dosing of their medications to allow them to fast. One study found 60% of Muslims made medication adjustments during Ramadan without seeking medical advice.³ It is possible that such alterations may be detrimental. During Ramadan, some Muslims wake up early in the morning to eat a pre-dawn meal, and often go back to sleep. This has been reported to cause a delay in sleep-wake times and to reduce rapid eye movement sleep.⁴ These circadian rhythm changes can be detrimental to patients with bipolar disorder. One study found higher rates of relapse to depression and mania in patients with bipolar disorder who were fasting during Ramadan.⁵ Circadian rhythm disturbances also may worsen depression.⁶ Another point of concern is patients with eating disorders. One small case series (N = 6) found that fasting during Ramadan exacerbated symptoms in patients with eating disorders.⁷

Another concern is that dehydration while fasting can lead to lithium toxicity. However, one study found lithium levels remained stable while fasting for 10 to 12 hours.⁵ Another showed that changing lithium dosing from twice a day to once a day allowed for easier administration without causing a subtherapeutic change in blood lithium levels.⁸

The practice also may have benefits for mental health

For many Muslims, Ramadan is the best time of the year, where they reconnect with their religion and experience the utmost spiritual growth. Studies have shown that the incidence of suicide is lowest during Ramadan compared to other months.⁹ A study of older men found that intermittent fasting and calorie restriction (not during Ramadan) resulted in decreases in tension, confusion, anger, and mood disturbance.¹⁰ Another study found that fasting during Ramadan had a positive impact on depression, anxiety, stress, and cognitive function.¹¹

Clinical considerations

To provide the best care for Muslim patients during Ramadan, clinicians should take a holistic approach and take all factors into consideration. It is common for circadian rhythm disruptions to exacerbate mood disorders, so encourage patients to maintain healthy sleep hygiene to their best ability during this month. Another important consideration is medication timing and dosing.¹² For patients prescribed a medication that typically is taken twice a day, determine if this dosing can be changed to once a day, or if both doses can be taken when it is permissible to eat (sunset to dawn). For medications that are absorbed with food, consider how these medications might be adjusted and maintained while a patient is fasting. Some medications may be sedating or activating, so the timing of administration may need to be adjusted to meet the patient’s needs. Lastly, keep in mind that certain medications can have withdrawal effects, and the likelihood of this occurring while a patient is fasting.

One vital point is that if a patient is at high risk of clinically decompensating due to fasting or medication adjustments or discontinuation, advise them to not fast. Muslims with physical or mental illnesses are excused from fasting. Bear in mind that because Ramadan is meant to be a month of heightened spirituality, many Muslims will prefer to fast.

The inaugural issue of GI & Hepatology News was published in January 2007, and the newspaper has gone on to become part of the fabric of the AGA. This year, we celebrate the newspaper’s 15th year with a special 15th Anniversary Series that will run from June through December 2022. We will feature reflections from GIHN’s three former editors-in-chief, Dr. Charles J. Lightdale, Dr. Colin Howden, and Dr. John Allen, on the evolution of the newspaper (and the field of GI) over the past 15 years. We also will present a series of Then and Now columns, highlighting high-impact areas of GI and hepatology covered in past GIHN issues, and reflecting on how the field has changed since that time.

In this month’s issue, we are pleased to kick off the 15th Anniversary Series with reflections by Dr. Lightdale, GIHN’s inaugural editor-in-chief, as well as a Then and Now column written by Dr. Kimberly M. Persley (GIHN associate editor and longstanding AGA member) reflecting on how the demographics of gastroenterology and of the AGA as an organization have changed over the past 15 years. I hope you will find these special contributions to be engaging and thought-provoking. Other issue highlights include a lead article describing impacts of social determinants of health in driving disparities in IBD care and offering recommendations for achieving IBD health equity, a new AGA Clinical Practice Update on dietary options for our many patients with irritable bowel syndrome, and new data on the safety of anti-TNF medications prior to surgery in patients with inflammatory bowel disease.

As summer vacation season commences, I hope you will join me in taking some well-deserved time away from work demands, spending some quality time with friends and family, and seizing the opportunity to rest and recharge.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

The inaugural issue of GI & Hepatology News was published in January 2007, and the newspaper has gone on to become part of the fabric of the AGA. This year, we celebrate the newspaper’s 15th year with a special 15th Anniversary Series that will run from June through December 2022. We will feature reflections from GIHN’s three former editors-in-chief, Dr. Charles J. Lightdale, Dr. Colin Howden, and Dr. John Allen, on the evolution of the newspaper (and the field of GI) over the past 15 years. We also will present a series of Then and Now columns, highlighting high-impact areas of GI and hepatology covered in past GIHN issues, and reflecting on how the field has changed since that time.

In this month’s issue, we are pleased to kick off the 15th Anniversary Series with reflections by Dr. Lightdale, GIHN’s inaugural editor-in-chief, as well as a Then and Now column written by Dr. Kimberly M. Persley (GIHN associate editor and longstanding AGA member) reflecting on how the demographics of gastroenterology and of the AGA as an organization have changed over the past 15 years. I hope you will find these special contributions to be engaging and thought-provoking. Other issue highlights include a lead article describing impacts of social determinants of health in driving disparities in IBD care and offering recommendations for achieving IBD health equity, a new AGA Clinical Practice Update on dietary options for our many patients with irritable bowel syndrome, and new data on the safety of anti-TNF medications prior to surgery in patients with inflammatory bowel disease.

As summer vacation season commences, I hope you will join me in taking some well-deserved time away from work demands, spending some quality time with friends and family, and seizing the opportunity to rest and recharge.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

The inaugural issue of GI & Hepatology News was published in January 2007, and the newspaper has gone on to become part of the fabric of the AGA. This year, we celebrate the newspaper’s 15th year with a special 15th Anniversary Series that will run from June through December 2022. We will feature reflections from GIHN’s three former editors-in-chief, Dr. Charles J. Lightdale, Dr. Colin Howden, and Dr. John Allen, on the evolution of the newspaper (and the field of GI) over the past 15 years. We also will present a series of Then and Now columns, highlighting high-impact areas of GI and hepatology covered in past GIHN issues, and reflecting on how the field has changed since that time.

In this month’s issue, we are pleased to kick off the 15th Anniversary Series with reflections by Dr. Lightdale, GIHN’s inaugural editor-in-chief, as well as a Then and Now column written by Dr. Kimberly M. Persley (GIHN associate editor and longstanding AGA member) reflecting on how the demographics of gastroenterology and of the AGA as an organization have changed over the past 15 years. I hope you will find these special contributions to be engaging and thought-provoking. Other issue highlights include a lead article describing impacts of social determinants of health in driving disparities in IBD care and offering recommendations for achieving IBD health equity, a new AGA Clinical Practice Update on dietary options for our many patients with irritable bowel syndrome, and new data on the safety of anti-TNF medications prior to surgery in patients with inflammatory bowel disease.

As summer vacation season commences, I hope you will join me in taking some well-deserved time away from work demands, spending some quality time with friends and family, and seizing the opportunity to rest and recharge.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

Here we go again, and again, and again.

There just aren’t enough tears, and before the bodies of 19 small children are identified, the political noise starts up. Mass shootings are a part of the American landscape, but when they happen at schools, we all feel a distinct sense of violation and gaping grief. Those children are so innocent, so deserving of a right to live their lives, hold their place with their families, create their own legacies, and die of natural causes at a ripe old age. And those children could have been our children. There was nothing special about them; they were just sent to school that day like every child who is sent to school every day.

Here is how the politics goes: The Republicans will blame the Democrats and the Democrats will blame the Republicans. Is Rachel Maddow at fault, or is it Tucker Carlson? Social media accounts blamed both of them for the racially motivated mass murder in a Buffalo grocery store on May 14.

Mass murders were previously defined as a shooting where four or more victims are killed, excluding the shooter, in a public place that is not related to the commission of another crime. In 2012, the definition was changed to include events with three victims. This definition excludes gang violence and the murder of family members.

When it comes to explaining mass murder, the camps divide: They are the result of some combination of mental illness, easy access to firearms, and terrorism and hate. For psychiatry, there is a unique place in the argument – half of all mass shooters have exhibited signs or symptoms of psychiatric illness, and for those who want to deflect the issue away from issues related to the regulation of firearms, it becomes easy to blame “mental illness,” as though that explains it all. Either the gunman “snapped” in such a way that no one could have predicted, or the mental health system is at fault for not preventing it.

There are many ways to be emotionally disturbed; mental illness is only one of them, and there is no psychiatric diagnosis that includes the symptom of shooting strangers, or shooting children. The vast majority of people, including nearly all psychiatrists, will never know someone who perpetrates a mass shooting. 

Can mental illness give us any insight into these senseless killings? Sometimes, but rarely. Take John Hinckley Jr., who shot President Ronald Reagan as a means to impress actress Jodie Foster. Sometimes these killings are motivated by delusional beliefs. But the planning and preparation that goes into most mass shootings involves a degree of organization and forethought that we don’t typically see in those with severe psychotic disorders.

The other psychological explanation that satisfies some of a nonmedical population is that these killers “just snap.” This, too, is a term that is not included in our diagnostic vocabulary, but it remains a way for some to explain that which can’t be explained. If mental illness, however, is the cause of mass murders, then more stringent gun control is unnecessary. Every state already has a mechanism to prevent those with criminal and specified psychiatric histories from buying legal firearms, and it may be inevitable that these screens are not perfect. 

The next line of political thinking moves to the psychiatric “if only.” If only there were more state hospital beds and if only it were easier to compel people with psychiatric disorders to get treatment against their will, then we could eliminate these crimes. The Virginia tech shooter was mandated to get outpatient psychiatric treatment after a brief hospitalization, yet he never went and there was no mechanism in place to track him.

In cases where a person with a psychotic illness has a history of repeated violent episodes after stopping medications, it does make sense to mandate treatment, not because they are likely to shoot strangers, but because some people do become violent when they are ill and mental illness is believed to play a role in 10% of murders.

Mass murders remain rare, and while advocates for legislation that would make it easier to mandate involuntary care have cited violence prevention as a reason, it is hard to imagine that we would force people to get care because they “might” commit such a crime – unless there was convincing evidence that someone was at risk of committing such a heinous act.

For those who oppose stronger gun control laws, the “what if” may circulate around the need for even more firearms. What if teachers carried guns? What if schools were more heavily policed? What if the criminals were made to be afraid?

We are left with the fact that other countries do not see these numbers of mass shooting events, yet mental illness is ubiquitous. While the presence of psychiatric disorders does little to explain school shootings, we still have no understanding of what motivated the Sandy Hook killer, and it remains to be seen what we will come to understand about the gunman in Uvalde, Texas.

Mental illness is not unique to the United States; however, the number of available firearms is. In a country of 323 million people (including children and people who live in institutions where they have no access to firearms), there are estimated to be over 400 million guns in the United States, 98% of which are owned by civilians. 

Hate crimes and terrorism are another explanation for mass murders. In these instances, the gunman makes his motive obvious: There are social media announcements, or the site of the shooting is a synagogue, a mosque, or a location where the victims are of a specific race or religion. But hate may come out of a psychotic illness, and easy access to firearms allows for these crimes to continue. 

Firearms are now the No. 1 cause of mortality in children. Very few of these deaths are the result of mass murders. Many more are from accidental deaths, targeted crime, or suicide. Still, school shootings rip at our hearts. Neither the victims nor their grieving families have any role in the act, and suffering leaves its mark on families, communities, and all of us.
 

Are there answers?

In many states, physicians can now request emergency removal of firearms from the home of someone who is both mentally ill and threatening either suicide or homicide. During the era when high-capacity firearms were banned, from 1994 to 2004, mass murders decreased in our country. While most gunmen use legal firearms they have purchased, I would contend that “smart guns” – firearms that allow only the legal owner to operate them based on biometrics – would prevent some mass shootings and many accidents, crimes, and suicides. Universal background checks and tracking gun purchases in the way we monitor controlled medications, or even Sudafed, might allow authorities to predict who might be at risk of committing these heinous acts.

In his newly released book, Trigger Points: Inside the Mission to Stop Mass Murders in America, journalist Mark Follman argues for a proactive community approach using threat assessment methods and providing wraparound services to those who are deemed to be at risk for violent acts. Mr. Follman’s voice is one of the few out there saying that these events are not random and are, in fact, preventable.

In psychiatry, we struggle with school shootings such as the one we just saw in Uvalde. Our own hearts ache as we hold our children close and empathize with the loss of strangers who have been through the unthinkable. We help our patients as they process their emotions. And we wonder whether any of our patients might ever do anything so horrific. The feelings get complicated, the sadness and anger intermingle while the frustration builds, and we are left with our fears and the hope that if that very rare person were to walk through our office door, we would know what to do.

Dr. Miller is a coauthor of Committed: The Battle Over Involuntary Psychiatric Care (Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore. A version of this article first appeared on Medscape.com.

Here we go again, and again, and again.

There just aren’t enough tears, and before the bodies of 19 small children are identified, the political noise starts up. Mass shootings are a part of the American landscape, but when they happen at schools, we all feel a distinct sense of violation and gaping grief. Those children are so innocent, so deserving of a right to live their lives, hold their place with their families, create their own legacies, and die of natural causes at a ripe old age. And those children could have been our children. There was nothing special about them; they were just sent to school that day like every child who is sent to school every day.

Here is how the politics goes: The Republicans will blame the Democrats and the Democrats will blame the Republicans. Is Rachel Maddow at fault, or is it Tucker Carlson? Social media accounts blamed both of them for the racially motivated mass murder in a Buffalo grocery store on May 14.

Mass murders were previously defined as a shooting where four or more victims are killed, excluding the shooter, in a public place that is not related to the commission of another crime. In 2012, the definition was changed to include events with three victims. This definition excludes gang violence and the murder of family members.

When it comes to explaining mass murder, the camps divide: They are the result of some combination of mental illness, easy access to firearms, and terrorism and hate. For psychiatry, there is a unique place in the argument – half of all mass shooters have exhibited signs or symptoms of psychiatric illness, and for those who want to deflect the issue away from issues related to the regulation of firearms, it becomes easy to blame “mental illness,” as though that explains it all. Either the gunman “snapped” in such a way that no one could have predicted, or the mental health system is at fault for not preventing it.

There are many ways to be emotionally disturbed; mental illness is only one of them, and there is no psychiatric diagnosis that includes the symptom of shooting strangers, or shooting children. The vast majority of people, including nearly all psychiatrists, will never know someone who perpetrates a mass shooting. 

Can mental illness give us any insight into these senseless killings? Sometimes, but rarely. Take John Hinckley Jr., who shot President Ronald Reagan as a means to impress actress Jodie Foster. Sometimes these killings are motivated by delusional beliefs. But the planning and preparation that goes into most mass shootings involves a degree of organization and forethought that we don’t typically see in those with severe psychotic disorders.

The other psychological explanation that satisfies some of a nonmedical population is that these killers “just snap.” This, too, is a term that is not included in our diagnostic vocabulary, but it remains a way for some to explain that which can’t be explained. If mental illness, however, is the cause of mass murders, then more stringent gun control is unnecessary. Every state already has a mechanism to prevent those with criminal and specified psychiatric histories from buying legal firearms, and it may be inevitable that these screens are not perfect. 

The next line of political thinking moves to the psychiatric “if only.” If only there were more state hospital beds and if only it were easier to compel people with psychiatric disorders to get treatment against their will, then we could eliminate these crimes. The Virginia tech shooter was mandated to get outpatient psychiatric treatment after a brief hospitalization, yet he never went and there was no mechanism in place to track him.

In cases where a person with a psychotic illness has a history of repeated violent episodes after stopping medications, it does make sense to mandate treatment, not because they are likely to shoot strangers, but because some people do become violent when they are ill and mental illness is believed to play a role in 10% of murders.

Mass murders remain rare, and while advocates for legislation that would make it easier to mandate involuntary care have cited violence prevention as a reason, it is hard to imagine that we would force people to get care because they “might” commit such a crime – unless there was convincing evidence that someone was at risk of committing such a heinous act.

For those who oppose stronger gun control laws, the “what if” may circulate around the need for even more firearms. What if teachers carried guns? What if schools were more heavily policed? What if the criminals were made to be afraid?

We are left with the fact that other countries do not see these numbers of mass shooting events, yet mental illness is ubiquitous. While the presence of psychiatric disorders does little to explain school shootings, we still have no understanding of what motivated the Sandy Hook killer, and it remains to be seen what we will come to understand about the gunman in Uvalde, Texas.

Mental illness is not unique to the United States; however, the number of available firearms is. In a country of 323 million people (including children and people who live in institutions where they have no access to firearms), there are estimated to be over 400 million guns in the United States, 98% of which are owned by civilians. 

Hate crimes and terrorism are another explanation for mass murders. In these instances, the gunman makes his motive obvious: There are social media announcements, or the site of the shooting is a synagogue, a mosque, or a location where the victims are of a specific race or religion. But hate may come out of a psychotic illness, and easy access to firearms allows for these crimes to continue. 

Firearms are now the No. 1 cause of mortality in children. Very few of these deaths are the result of mass murders. Many more are from accidental deaths, targeted crime, or suicide. Still, school shootings rip at our hearts. Neither the victims nor their grieving families have any role in the act, and suffering leaves its mark on families, communities, and all of us.
 

Are there answers?

In many states, physicians can now request emergency removal of firearms from the home of someone who is both mentally ill and threatening either suicide or homicide. During the era when high-capacity firearms were banned, from 1994 to 2004, mass murders decreased in our country. While most gunmen use legal firearms they have purchased, I would contend that “smart guns” – firearms that allow only the legal owner to operate them based on biometrics – would prevent some mass shootings and many accidents, crimes, and suicides. Universal background checks and tracking gun purchases in the way we monitor controlled medications, or even Sudafed, might allow authorities to predict who might be at risk of committing these heinous acts.

In his newly released book, Trigger Points: Inside the Mission to Stop Mass Murders in America, journalist Mark Follman argues for a proactive community approach using threat assessment methods and providing wraparound services to those who are deemed to be at risk for violent acts. Mr. Follman’s voice is one of the few out there saying that these events are not random and are, in fact, preventable.

In psychiatry, we struggle with school shootings such as the one we just saw in Uvalde. Our own hearts ache as we hold our children close and empathize with the loss of strangers who have been through the unthinkable. We help our patients as they process their emotions. And we wonder whether any of our patients might ever do anything so horrific. The feelings get complicated, the sadness and anger intermingle while the frustration builds, and we are left with our fears and the hope that if that very rare person were to walk through our office door, we would know what to do.

Dr. Miller is a coauthor of Committed: The Battle Over Involuntary Psychiatric Care (Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore. A version of this article first appeared on Medscape.com.

Here we go again, and again, and again.

There just aren’t enough tears, and before the bodies of 19 small children are identified, the political noise starts up. Mass shootings are a part of the American landscape, but when they happen at schools, we all feel a distinct sense of violation and gaping grief. Those children are so innocent, so deserving of a right to live their lives, hold their place with their families, create their own legacies, and die of natural causes at a ripe old age. And those children could have been our children. There was nothing special about them; they were just sent to school that day like every child who is sent to school every day.

Here is how the politics goes: The Republicans will blame the Democrats and the Democrats will blame the Republicans. Is Rachel Maddow at fault, or is it Tucker Carlson? Social media accounts blamed both of them for the racially motivated mass murder in a Buffalo grocery store on May 14.

Mass murders were previously defined as a shooting where four or more victims are killed, excluding the shooter, in a public place that is not related to the commission of another crime. In 2012, the definition was changed to include events with three victims. This definition excludes gang violence and the murder of family members.

When it comes to explaining mass murder, the camps divide: They are the result of some combination of mental illness, easy access to firearms, and terrorism and hate. For psychiatry, there is a unique place in the argument – half of all mass shooters have exhibited signs or symptoms of psychiatric illness, and for those who want to deflect the issue away from issues related to the regulation of firearms, it becomes easy to blame “mental illness,” as though that explains it all. Either the gunman “snapped” in such a way that no one could have predicted, or the mental health system is at fault for not preventing it.

There are many ways to be emotionally disturbed; mental illness is only one of them, and there is no psychiatric diagnosis that includes the symptom of shooting strangers, or shooting children. The vast majority of people, including nearly all psychiatrists, will never know someone who perpetrates a mass shooting. 

Can mental illness give us any insight into these senseless killings? Sometimes, but rarely. Take John Hinckley Jr., who shot President Ronald Reagan as a means to impress actress Jodie Foster. Sometimes these killings are motivated by delusional beliefs. But the planning and preparation that goes into most mass shootings involves a degree of organization and forethought that we don’t typically see in those with severe psychotic disorders.

The other psychological explanation that satisfies some of a nonmedical population is that these killers “just snap.” This, too, is a term that is not included in our diagnostic vocabulary, but it remains a way for some to explain that which can’t be explained. If mental illness, however, is the cause of mass murders, then more stringent gun control is unnecessary. Every state already has a mechanism to prevent those with criminal and specified psychiatric histories from buying legal firearms, and it may be inevitable that these screens are not perfect. 

The next line of political thinking moves to the psychiatric “if only.” If only there were more state hospital beds and if only it were easier to compel people with psychiatric disorders to get treatment against their will, then we could eliminate these crimes. The Virginia tech shooter was mandated to get outpatient psychiatric treatment after a brief hospitalization, yet he never went and there was no mechanism in place to track him.

In cases where a person with a psychotic illness has a history of repeated violent episodes after stopping medications, it does make sense to mandate treatment, not because they are likely to shoot strangers, but because some people do become violent when they are ill and mental illness is believed to play a role in 10% of murders.

Mass murders remain rare, and while advocates for legislation that would make it easier to mandate involuntary care have cited violence prevention as a reason, it is hard to imagine that we would force people to get care because they “might” commit such a crime – unless there was convincing evidence that someone was at risk of committing such a heinous act.

For those who oppose stronger gun control laws, the “what if” may circulate around the need for even more firearms. What if teachers carried guns? What if schools were more heavily policed? What if the criminals were made to be afraid?

We are left with the fact that other countries do not see these numbers of mass shooting events, yet mental illness is ubiquitous. While the presence of psychiatric disorders does little to explain school shootings, we still have no understanding of what motivated the Sandy Hook killer, and it remains to be seen what we will come to understand about the gunman in Uvalde, Texas.

Mental illness is not unique to the United States; however, the number of available firearms is. In a country of 323 million people (including children and people who live in institutions where they have no access to firearms), there are estimated to be over 400 million guns in the United States, 98% of which are owned by civilians. 

Hate crimes and terrorism are another explanation for mass murders. In these instances, the gunman makes his motive obvious: There are social media announcements, or the site of the shooting is a synagogue, a mosque, or a location where the victims are of a specific race or religion. But hate may come out of a psychotic illness, and easy access to firearms allows for these crimes to continue. 

Firearms are now the No. 1 cause of mortality in children. Very few of these deaths are the result of mass murders. Many more are from accidental deaths, targeted crime, or suicide. Still, school shootings rip at our hearts. Neither the victims nor their grieving families have any role in the act, and suffering leaves its mark on families, communities, and all of us.
 

Are there answers?

In many states, physicians can now request emergency removal of firearms from the home of someone who is both mentally ill and threatening either suicide or homicide. During the era when high-capacity firearms were banned, from 1994 to 2004, mass murders decreased in our country. While most gunmen use legal firearms they have purchased, I would contend that “smart guns” – firearms that allow only the legal owner to operate them based on biometrics – would prevent some mass shootings and many accidents, crimes, and suicides. Universal background checks and tracking gun purchases in the way we monitor controlled medications, or even Sudafed, might allow authorities to predict who might be at risk of committing these heinous acts.

In his newly released book, Trigger Points: Inside the Mission to Stop Mass Murders in America, journalist Mark Follman argues for a proactive community approach using threat assessment methods and providing wraparound services to those who are deemed to be at risk for violent acts. Mr. Follman’s voice is one of the few out there saying that these events are not random and are, in fact, preventable.

In psychiatry, we struggle with school shootings such as the one we just saw in Uvalde. Our own hearts ache as we hold our children close and empathize with the loss of strangers who have been through the unthinkable. We help our patients as they process their emotions. And we wonder whether any of our patients might ever do anything so horrific. The feelings get complicated, the sadness and anger intermingle while the frustration builds, and we are left with our fears and the hope that if that very rare person were to walk through our office door, we would know what to do.

Dr. Miller is a coauthor of Committed: The Battle Over Involuntary Psychiatric Care (Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore. A version of this article first appeared on Medscape.com.

“It must be mental illness. My mind cannot possibly conceive of an alternative. A rational healthy mind cannot be capable of this, Doc.”

These were the opening words of one of many discussions that I had with patients in the wake of yet another gut-wrenching tragedy where we saw innocent children and their teachers murdered in school.

Courtesy of Mena Mirhom

Do any mass shooters have untreated mental illness?

There are data to suggest that of 14,785 murders studied in a database to track death by guns, 1,315 mass shootings were identified. Of these mass shootings, 11% of the shooters had serious mental illness. Could we have diagnosed those cases earlier? Intervened sooner? Offered more effective treatment? Certainly. Would that have explain away the rest of the cases? Unfortunately, no.

What is it, then?

The scary answer is that the people who are capable of doing this are not so far away. They are not the folks that we would image locking up in a “psych ward” and throwing away the key. They are, rather, people who are lonely, neglected, rejected, bullied, and broken down by life. Anger, hatred, racism, and evil may be ailments of the soul, but they are not mental illnesses. The carnage they produce is just as tangible. As a psychiatrist, I must admit to you that I do not have a good medication to treat these manifestations of the human condition.

What do we do as a society?

Gun reform is the first obvious and essential answer, without which little else is truly as impactful. We must advocate for it and fight tirelessly.

But at the time you will read this article, your disgruntled coworker will be able to walk into a local store in a moment of despair, anguish, and hopelessness and purchase a semiautomatic weapon of war.

What if we were to start seeing, as a society, that our lives are interwoven? What if we saw that our health is truly interdependent? The COVID-19 pandemic shattered many things in our lives, but one element in particular is our radical individualism. We saw that the choices you make certainly affect me and vice versa. We saw that public health is just that – a public matter, not a private one. We saw that there are some areas of our lives that force us to come together for our own survival.

Perhaps politicians will not save us here. Perhaps kindness will. Empathy can be as potent as legislation, and compassion as impactful as a Twitter hashtag. We each know a lonely coworker, an isolated neighbor, a bullied student, or someone beaten down by life.

What if some of the prevention is in fact in our hands? Together.

“Darkness cannot drive out darkness. Only light can do that. Hate cannot drive out hate; only love can do that.” – Reverend Dr. Martin Luther King, Jr.

Mena Mirhom, MD, is an assistant professor of psychiatry at Columbia University and teaches writing to public psychiatry fellows. He is a board-certified psychiatrist and a consultant for the National Basketball Players Association, treating NBA players and staff.

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

“It must be mental illness. My mind cannot possibly conceive of an alternative. A rational healthy mind cannot be capable of this, Doc.”

These were the opening words of one of many discussions that I had with patients in the wake of yet another gut-wrenching tragedy where we saw innocent children and their teachers murdered in school.

Courtesy of Mena Mirhom

Do any mass shooters have untreated mental illness?

There are data to suggest that of 14,785 murders studied in a database to track death by guns, 1,315 mass shootings were identified. Of these mass shootings, 11% of the shooters had serious mental illness. Could we have diagnosed those cases earlier? Intervened sooner? Offered more effective treatment? Certainly. Would that have explain away the rest of the cases? Unfortunately, no.

What is it, then?

The scary answer is that the people who are capable of doing this are not so far away. They are not the folks that we would image locking up in a “psych ward” and throwing away the key. They are, rather, people who are lonely, neglected, rejected, bullied, and broken down by life. Anger, hatred, racism, and evil may be ailments of the soul, but they are not mental illnesses. The carnage they produce is just as tangible. As a psychiatrist, I must admit to you that I do not have a good medication to treat these manifestations of the human condition.

What do we do as a society?

Gun reform is the first obvious and essential answer, without which little else is truly as impactful. We must advocate for it and fight tirelessly.

But at the time you will read this article, your disgruntled coworker will be able to walk into a local store in a moment of despair, anguish, and hopelessness and purchase a semiautomatic weapon of war.

What if we were to start seeing, as a society, that our lives are interwoven? What if we saw that our health is truly interdependent? The COVID-19 pandemic shattered many things in our lives, but one element in particular is our radical individualism. We saw that the choices you make certainly affect me and vice versa. We saw that public health is just that – a public matter, not a private one. We saw that there are some areas of our lives that force us to come together for our own survival.

Perhaps politicians will not save us here. Perhaps kindness will. Empathy can be as potent as legislation, and compassion as impactful as a Twitter hashtag. We each know a lonely coworker, an isolated neighbor, a bullied student, or someone beaten down by life.

What if some of the prevention is in fact in our hands? Together.

“Darkness cannot drive out darkness. Only light can do that. Hate cannot drive out hate; only love can do that.” – Reverend Dr. Martin Luther King, Jr.

Mena Mirhom, MD, is an assistant professor of psychiatry at Columbia University and teaches writing to public psychiatry fellows. He is a board-certified psychiatrist and a consultant for the National Basketball Players Association, treating NBA players and staff.

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

“It must be mental illness. My mind cannot possibly conceive of an alternative. A rational healthy mind cannot be capable of this, Doc.”

These were the opening words of one of many discussions that I had with patients in the wake of yet another gut-wrenching tragedy where we saw innocent children and their teachers murdered in school.

Courtesy of Mena Mirhom

Do any mass shooters have untreated mental illness?

There are data to suggest that of 14,785 murders studied in a database to track death by guns, 1,315 mass shootings were identified. Of these mass shootings, 11% of the shooters had serious mental illness. Could we have diagnosed those cases earlier? Intervened sooner? Offered more effective treatment? Certainly. Would that have explain away the rest of the cases? Unfortunately, no.

What is it, then?

The scary answer is that the people who are capable of doing this are not so far away. They are not the folks that we would image locking up in a “psych ward” and throwing away the key. They are, rather, people who are lonely, neglected, rejected, bullied, and broken down by life. Anger, hatred, racism, and evil may be ailments of the soul, but they are not mental illnesses. The carnage they produce is just as tangible. As a psychiatrist, I must admit to you that I do not have a good medication to treat these manifestations of the human condition.

What do we do as a society?

Gun reform is the first obvious and essential answer, without which little else is truly as impactful. We must advocate for it and fight tirelessly.

But at the time you will read this article, your disgruntled coworker will be able to walk into a local store in a moment of despair, anguish, and hopelessness and purchase a semiautomatic weapon of war.

What if we were to start seeing, as a society, that our lives are interwoven? What if we saw that our health is truly interdependent? The COVID-19 pandemic shattered many things in our lives, but one element in particular is our radical individualism. We saw that the choices you make certainly affect me and vice versa. We saw that public health is just that – a public matter, not a private one. We saw that there are some areas of our lives that force us to come together for our own survival.

Perhaps politicians will not save us here. Perhaps kindness will. Empathy can be as potent as legislation, and compassion as impactful as a Twitter hashtag. We each know a lonely coworker, an isolated neighbor, a bullied student, or someone beaten down by life.

What if some of the prevention is in fact in our hands? Together.

“Darkness cannot drive out darkness. Only light can do that. Hate cannot drive out hate; only love can do that.” – Reverend Dr. Martin Luther King, Jr.

Mena Mirhom, MD, is an assistant professor of psychiatry at Columbia University and teaches writing to public psychiatry fellows. He is a board-certified psychiatrist and a consultant for the National Basketball Players Association, treating NBA players and staff.

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

A 75-year-old male is seen in the emergency department for shortness of breath. D-dimer is very high, and a CT scan chest reveals bilateral pulmonary emboli without right heart strain. He is admitted and started on enoxaparin 1 mg/kg subcutaneously every 12 hours.

By the next morning, he is feeling better and wants to discuss discharge to home and follow-up plans.

Two months ago he presented with abdominal pain and evaluation revealed he had a pancreatic head mass with liver metastases. A liver biopsy was positive for adenocarcinoma consistent with pancreas primary. CA 19-9 level was 1,200 U/mL and he was started on FOLFIRINOX chemotherapy – which he has tolerated well thus far. CA 19-9 and follow-up CT scan show early response to chemotherapy.

Of course, this case raises many questions. Given how successful some directed biomarker-positive therapies are now, you would want to know his microsatellite instability (MSI)/progressive death–ligand 1 (PD-L1) and BRCA mutation status. A high PD-L1 positivity or MSI deficiency would suggest immunoantibody therapy and a BRCA mutation might suggest a poly (ADP-ribose) polymerase inhibitor could play a role.

However, let’s use this case to discuss his venous thromboembolism (VTE) .

Studies show that metastatic cancer patients on chemotherapy might experience a VTE episode of deep vein thrombosis (DVT) or pulmonary embolism (PE) or both as high as 20% of the time during their cancer course and therapy. This patient would be among those who experience the highest incidence of VTE because of the liver metastasis from the pancreatic adenocarcinoma.

So, what to do? Standard treatment of his pulmonary emboli would include either enoxaparin therapeutic dosing 1 mg/kg subcutaneously q12H or 1.5 mg/kg q24H for 3 months. At 3 months, repeat a CT chest scan to show resolution of pulmonary emboli and/or DVT or both, and repeat D-dimer, which should now be well under 1.

But then, there is a second decision to make: Can you stop anticoagulation if his clots have resolved? The answer is yes. If the clots were provoked and the provoking feature is gone you can stop anticoagulation. Patients with pregnancy, on a birth control pill, or on a long trip where immobilization occurred for a extended time (such as driving or flying) can have anticoagulation stopped because the provoking feature is gone, but this is not true in this case. This patient’s pancreas cancer and chemotherapy are ongoing and he will be at increased risk to clot once again if anticoagulation is stopped.

Should this patient have a hypercoagulable workup which might include protein C, protein S, and antithrombin levels? Remember this is quite rare and patients with these deficiencies usually present in their teens or 20s with increased clotting issues. The more common hypercoagulable workup would include checking for factor V Leiden and prothrombin G20210A mutations, as well as acquired antiphospholipid antibodies such as beta₂ glycoprotein I, anticardiolipin, and the lupus inhibitor. However, in this 75-year-old cancer patient, these are not necessary or even relevant since his VTE was clearly provoked by metastatic cancer on chemotherapy.

Unfortunately, with metastatic active cancer, anticoagulation would need to be continued at full or possibly half therapeutic dose. Of course, enoxaparin injections can get tiresome for the patient and data suggest the same result can be achieved either with initial management or by continuing anticoagulation management using either rivaroxaban or apixaban.

Wouldn’t it have been better if this patient had never experienced VTE in the first place? Is that possible?

Yes, data suggest that it is. Higher-risk patients like this one could benefit from prophylactic anticoagulation. The Khorana predictive model gives us a simple clinical means to evaluate this and decide who might be at highest VTE risk and who could benefit from low-dose preventive anticoagulation.

In summary, cancer patients undergoing treatment for metastatic disease are at increased risk for symptomatic VTE. Once diagnosed, therapy is usually very effective, but may need to be prolonged as long as the cancer is still active or else, the VTE could recur. Preventive therapy for high-risk patients would be reasonable.

Dr. Henry is a medical oncologist with the Abramson Cancer Center at the University of Pennsylvania, Philadelphia.

A 75-year-old male is seen in the emergency department for shortness of breath. D-dimer is very high, and a CT scan chest reveals bilateral pulmonary emboli without right heart strain. He is admitted and started on enoxaparin 1 mg/kg subcutaneously every 12 hours.

By the next morning, he is feeling better and wants to discuss discharge to home and follow-up plans.

Two months ago he presented with abdominal pain and evaluation revealed he had a pancreatic head mass with liver metastases. A liver biopsy was positive for adenocarcinoma consistent with pancreas primary. CA 19-9 level was 1,200 U/mL and he was started on FOLFIRINOX chemotherapy – which he has tolerated well thus far. CA 19-9 and follow-up CT scan show early response to chemotherapy.

Of course, this case raises many questions. Given how successful some directed biomarker-positive therapies are now, you would want to know his microsatellite instability (MSI)/progressive death–ligand 1 (PD-L1) and BRCA mutation status. A high PD-L1 positivity or MSI deficiency would suggest immunoantibody therapy and a BRCA mutation might suggest a poly (ADP-ribose) polymerase inhibitor could play a role.

However, let’s use this case to discuss his venous thromboembolism (VTE) .

Studies show that metastatic cancer patients on chemotherapy might experience a VTE episode of deep vein thrombosis (DVT) or pulmonary embolism (PE) or both as high as 20% of the time during their cancer course and therapy. This patient would be among those who experience the highest incidence of VTE because of the liver metastasis from the pancreatic adenocarcinoma.

So, what to do? Standard treatment of his pulmonary emboli would include either enoxaparin therapeutic dosing 1 mg/kg subcutaneously q12H or 1.5 mg/kg q24H for 3 months. At 3 months, repeat a CT chest scan to show resolution of pulmonary emboli and/or DVT or both, and repeat D-dimer, which should now be well under 1.

But then, there is a second decision to make: Can you stop anticoagulation if his clots have resolved? The answer is yes. If the clots were provoked and the provoking feature is gone you can stop anticoagulation. Patients with pregnancy, on a birth control pill, or on a long trip where immobilization occurred for a extended time (such as driving or flying) can have anticoagulation stopped because the provoking feature is gone, but this is not true in this case. This patient’s pancreas cancer and chemotherapy are ongoing and he will be at increased risk to clot once again if anticoagulation is stopped.

Should this patient have a hypercoagulable workup which might include protein C, protein S, and antithrombin levels? Remember this is quite rare and patients with these deficiencies usually present in their teens or 20s with increased clotting issues. The more common hypercoagulable workup would include checking for factor V Leiden and prothrombin G20210A mutations, as well as acquired antiphospholipid antibodies such as beta₂ glycoprotein I, anticardiolipin, and the lupus inhibitor. However, in this 75-year-old cancer patient, these are not necessary or even relevant since his VTE was clearly provoked by metastatic cancer on chemotherapy.

Unfortunately, with metastatic active cancer, anticoagulation would need to be continued at full or possibly half therapeutic dose. Of course, enoxaparin injections can get tiresome for the patient and data suggest the same result can be achieved either with initial management or by continuing anticoagulation management using either rivaroxaban or apixaban.

Wouldn’t it have been better if this patient had never experienced VTE in the first place? Is that possible?

Yes, data suggest that it is. Higher-risk patients like this one could benefit from prophylactic anticoagulation. The Khorana predictive model gives us a simple clinical means to evaluate this and decide who might be at highest VTE risk and who could benefit from low-dose preventive anticoagulation.

In summary, cancer patients undergoing treatment for metastatic disease are at increased risk for symptomatic VTE. Once diagnosed, therapy is usually very effective, but may need to be prolonged as long as the cancer is still active or else, the VTE could recur. Preventive therapy for high-risk patients would be reasonable.

Dr. Henry is a medical oncologist with the Abramson Cancer Center at the University of Pennsylvania, Philadelphia.

A 75-year-old male is seen in the emergency department for shortness of breath. D-dimer is very high, and a CT scan chest reveals bilateral pulmonary emboli without right heart strain. He is admitted and started on enoxaparin 1 mg/kg subcutaneously every 12 hours.

By the next morning, he is feeling better and wants to discuss discharge to home and follow-up plans.

Two months ago he presented with abdominal pain and evaluation revealed he had a pancreatic head mass with liver metastases. A liver biopsy was positive for adenocarcinoma consistent with pancreas primary. CA 19-9 level was 1,200 U/mL and he was started on FOLFIRINOX chemotherapy – which he has tolerated well thus far. CA 19-9 and follow-up CT scan show early response to chemotherapy.

Of course, this case raises many questions. Given how successful some directed biomarker-positive therapies are now, you would want to know his microsatellite instability (MSI)/progressive death–ligand 1 (PD-L1) and BRCA mutation status. A high PD-L1 positivity or MSI deficiency would suggest immunoantibody therapy and a BRCA mutation might suggest a poly (ADP-ribose) polymerase inhibitor could play a role.

However, let’s use this case to discuss his venous thromboembolism (VTE) .

Studies show that metastatic cancer patients on chemotherapy might experience a VTE episode of deep vein thrombosis (DVT) or pulmonary embolism (PE) or both as high as 20% of the time during their cancer course and therapy. This patient would be among those who experience the highest incidence of VTE because of the liver metastasis from the pancreatic adenocarcinoma.

So, what to do? Standard treatment of his pulmonary emboli would include either enoxaparin therapeutic dosing 1 mg/kg subcutaneously q12H or 1.5 mg/kg q24H for 3 months. At 3 months, repeat a CT chest scan to show resolution of pulmonary emboli and/or DVT or both, and repeat D-dimer, which should now be well under 1.

But then, there is a second decision to make: Can you stop anticoagulation if his clots have resolved? The answer is yes. If the clots were provoked and the provoking feature is gone you can stop anticoagulation. Patients with pregnancy, on a birth control pill, or on a long trip where immobilization occurred for a extended time (such as driving or flying) can have anticoagulation stopped because the provoking feature is gone, but this is not true in this case. This patient’s pancreas cancer and chemotherapy are ongoing and he will be at increased risk to clot once again if anticoagulation is stopped.

Should this patient have a hypercoagulable workup which might include protein C, protein S, and antithrombin levels? Remember this is quite rare and patients with these deficiencies usually present in their teens or 20s with increased clotting issues. The more common hypercoagulable workup would include checking for factor V Leiden and prothrombin G20210A mutations, as well as acquired antiphospholipid antibodies such as beta₂ glycoprotein I, anticardiolipin, and the lupus inhibitor. However, in this 75-year-old cancer patient, these are not necessary or even relevant since his VTE was clearly provoked by metastatic cancer on chemotherapy.

Unfortunately, with metastatic active cancer, anticoagulation would need to be continued at full or possibly half therapeutic dose. Of course, enoxaparin injections can get tiresome for the patient and data suggest the same result can be achieved either with initial management or by continuing anticoagulation management using either rivaroxaban or apixaban.

Wouldn’t it have been better if this patient had never experienced VTE in the first place? Is that possible?

Yes, data suggest that it is. Higher-risk patients like this one could benefit from prophylactic anticoagulation. The Khorana predictive model gives us a simple clinical means to evaluate this and decide who might be at highest VTE risk and who could benefit from low-dose preventive anticoagulation.

In summary, cancer patients undergoing treatment for metastatic disease are at increased risk for symptomatic VTE. Once diagnosed, therapy is usually very effective, but may need to be prolonged as long as the cancer is still active or else, the VTE could recur. Preventive therapy for high-risk patients would be reasonable.

Dr. Henry is a medical oncologist with the Abramson Cancer Center at the University of Pennsylvania, Philadelphia.