Commentary

The US government has a legacy of providing support for veterans. Pensions were offered to disabled veterans as early as 1776, and benefits were expanded to cover medical needs as the country grew and modernized.^1,2 Enacted during the Civil War, the General Pension Act increased benefits for widows and dependents.² Rehabilitation and vocational training assistance benefits were added after World War I, and the US Department of Veterans Affairs (VA) was created in 1930 to consolidate all benefits under one umbrella organization.^2,3

Prior to World War II, the VA lacked the bed capacity for the 4 million veterans who were eligible for care. This shortage became more acute by the end of the war, when the number of eligible veterans increased by 15 million.⁴ Although the VA successfully built bed capacity through acquisition of military hospitals, VA hospitals struggled to recruit clinical staff.² Physicians were hesitant to join the VA because civil service salaries were lower than comparable positions in the community, and the VA offered limited opportunities for research or continuing education. These limitations negatively impacted the overall reputation of the VA. The American Medical Association (AMA) was reluctant to directly admit VA physicians for membership because of a “lower” standard of care at VA hospitals.² This review will describe how passage of 2 legislative actions, the Servicemen’s Readjustment Act and Public Law (PL)79-293, and a key policy memorandum set the foundation for the partnership between the VA and academic medical centers. This led to improved medical care for veterans and expansion of health professions education for VA and the nation.^5,6

GI Bill of Rights

The passage of the Servicemen’s Readjustment Act of 1944, better known as the GI Bill of Rights, provided education assistance, guaranteed home loans, and unemployment payments to veterans.⁵ All medical officers serving during the war were eligible for this benefit, which effectively increased the number of potential physician trainees at the end of World War II by almost 60,000.⁷ Medical education at the time was simultaneously undergoing a transformation with more rigorous training and a push to standardize medical education across state lines. While prerequisite training was not required for admission to many medical schools and curricula varied in length based on state licensing requirements, more programs were adding premedical education requirements and transitioning to the 4-year curricula seen today. At this time, only 23 states required postgraduate internships for licensure, but this number was growing.⁸ The American Board of Medical Specialties was established several years prior to World War II in 1934 to elevate the quality of care; the desire for residency training and board certification continued to gain traction during the 1940s.⁹

Medical Training

In anticipation of an influx of medical trainees, the Committee on Postwar Medical Service conducted a comprehensive survey to understand the training needs of physician veterans returning from World War II.⁷ The survey collected data from medical officers on their desired length of training, interest in specialty board certification, time served, and type of medical practice prior to enlisting. Length of desired training was categorized as short (up to 6 months), which would serve as a refresher course and provide updates on recent advances in medicine and surgery, and long (> 6 months), which resembled a modern internship or residency. Nineteen percent did not want additional training, 22% wished to pursue short courses, and 51% were interested in longer courses. Most respondents also wished to obtain board certification.⁷ The AMA played a significant role in supporting the expansion of training opportunities, encouraging all accredited hospitals to assess their capacity to determine the number of additional residents they could accommodate. The AMA also awarded hospitals with existing internship programs temporary accreditation to allow them to add extended training through residency programs.⁷

Medical schools devised creative solutions to meet the needs of returning physician veterans and capitalize on the available educational benefits. Postgraduate refresher courses that varied in length from hours to months were developed focusing on an array of topics. In addition to basic medical principles, courses covered general topics, such as advances in medicine, to specialty topics, such as nutrition or ophthalmology.⁷ Although the courses could not be counted toward board certification, participation increased by almost 300% in the 1945/1946 academic year relative to the previous year.⁷ Increasing access to the longer training courses, including internships and residencies, was often achieved through experiences outside the clinical setting. Yale University modified its curriculum to reduce time devoted to lectures on published materials and encourage active learning and community outreach.¹⁰ Northwestern University assigned residents to spend 1 of their 3 years “out of residence” in basic science and clinical instruction provided by the medical school. Tuition assistance from the GI Bill supported the additional expenses incurred by the medical school to fund laboratory space, equipment, and the salaries of the basic science instructors and administrative staff.¹¹

Public Law 79-293

Public Law 79-293 was passed on January 3, 1946, establishing the Department of Medicine and Surgery within the VA. The law, which became the basis for Title 38 chapters 73 and 74, allowed VA hospitals flexibility to hire doctors, dentists, and nurses without regard to the civil service regulations and salary restrictions associated with other federal positions.⁶

Concerns about quality of care had been mounting for years, and the release of several sensationalized and critical articles motivated VA leadership to make sweeping changes. One article described neglect at VA hospitals.¹² Excessive paperwork and low economic benefits were identified as barriers to the recruitment of qualified clinicians at the VA.² The VA Special Medical Advisory Group investigating the claims recommended that the VA encourage their hospitals to affiliate with medical schools to improve the quality of care. This group also recommended that new VA hospitals be constructed near academic medical centers to allow access to consultants.² Three large veterans service organizations (American Legion, Veterans of Foreign Wars, and Disabled American Veterans) conducted their own investigations in response to the media reports. The organizations reported that the quality of care in most VA hospitals was already on par with the community but indicated that the VA would benefit from expansion of medical research and training, increased bed capacity, reduction in the administrative burden on clinicians, and increased salaries for clinical staff.²

Policy Memorandum No. 2

The relationship between VA and academic medical centers was solidified on January 30, 1946, with adoption of Policy Memorandum No. 2.¹³ This memorandum allowed for the establishment of relationships with academic medical centers to provide “the veteran a much higher standard of medical care than could be given him with a wholly full-time medical staff.” Shortly after this memorandum was signed, residents from Northwestern University and the University of Illinois at Chicago began clinical rotations at the Hines VA facility in Chicago, Illinois.² By 1947, 62 medical schools had committed to an affiliation with local VA hospitals and 21 deans’ committees were in operation, which were responsible for the appointment of physician residents and consultants. The AMA extended direct membership privileges to VA physicians, and by 1947 the number of residency positions doubled nationally.^14,15 The almost universal support of the relationship between VA and academic affiliates provided educational opportunities for returning veterans and raised standards for medical education nationally.

Current State

Since the passage of PL 79-293 and PM No. 2, the VA-academic health professions education partnership has grown to include 113,000 trainees rotating through 150 VA medical centers annually from more than 1400 colleges and universities.¹⁶ Most VA podiatrists, psychologists, optometrists, and physicians working in VA medical centers also trained at VA, and trainees are 37% more likely to consider a job at VA after completing their clinical rotations. This unique partnership began 76 years ago and continues to provide clinicians “for VA and the nation.”

The US government has a legacy of providing support for veterans. Pensions were offered to disabled veterans as early as 1776, and benefits were expanded to cover medical needs as the country grew and modernized.^1,2 Enacted during the Civil War, the General Pension Act increased benefits for widows and dependents.² Rehabilitation and vocational training assistance benefits were added after World War I, and the US Department of Veterans Affairs (VA) was created in 1930 to consolidate all benefits under one umbrella organization.^2,3

Prior to World War II, the VA lacked the bed capacity for the 4 million veterans who were eligible for care. This shortage became more acute by the end of the war, when the number of eligible veterans increased by 15 million.⁴ Although the VA successfully built bed capacity through acquisition of military hospitals, VA hospitals struggled to recruit clinical staff.² Physicians were hesitant to join the VA because civil service salaries were lower than comparable positions in the community, and the VA offered limited opportunities for research or continuing education. These limitations negatively impacted the overall reputation of the VA. The American Medical Association (AMA) was reluctant to directly admit VA physicians for membership because of a “lower” standard of care at VA hospitals.² This review will describe how passage of 2 legislative actions, the Servicemen’s Readjustment Act and Public Law (PL)79-293, and a key policy memorandum set the foundation for the partnership between the VA and academic medical centers. This led to improved medical care for veterans and expansion of health professions education for VA and the nation.^5,6

GI Bill of Rights

The passage of the Servicemen’s Readjustment Act of 1944, better known as the GI Bill of Rights, provided education assistance, guaranteed home loans, and unemployment payments to veterans.⁵ All medical officers serving during the war were eligible for this benefit, which effectively increased the number of potential physician trainees at the end of World War II by almost 60,000.⁷ Medical education at the time was simultaneously undergoing a transformation with more rigorous training and a push to standardize medical education across state lines. While prerequisite training was not required for admission to many medical schools and curricula varied in length based on state licensing requirements, more programs were adding premedical education requirements and transitioning to the 4-year curricula seen today. At this time, only 23 states required postgraduate internships for licensure, but this number was growing.⁸ The American Board of Medical Specialties was established several years prior to World War II in 1934 to elevate the quality of care; the desire for residency training and board certification continued to gain traction during the 1940s.⁹

Medical Training

In anticipation of an influx of medical trainees, the Committee on Postwar Medical Service conducted a comprehensive survey to understand the training needs of physician veterans returning from World War II.⁷ The survey collected data from medical officers on their desired length of training, interest in specialty board certification, time served, and type of medical practice prior to enlisting. Length of desired training was categorized as short (up to 6 months), which would serve as a refresher course and provide updates on recent advances in medicine and surgery, and long (> 6 months), which resembled a modern internship or residency. Nineteen percent did not want additional training, 22% wished to pursue short courses, and 51% were interested in longer courses. Most respondents also wished to obtain board certification.⁷ The AMA played a significant role in supporting the expansion of training opportunities, encouraging all accredited hospitals to assess their capacity to determine the number of additional residents they could accommodate. The AMA also awarded hospitals with existing internship programs temporary accreditation to allow them to add extended training through residency programs.⁷

Medical schools devised creative solutions to meet the needs of returning physician veterans and capitalize on the available educational benefits. Postgraduate refresher courses that varied in length from hours to months were developed focusing on an array of topics. In addition to basic medical principles, courses covered general topics, such as advances in medicine, to specialty topics, such as nutrition or ophthalmology.⁷ Although the courses could not be counted toward board certification, participation increased by almost 300% in the 1945/1946 academic year relative to the previous year.⁷ Increasing access to the longer training courses, including internships and residencies, was often achieved through experiences outside the clinical setting. Yale University modified its curriculum to reduce time devoted to lectures on published materials and encourage active learning and community outreach.¹⁰ Northwestern University assigned residents to spend 1 of their 3 years “out of residence” in basic science and clinical instruction provided by the medical school. Tuition assistance from the GI Bill supported the additional expenses incurred by the medical school to fund laboratory space, equipment, and the salaries of the basic science instructors and administrative staff.¹¹

Public Law 79-293

Public Law 79-293 was passed on January 3, 1946, establishing the Department of Medicine and Surgery within the VA. The law, which became the basis for Title 38 chapters 73 and 74, allowed VA hospitals flexibility to hire doctors, dentists, and nurses without regard to the civil service regulations and salary restrictions associated with other federal positions.⁶

Concerns about quality of care had been mounting for years, and the release of several sensationalized and critical articles motivated VA leadership to make sweeping changes. One article described neglect at VA hospitals.¹² Excessive paperwork and low economic benefits were identified as barriers to the recruitment of qualified clinicians at the VA.² The VA Special Medical Advisory Group investigating the claims recommended that the VA encourage their hospitals to affiliate with medical schools to improve the quality of care. This group also recommended that new VA hospitals be constructed near academic medical centers to allow access to consultants.² Three large veterans service organizations (American Legion, Veterans of Foreign Wars, and Disabled American Veterans) conducted their own investigations in response to the media reports. The organizations reported that the quality of care in most VA hospitals was already on par with the community but indicated that the VA would benefit from expansion of medical research and training, increased bed capacity, reduction in the administrative burden on clinicians, and increased salaries for clinical staff.²

Policy Memorandum No. 2

The relationship between VA and academic medical centers was solidified on January 30, 1946, with adoption of Policy Memorandum No. 2.¹³ This memorandum allowed for the establishment of relationships with academic medical centers to provide “the veteran a much higher standard of medical care than could be given him with a wholly full-time medical staff.” Shortly after this memorandum was signed, residents from Northwestern University and the University of Illinois at Chicago began clinical rotations at the Hines VA facility in Chicago, Illinois.² By 1947, 62 medical schools had committed to an affiliation with local VA hospitals and 21 deans’ committees were in operation, which were responsible for the appointment of physician residents and consultants. The AMA extended direct membership privileges to VA physicians, and by 1947 the number of residency positions doubled nationally.^14,15 The almost universal support of the relationship between VA and academic affiliates provided educational opportunities for returning veterans and raised standards for medical education nationally.

Current State

Since the passage of PL 79-293 and PM No. 2, the VA-academic health professions education partnership has grown to include 113,000 trainees rotating through 150 VA medical centers annually from more than 1400 colleges and universities.¹⁶ Most VA podiatrists, psychologists, optometrists, and physicians working in VA medical centers also trained at VA, and trainees are 37% more likely to consider a job at VA after completing their clinical rotations. This unique partnership began 76 years ago and continues to provide clinicians “for VA and the nation.”

The US government has a legacy of providing support for veterans. Pensions were offered to disabled veterans as early as 1776, and benefits were expanded to cover medical needs as the country grew and modernized.^1,2 Enacted during the Civil War, the General Pension Act increased benefits for widows and dependents.² Rehabilitation and vocational training assistance benefits were added after World War I, and the US Department of Veterans Affairs (VA) was created in 1930 to consolidate all benefits under one umbrella organization.^2,3

Prior to World War II, the VA lacked the bed capacity for the 4 million veterans who were eligible for care. This shortage became more acute by the end of the war, when the number of eligible veterans increased by 15 million.⁴ Although the VA successfully built bed capacity through acquisition of military hospitals, VA hospitals struggled to recruit clinical staff.² Physicians were hesitant to join the VA because civil service salaries were lower than comparable positions in the community, and the VA offered limited opportunities for research or continuing education. These limitations negatively impacted the overall reputation of the VA. The American Medical Association (AMA) was reluctant to directly admit VA physicians for membership because of a “lower” standard of care at VA hospitals.² This review will describe how passage of 2 legislative actions, the Servicemen’s Readjustment Act and Public Law (PL)79-293, and a key policy memorandum set the foundation for the partnership between the VA and academic medical centers. This led to improved medical care for veterans and expansion of health professions education for VA and the nation.^5,6

GI Bill of Rights

The passage of the Servicemen’s Readjustment Act of 1944, better known as the GI Bill of Rights, provided education assistance, guaranteed home loans, and unemployment payments to veterans.⁵ All medical officers serving during the war were eligible for this benefit, which effectively increased the number of potential physician trainees at the end of World War II by almost 60,000.⁷ Medical education at the time was simultaneously undergoing a transformation with more rigorous training and a push to standardize medical education across state lines. While prerequisite training was not required for admission to many medical schools and curricula varied in length based on state licensing requirements, more programs were adding premedical education requirements and transitioning to the 4-year curricula seen today. At this time, only 23 states required postgraduate internships for licensure, but this number was growing.⁸ The American Board of Medical Specialties was established several years prior to World War II in 1934 to elevate the quality of care; the desire for residency training and board certification continued to gain traction during the 1940s.⁹

Medical Training

In anticipation of an influx of medical trainees, the Committee on Postwar Medical Service conducted a comprehensive survey to understand the training needs of physician veterans returning from World War II.⁷ The survey collected data from medical officers on their desired length of training, interest in specialty board certification, time served, and type of medical practice prior to enlisting. Length of desired training was categorized as short (up to 6 months), which would serve as a refresher course and provide updates on recent advances in medicine and surgery, and long (> 6 months), which resembled a modern internship or residency. Nineteen percent did not want additional training, 22% wished to pursue short courses, and 51% were interested in longer courses. Most respondents also wished to obtain board certification.⁷ The AMA played a significant role in supporting the expansion of training opportunities, encouraging all accredited hospitals to assess their capacity to determine the number of additional residents they could accommodate. The AMA also awarded hospitals with existing internship programs temporary accreditation to allow them to add extended training through residency programs.⁷

Medical schools devised creative solutions to meet the needs of returning physician veterans and capitalize on the available educational benefits. Postgraduate refresher courses that varied in length from hours to months were developed focusing on an array of topics. In addition to basic medical principles, courses covered general topics, such as advances in medicine, to specialty topics, such as nutrition or ophthalmology.⁷ Although the courses could not be counted toward board certification, participation increased by almost 300% in the 1945/1946 academic year relative to the previous year.⁷ Increasing access to the longer training courses, including internships and residencies, was often achieved through experiences outside the clinical setting. Yale University modified its curriculum to reduce time devoted to lectures on published materials and encourage active learning and community outreach.¹⁰ Northwestern University assigned residents to spend 1 of their 3 years “out of residence” in basic science and clinical instruction provided by the medical school. Tuition assistance from the GI Bill supported the additional expenses incurred by the medical school to fund laboratory space, equipment, and the salaries of the basic science instructors and administrative staff.¹¹

Public Law 79-293

Public Law 79-293 was passed on January 3, 1946, establishing the Department of Medicine and Surgery within the VA. The law, which became the basis for Title 38 chapters 73 and 74, allowed VA hospitals flexibility to hire doctors, dentists, and nurses without regard to the civil service regulations and salary restrictions associated with other federal positions.⁶

Concerns about quality of care had been mounting for years, and the release of several sensationalized and critical articles motivated VA leadership to make sweeping changes. One article described neglect at VA hospitals.¹² Excessive paperwork and low economic benefits were identified as barriers to the recruitment of qualified clinicians at the VA.² The VA Special Medical Advisory Group investigating the claims recommended that the VA encourage their hospitals to affiliate with medical schools to improve the quality of care. This group also recommended that new VA hospitals be constructed near academic medical centers to allow access to consultants.² Three large veterans service organizations (American Legion, Veterans of Foreign Wars, and Disabled American Veterans) conducted their own investigations in response to the media reports. The organizations reported that the quality of care in most VA hospitals was already on par with the community but indicated that the VA would benefit from expansion of medical research and training, increased bed capacity, reduction in the administrative burden on clinicians, and increased salaries for clinical staff.²

Policy Memorandum No. 2

The relationship between VA and academic medical centers was solidified on January 30, 1946, with adoption of Policy Memorandum No. 2.¹³ This memorandum allowed for the establishment of relationships with academic medical centers to provide “the veteran a much higher standard of medical care than could be given him with a wholly full-time medical staff.” Shortly after this memorandum was signed, residents from Northwestern University and the University of Illinois at Chicago began clinical rotations at the Hines VA facility in Chicago, Illinois.² By 1947, 62 medical schools had committed to an affiliation with local VA hospitals and 21 deans’ committees were in operation, which were responsible for the appointment of physician residents and consultants. The AMA extended direct membership privileges to VA physicians, and by 1947 the number of residency positions doubled nationally.^14,15 The almost universal support of the relationship between VA and academic affiliates provided educational opportunities for returning veterans and raised standards for medical education nationally.

Current State

Since the passage of PL 79-293 and PM No. 2, the VA-academic health professions education partnership has grown to include 113,000 trainees rotating through 150 VA medical centers annually from more than 1400 colleges and universities.¹⁶ Most VA podiatrists, psychologists, optometrists, and physicians working in VA medical centers also trained at VA, and trainees are 37% more likely to consider a job at VA after completing their clinical rotations. This unique partnership began 76 years ago and continues to provide clinicians “for VA and the nation.”

Not long ago, the grandmother of my son’s friend died of COVID-19 infection. She was elderly and unvaccinated. Her grandson had no regrets over her unvaccinated status. “Why would she inject poison into her body?” he said, and then expressed a strong opinion that she had died because the hospital physicians refused to give her ivermectin and hydroxychloroquine. My son, wisely, did not push the issue.

Soon thereafter, my personal family physician emailed a newsletter to his patients (me included) with 3 important messages: (1) COVID vaccines were available in the office; (2) He was not going to prescribe hydroxychloroquine, no matter how adamantly it was requested; and (3) He warned against threatening him or his staff with lawsuits or violence over refusal to prescribe any unproven medication.

Mistakes will be made; corrections will be issued. This is the scientific process in action.

How, as a country, have we come to this? A sizeable portion of the public trusts the advice of quacks, hacks, and political opportunists over that of the nation’s most expert scientists and physicians. The National Institutes of Health maintains a website with up-to-date recommendations on the use of treatments for COVID-19. They assess the existing evidence and make recommendations for or against a wide array of interventions. (They recommend against the use of both ivermectin and hydroxychloroquine.) The Centers for Disease Control and Prevention publishes extensively about the current knowledge on the safety and efficacy of vaccines. Neither agency is part of a “deep state” or conspiracy. They are comprised of some of the nation’s leading scientists, including physicians, trying to protect the public from disease and foster good health.

Sadly, some physicians have been a source of inaccurate vaccine information; some even prescribe ineffective treatments despite the evidence. These physicians are either letting their politics override their good sense or are improperly assessing the scientific literature, or both. Medical licensing agencies, and specialty certification boards, need to find ways to prevent this—ways that can survive judicial scrutiny and allow for legitimate scientific debate.

I have been tempted to just accept the current situation as the inevitable outcome of social media–fueled tribalism. But when we know that the COVID death rate among the unvaccinated is 9 times that of people who have received a booster dose,¹ I can’t sit idly and watch the Internet pundits prevail. Instead, I continue to advise and teach my students to have confidence in trustworthy authorities and websites. Mistakes will be made; corrections will be issued. However, this is not evidence of malintent or incompetence, but rather, the scientific process in action.

I tell my students that one of the biggest challenges facing them and society is to figure out how to stop, or at least minimize the effects of, incorrect information, misleading statements, and outright lies in a society that values free speech. Physicians—young and old alike—must remain committed to communicating factual information to a not-always-receptive audience. And I wish my young colleagues luck; I hope that their passion for family medicine and their insights into social media may be just the combination that’s needed to redirect the public’s trust back to where it belongs during a health care crisis.

Not long ago, the grandmother of my son’s friend died of COVID-19 infection. She was elderly and unvaccinated. Her grandson had no regrets over her unvaccinated status. “Why would she inject poison into her body?” he said, and then expressed a strong opinion that she had died because the hospital physicians refused to give her ivermectin and hydroxychloroquine. My son, wisely, did not push the issue.

Soon thereafter, my personal family physician emailed a newsletter to his patients (me included) with 3 important messages: (1) COVID vaccines were available in the office; (2) He was not going to prescribe hydroxychloroquine, no matter how adamantly it was requested; and (3) He warned against threatening him or his staff with lawsuits or violence over refusal to prescribe any unproven medication.

Mistakes will be made; corrections will be issued. This is the scientific process in action.

How, as a country, have we come to this? A sizeable portion of the public trusts the advice of quacks, hacks, and political opportunists over that of the nation’s most expert scientists and physicians. The National Institutes of Health maintains a website with up-to-date recommendations on the use of treatments for COVID-19. They assess the existing evidence and make recommendations for or against a wide array of interventions. (They recommend against the use of both ivermectin and hydroxychloroquine.) The Centers for Disease Control and Prevention publishes extensively about the current knowledge on the safety and efficacy of vaccines. Neither agency is part of a “deep state” or conspiracy. They are comprised of some of the nation’s leading scientists, including physicians, trying to protect the public from disease and foster good health.

Sadly, some physicians have been a source of inaccurate vaccine information; some even prescribe ineffective treatments despite the evidence. These physicians are either letting their politics override their good sense or are improperly assessing the scientific literature, or both. Medical licensing agencies, and specialty certification boards, need to find ways to prevent this—ways that can survive judicial scrutiny and allow for legitimate scientific debate.

I have been tempted to just accept the current situation as the inevitable outcome of social media–fueled tribalism. But when we know that the COVID death rate among the unvaccinated is 9 times that of people who have received a booster dose,¹ I can’t sit idly and watch the Internet pundits prevail. Instead, I continue to advise and teach my students to have confidence in trustworthy authorities and websites. Mistakes will be made; corrections will be issued. However, this is not evidence of malintent or incompetence, but rather, the scientific process in action.

I tell my students that one of the biggest challenges facing them and society is to figure out how to stop, or at least minimize the effects of, incorrect information, misleading statements, and outright lies in a society that values free speech. Physicians—young and old alike—must remain committed to communicating factual information to a not-always-receptive audience. And I wish my young colleagues luck; I hope that their passion for family medicine and their insights into social media may be just the combination that’s needed to redirect the public’s trust back to where it belongs during a health care crisis.

Not long ago, the grandmother of my son’s friend died of COVID-19 infection. She was elderly and unvaccinated. Her grandson had no regrets over her unvaccinated status. “Why would she inject poison into her body?” he said, and then expressed a strong opinion that she had died because the hospital physicians refused to give her ivermectin and hydroxychloroquine. My son, wisely, did not push the issue.

Soon thereafter, my personal family physician emailed a newsletter to his patients (me included) with 3 important messages: (1) COVID vaccines were available in the office; (2) He was not going to prescribe hydroxychloroquine, no matter how adamantly it was requested; and (3) He warned against threatening him or his staff with lawsuits or violence over refusal to prescribe any unproven medication.

Mistakes will be made; corrections will be issued. This is the scientific process in action.

How, as a country, have we come to this? A sizeable portion of the public trusts the advice of quacks, hacks, and political opportunists over that of the nation’s most expert scientists and physicians. The National Institutes of Health maintains a website with up-to-date recommendations on the use of treatments for COVID-19. They assess the existing evidence and make recommendations for or against a wide array of interventions. (They recommend against the use of both ivermectin and hydroxychloroquine.) The Centers for Disease Control and Prevention publishes extensively about the current knowledge on the safety and efficacy of vaccines. Neither agency is part of a “deep state” or conspiracy. They are comprised of some of the nation’s leading scientists, including physicians, trying to protect the public from disease and foster good health.

Sadly, some physicians have been a source of inaccurate vaccine information; some even prescribe ineffective treatments despite the evidence. These physicians are either letting their politics override their good sense or are improperly assessing the scientific literature, or both. Medical licensing agencies, and specialty certification boards, need to find ways to prevent this—ways that can survive judicial scrutiny and allow for legitimate scientific debate.

I have been tempted to just accept the current situation as the inevitable outcome of social media–fueled tribalism. But when we know that the COVID death rate among the unvaccinated is 9 times that of people who have received a booster dose,¹ I can’t sit idly and watch the Internet pundits prevail. Instead, I continue to advise and teach my students to have confidence in trustworthy authorities and websites. Mistakes will be made; corrections will be issued. However, this is not evidence of malintent or incompetence, but rather, the scientific process in action.

I tell my students that one of the biggest challenges facing them and society is to figure out how to stop, or at least minimize the effects of, incorrect information, misleading statements, and outright lies in a society that values free speech. Physicians—young and old alike—must remain committed to communicating factual information to a not-always-receptive audience. And I wish my young colleagues luck; I hope that their passion for family medicine and their insights into social media may be just the combination that’s needed to redirect the public’s trust back to where it belongs during a health care crisis.

We’ve been told for decades that a child who doesn’t start the day with a good breakfast is entering school at a serious disadvantage. The brain needs a good supply of energy to learn optimally. So the standard wisdom goes. Subsidized school breakfast programs have been built around this chestnut. But, is there solid evidence to support the notion that simply adding a morning meal to a child’s schedule will improve his or her school performance? It sounds like common sense, but is it just one of those old grandmother’s nuggets that doesn’t stand up under close scrutiny?

A recent study from Spain suggests that the relationship between breakfast and school performance is not merely related to the nutritional needs of a growing brain. Using data from nearly 4,000 Spanish children aged 4-14 collected in a 2017 national health survey, the investigators found “skipping breakfast and eating breakfast out of the home were linked to greater odds of psychosocial behavioral problems than eating breakfast at home.” And, we already know that, in general, children who misbehave in school don’t thrive academically.

There were also associations between the absence or presence of certain food groups in the morning meal with behavioral problems. But the data lacked the granularity to draw any firm conclusions – although the authors felt that what they consider a healthy Spanish diet may have had a positive influence on behavior.

The findings in this study may simply be another example of the many positive influences that have been associated with family meals and have little to do with what is actually consumed. The association may not have much to do with the family gathering together at a single Norman Rockwell sitting, a reality that I suspect seldom occurs. The apparent positive influence of breakfast may be that it reflects a family’s priorities: that food is important, that sleep is important, and that school is important – so important that scheduling the morning should focus on sending the child off well prepared. The child who is allowed to stay up to an unhealthy hour is likely to be difficult to arouse in the morning for breakfast and getting off to school.

It may be that the child’s behavior problems are so disruptive and taxing for the family that even with their best efforts, the parents can’t find the time and energy to provide a breakfast in the home.

On the other hand, the study doesn’t tell us how many children aren’t offered breakfast at home because their families simply can’t afford it. Obviously, the answer depends on the socioeconomic mix of a given community. In some localities this may represent a sizable percentage of the population.

So where does this leave us? Unfortunately, as I read through the discussion at the end of this paper I felt that the authors were leaning too much toward further research based on the potential associations between behavior and specific food groups their data suggested.

For me, the take-home message from this paper is that our existing efforts to improve academic success with food offered in school should also include strategies that promote eating breakfast at home. For example, the backpack take-home food distribution programs that seem to have been effective could include breakfast-targeted items packaged in a way that encourage families to provide breakfast at home.

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

We’ve been told for decades that a child who doesn’t start the day with a good breakfast is entering school at a serious disadvantage. The brain needs a good supply of energy to learn optimally. So the standard wisdom goes. Subsidized school breakfast programs have been built around this chestnut. But, is there solid evidence to support the notion that simply adding a morning meal to a child’s schedule will improve his or her school performance? It sounds like common sense, but is it just one of those old grandmother’s nuggets that doesn’t stand up under close scrutiny?

A recent study from Spain suggests that the relationship between breakfast and school performance is not merely related to the nutritional needs of a growing brain. Using data from nearly 4,000 Spanish children aged 4-14 collected in a 2017 national health survey, the investigators found “skipping breakfast and eating breakfast out of the home were linked to greater odds of psychosocial behavioral problems than eating breakfast at home.” And, we already know that, in general, children who misbehave in school don’t thrive academically.

There were also associations between the absence or presence of certain food groups in the morning meal with behavioral problems. But the data lacked the granularity to draw any firm conclusions – although the authors felt that what they consider a healthy Spanish diet may have had a positive influence on behavior.

The findings in this study may simply be another example of the many positive influences that have been associated with family meals and have little to do with what is actually consumed. The association may not have much to do with the family gathering together at a single Norman Rockwell sitting, a reality that I suspect seldom occurs. The apparent positive influence of breakfast may be that it reflects a family’s priorities: that food is important, that sleep is important, and that school is important – so important that scheduling the morning should focus on sending the child off well prepared. The child who is allowed to stay up to an unhealthy hour is likely to be difficult to arouse in the morning for breakfast and getting off to school.

It may be that the child’s behavior problems are so disruptive and taxing for the family that even with their best efforts, the parents can’t find the time and energy to provide a breakfast in the home.

On the other hand, the study doesn’t tell us how many children aren’t offered breakfast at home because their families simply can’t afford it. Obviously, the answer depends on the socioeconomic mix of a given community. In some localities this may represent a sizable percentage of the population.

So where does this leave us? Unfortunately, as I read through the discussion at the end of this paper I felt that the authors were leaning too much toward further research based on the potential associations between behavior and specific food groups their data suggested.

For me, the take-home message from this paper is that our existing efforts to improve academic success with food offered in school should also include strategies that promote eating breakfast at home. For example, the backpack take-home food distribution programs that seem to have been effective could include breakfast-targeted items packaged in a way that encourage families to provide breakfast at home.

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

We’ve been told for decades that a child who doesn’t start the day with a good breakfast is entering school at a serious disadvantage. The brain needs a good supply of energy to learn optimally. So the standard wisdom goes. Subsidized school breakfast programs have been built around this chestnut. But, is there solid evidence to support the notion that simply adding a morning meal to a child’s schedule will improve his or her school performance? It sounds like common sense, but is it just one of those old grandmother’s nuggets that doesn’t stand up under close scrutiny?

A recent study from Spain suggests that the relationship between breakfast and school performance is not merely related to the nutritional needs of a growing brain. Using data from nearly 4,000 Spanish children aged 4-14 collected in a 2017 national health survey, the investigators found “skipping breakfast and eating breakfast out of the home were linked to greater odds of psychosocial behavioral problems than eating breakfast at home.” And, we already know that, in general, children who misbehave in school don’t thrive academically.

There were also associations between the absence or presence of certain food groups in the morning meal with behavioral problems. But the data lacked the granularity to draw any firm conclusions – although the authors felt that what they consider a healthy Spanish diet may have had a positive influence on behavior.

The findings in this study may simply be another example of the many positive influences that have been associated with family meals and have little to do with what is actually consumed. The association may not have much to do with the family gathering together at a single Norman Rockwell sitting, a reality that I suspect seldom occurs. The apparent positive influence of breakfast may be that it reflects a family’s priorities: that food is important, that sleep is important, and that school is important – so important that scheduling the morning should focus on sending the child off well prepared. The child who is allowed to stay up to an unhealthy hour is likely to be difficult to arouse in the morning for breakfast and getting off to school.

It may be that the child’s behavior problems are so disruptive and taxing for the family that even with their best efforts, the parents can’t find the time and energy to provide a breakfast in the home.

On the other hand, the study doesn’t tell us how many children aren’t offered breakfast at home because their families simply can’t afford it. Obviously, the answer depends on the socioeconomic mix of a given community. In some localities this may represent a sizable percentage of the population.

So where does this leave us? Unfortunately, as I read through the discussion at the end of this paper I felt that the authors were leaning too much toward further research based on the potential associations between behavior and specific food groups their data suggested.

For me, the take-home message from this paper is that our existing efforts to improve academic success with food offered in school should also include strategies that promote eating breakfast at home. For example, the backpack take-home food distribution programs that seem to have been effective could include breakfast-targeted items packaged in a way that encourage families to provide breakfast at home.

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

Recruiting health care workers is a challenge these days for both private practice and hospital employers, and competition can be fierce. In order to be competitive, employers need to review the package they are offering potential candidates and understand that it’s more than just compensation and benefits that matter.

When all else is equal, contract language can end up being the difference between capturing or losing a candidate.

As someone who reviews physician contracts extensively, there are some common examples of language that may cause a candidate to choose a different position.
 

Probationary period

Although every employer wants to find out if they like the physician or midlevel employee that they have just hired before fully committing, the inclusion of a probationary period (usually 90 days) is offensive to a candidate, especially one with a choice of contracts.

Essentially, the employer is asking the employee to (potentially) relocate, go through the credentialing process, and turn down other potential offers, all for the possibility that they could easily be terminated. Probationary periods typically allow an employee to be immediately terminated without notice or cause, which can then leave them stranded without a paycheck (and with a new home and/or other recent commitments).

Moreover, contracts with probationary periods tend to terminate the employee without covering any tail costs or clarifying that the employer will not enforce restrictive provisions (even if unlikely to be legally enforceable based on the short relationship).

It is important to understand that the process of a person finding a new position, which includes interviewing, contract negotiation, and credentialing, can take up to 6 months. For this reason, probationary provisions create real job insecurity for a candidate.

Entering into a new affiliation is a leap of faith both for the employer and the employee. If the circumstances do not work out, the employer should fairly compensate the employee for the notice period and ask them not to return to work or otherwise allow them to keep working the notice period while they search for a new position.
 

Acceleration of notice

Another objectionable provision that employers like to include in their contracts is one which allows the employer to accelerate and immediately terminate an employee who has given proper notice.

The contract will contain a standard notice provision, but when the health care professional submits notice, their last date is suddenly accelerated, and they are released without further compensation, notice, or benefits. This type of provision is particularly offensive to health care employees who take the step of giving proper contractual notice and, similar to the probationary language, can create real job insecurity for an employee who suddenly loses their paycheck and has no new job to start.

Medical workers should be paid for the entire notice period whether or not they are allowed to work. Unfortunately, this type of provision is sometimes hidden in contracts and not noticed by employees, who tend to focus on the notice provision itself. I consider this provision to be a red flag about the employer when I review clients’ contracts.
 

Malpractice tail

Although many employers will claim it is not unusual for an employee to pay for their own malpractice tail, in the current marketplace, the payment of tail can be a deciding factor in whether a candidate accepts a contract.

At a minimum, employers should consider paying for the tail under circumstances where they non-renew a contract, terminate without cause, or the contract is terminated for the employer’s breach. Similarly, I like to seek out payment of the tail by the employer where the contract is terminated owing to a change in the law, use of a force majeure provision, loss of the employer’s hospital contract, or similar provisions where termination is outside the control of the employee.

Employers should also consider a provision where they share the cost of a tail or cover the entire cost on the basis of years of service in order to stand out to a potential candidate.
 

Noncompete provisions

I do not find noncompete provisions to be generally unacceptable when properly written; however, employers should reevaluate the reasonableness of their noncompete language frequently, because such language can make the difference in whether a candidate accepts a contract.

A reasonable noncompete that only protects the employer as necessary and does not restrict the reasonable practice of medicine is always preferable and can be the deciding factor for a candidate. Tying enforcement of a noncompete to reasons for termination (similar to the tail) can also make a positive difference in a candidate’s review of a contract.

Egregious noncompetes, where the candidate is simply informed that the language is “not negotiable,” are unlikely to be compelling to a candidate with other options.
 

Specifics on location, call, schedule

One item potential employees find extremely frustrating about contracts is when it fails to include promises made regarding location, call, and schedule.

These particular items affect a physician’s expectations about a job, including commute time, family life, and lifestyle. An employer or recruiter that makes a lot of promises on these points but won’t commit to the details in writing (or at least offer mutual agreement on these issues) can cause an uncertain candidate to choose the job that offers greater certainty.

There are many provisions of a contract that can make a difference to a particular job applicant. A savvy employer seeking to capture a particular health care professional should find out what the specific goals and needs of the candidate might be and consider adjusting the contract to best satisfy the candidate.

At the end of the day, however, at least for those physicians and others reviewing contracts that are fairly equivalent, it may be the fairness of the contract provisions that end up being the deciding factor.

Ms. Adler is Health Law Group Practice Leader for the law firm Roetzel in Chicago. She reported no relevant conflicts of interest.

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

Recruiting health care workers is a challenge these days for both private practice and hospital employers, and competition can be fierce. In order to be competitive, employers need to review the package they are offering potential candidates and understand that it’s more than just compensation and benefits that matter.

When all else is equal, contract language can end up being the difference between capturing or losing a candidate.

As someone who reviews physician contracts extensively, there are some common examples of language that may cause a candidate to choose a different position.
 

Probationary period

Although every employer wants to find out if they like the physician or midlevel employee that they have just hired before fully committing, the inclusion of a probationary period (usually 90 days) is offensive to a candidate, especially one with a choice of contracts.

Essentially, the employer is asking the employee to (potentially) relocate, go through the credentialing process, and turn down other potential offers, all for the possibility that they could easily be terminated. Probationary periods typically allow an employee to be immediately terminated without notice or cause, which can then leave them stranded without a paycheck (and with a new home and/or other recent commitments).

Moreover, contracts with probationary periods tend to terminate the employee without covering any tail costs or clarifying that the employer will not enforce restrictive provisions (even if unlikely to be legally enforceable based on the short relationship).

It is important to understand that the process of a person finding a new position, which includes interviewing, contract negotiation, and credentialing, can take up to 6 months. For this reason, probationary provisions create real job insecurity for a candidate.

Entering into a new affiliation is a leap of faith both for the employer and the employee. If the circumstances do not work out, the employer should fairly compensate the employee for the notice period and ask them not to return to work or otherwise allow them to keep working the notice period while they search for a new position.
 

Acceleration of notice

Another objectionable provision that employers like to include in their contracts is one which allows the employer to accelerate and immediately terminate an employee who has given proper notice.

The contract will contain a standard notice provision, but when the health care professional submits notice, their last date is suddenly accelerated, and they are released without further compensation, notice, or benefits. This type of provision is particularly offensive to health care employees who take the step of giving proper contractual notice and, similar to the probationary language, can create real job insecurity for an employee who suddenly loses their paycheck and has no new job to start.

Medical workers should be paid for the entire notice period whether or not they are allowed to work. Unfortunately, this type of provision is sometimes hidden in contracts and not noticed by employees, who tend to focus on the notice provision itself. I consider this provision to be a red flag about the employer when I review clients’ contracts.
 

Malpractice tail

Although many employers will claim it is not unusual for an employee to pay for their own malpractice tail, in the current marketplace, the payment of tail can be a deciding factor in whether a candidate accepts a contract.

At a minimum, employers should consider paying for the tail under circumstances where they non-renew a contract, terminate without cause, or the contract is terminated for the employer’s breach. Similarly, I like to seek out payment of the tail by the employer where the contract is terminated owing to a change in the law, use of a force majeure provision, loss of the employer’s hospital contract, or similar provisions where termination is outside the control of the employee.

Employers should also consider a provision where they share the cost of a tail or cover the entire cost on the basis of years of service in order to stand out to a potential candidate.
 

Noncompete provisions

I do not find noncompete provisions to be generally unacceptable when properly written; however, employers should reevaluate the reasonableness of their noncompete language frequently, because such language can make the difference in whether a candidate accepts a contract.

A reasonable noncompete that only protects the employer as necessary and does not restrict the reasonable practice of medicine is always preferable and can be the deciding factor for a candidate. Tying enforcement of a noncompete to reasons for termination (similar to the tail) can also make a positive difference in a candidate’s review of a contract.

Egregious noncompetes, where the candidate is simply informed that the language is “not negotiable,” are unlikely to be compelling to a candidate with other options.
 

Specifics on location, call, schedule

One item potential employees find extremely frustrating about contracts is when it fails to include promises made regarding location, call, and schedule.

These particular items affect a physician’s expectations about a job, including commute time, family life, and lifestyle. An employer or recruiter that makes a lot of promises on these points but won’t commit to the details in writing (or at least offer mutual agreement on these issues) can cause an uncertain candidate to choose the job that offers greater certainty.

There are many provisions of a contract that can make a difference to a particular job applicant. A savvy employer seeking to capture a particular health care professional should find out what the specific goals and needs of the candidate might be and consider adjusting the contract to best satisfy the candidate.

At the end of the day, however, at least for those physicians and others reviewing contracts that are fairly equivalent, it may be the fairness of the contract provisions that end up being the deciding factor.

Ms. Adler is Health Law Group Practice Leader for the law firm Roetzel in Chicago. She reported no relevant conflicts of interest.

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

Recruiting health care workers is a challenge these days for both private practice and hospital employers, and competition can be fierce. In order to be competitive, employers need to review the package they are offering potential candidates and understand that it’s more than just compensation and benefits that matter.

When all else is equal, contract language can end up being the difference between capturing or losing a candidate.

As someone who reviews physician contracts extensively, there are some common examples of language that may cause a candidate to choose a different position.
 

Probationary period

Although every employer wants to find out if they like the physician or midlevel employee that they have just hired before fully committing, the inclusion of a probationary period (usually 90 days) is offensive to a candidate, especially one with a choice of contracts.

Essentially, the employer is asking the employee to (potentially) relocate, go through the credentialing process, and turn down other potential offers, all for the possibility that they could easily be terminated. Probationary periods typically allow an employee to be immediately terminated without notice or cause, which can then leave them stranded without a paycheck (and with a new home and/or other recent commitments).

Moreover, contracts with probationary periods tend to terminate the employee without covering any tail costs or clarifying that the employer will not enforce restrictive provisions (even if unlikely to be legally enforceable based on the short relationship).

It is important to understand that the process of a person finding a new position, which includes interviewing, contract negotiation, and credentialing, can take up to 6 months. For this reason, probationary provisions create real job insecurity for a candidate.

Entering into a new affiliation is a leap of faith both for the employer and the employee. If the circumstances do not work out, the employer should fairly compensate the employee for the notice period and ask them not to return to work or otherwise allow them to keep working the notice period while they search for a new position.
 

Acceleration of notice

Another objectionable provision that employers like to include in their contracts is one which allows the employer to accelerate and immediately terminate an employee who has given proper notice.

The contract will contain a standard notice provision, but when the health care professional submits notice, their last date is suddenly accelerated, and they are released without further compensation, notice, or benefits. This type of provision is particularly offensive to health care employees who take the step of giving proper contractual notice and, similar to the probationary language, can create real job insecurity for an employee who suddenly loses their paycheck and has no new job to start.

Medical workers should be paid for the entire notice period whether or not they are allowed to work. Unfortunately, this type of provision is sometimes hidden in contracts and not noticed by employees, who tend to focus on the notice provision itself. I consider this provision to be a red flag about the employer when I review clients’ contracts.
 

Malpractice tail

Although many employers will claim it is not unusual for an employee to pay for their own malpractice tail, in the current marketplace, the payment of tail can be a deciding factor in whether a candidate accepts a contract.

At a minimum, employers should consider paying for the tail under circumstances where they non-renew a contract, terminate without cause, or the contract is terminated for the employer’s breach. Similarly, I like to seek out payment of the tail by the employer where the contract is terminated owing to a change in the law, use of a force majeure provision, loss of the employer’s hospital contract, or similar provisions where termination is outside the control of the employee.

Employers should also consider a provision where they share the cost of a tail or cover the entire cost on the basis of years of service in order to stand out to a potential candidate.
 

Noncompete provisions

I do not find noncompete provisions to be generally unacceptable when properly written; however, employers should reevaluate the reasonableness of their noncompete language frequently, because such language can make the difference in whether a candidate accepts a contract.

A reasonable noncompete that only protects the employer as necessary and does not restrict the reasonable practice of medicine is always preferable and can be the deciding factor for a candidate. Tying enforcement of a noncompete to reasons for termination (similar to the tail) can also make a positive difference in a candidate’s review of a contract.

Egregious noncompetes, where the candidate is simply informed that the language is “not negotiable,” are unlikely to be compelling to a candidate with other options.
 

Specifics on location, call, schedule

One item potential employees find extremely frustrating about contracts is when it fails to include promises made regarding location, call, and schedule.

These particular items affect a physician’s expectations about a job, including commute time, family life, and lifestyle. An employer or recruiter that makes a lot of promises on these points but won’t commit to the details in writing (or at least offer mutual agreement on these issues) can cause an uncertain candidate to choose the job that offers greater certainty.

There are many provisions of a contract that can make a difference to a particular job applicant. A savvy employer seeking to capture a particular health care professional should find out what the specific goals and needs of the candidate might be and consider adjusting the contract to best satisfy the candidate.

At the end of the day, however, at least for those physicians and others reviewing contracts that are fairly equivalent, it may be the fairness of the contract provisions that end up being the deciding factor.

Ms. Adler is Health Law Group Practice Leader for the law firm Roetzel in Chicago. She reported no relevant conflicts of interest.

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

Health literacy is a multifaceted construct that encompasses the knowledge of health and health systems, utilization of information related to health, and ability to maintain health.¹ Low health literacy impairs health outcomes, disproportionately affecting socioeconomically disadvantaged populations, including racial minorities and the older population. Consistently, it is associated with fewer vaccinations and screenings, higher health care utilization, and poorer ability to take medications or interpret health information.²

With growing utilization of the Internet for health information,³ much patient education now occurs outside the clinic. Differential utilization of the Internet can exacerbate disparities in health outcomes: people with a lower family income more frequently engage in health information and dialogue online.³ Despite opportunities to improve literacy and narrow gaps in care, a lack of awareness, advocacy, and funding limit patient- and community-based initiatives. Herein, we discuss health literacy challenges in dermatology, offer potential solutions, and propose ways that stakeholders can prioritize health literacy advocacy to improve outcomes.

The Importance of Health Literacy in Dermatology

Dermatology patients often face challenges that demand greater health literacy. Active participation in health promotion, protection, and maintenance can remarkably improve outcomes. When patients understand disease pathogenesis and the rationale behind treatment choices, adherence to a treatment regimen might improve.

However, understanding dermatologic diseases and disorders can be challenging. First, many are chronic inflammatory conditions that require intricate treatment regimens. Second, the complexity of those diseases and disorders continues to grow in the era of new research and unprecedented expansion of treatment options.

For chronic conditions that require ongoing complex management, researchers have developed advanced patient tools. For instance, the eczema action plan helps atopic dermatitis patients manage conditions from home.⁴ However, patients with greater literacy and the ability to participate will better utilize such tools and have fewer uncontrolled flares. Patient tools meant to improve outcomes might, instead, widen gaps in care. Even with nonchronic conditions, such as nonmelanoma skin cancer, continued awareness and the need for preventive care, timely diagnosis, and appropriate intervention remain critical.

Limited Accessibility of Patient Education Materials

Patient education in dermatology occurs through several formats. Because online health resources are more readily available to those with less access to health care, the potential for such resources to narrow health disparities is immense. However, online resources have not adequately taken advantage of the opportunity to make health information openly accessible to its users. The readability of online patient education materials on a large expanse of dermatologic conditions is far too advanced.⁵ The readability level of some resources is as high as 17th grade (graduate school), which is much higher than the American Medical Association recommendation⁶ that patient education materials be presented at a 6th-grade level or less. Furthermore, the quality and comprehensiveness of content is highly variable. Rather than serving as an equalizer, the Internet may widen the gap as low health literacy continues to impair the accessibility of health information.

Solutions to Level the Playing Field

What can be done to increase the readability of patient education materials? Leveling the playing field begins with creating materials at an appropriate readability level, including online content, printed handouts, and after-visit summaries in the clinic. Writers of patient education materials should be cognizant of their choice of language and routinely use a free readability checker (https://readabilityformulas.com). Patient education materials should reflect the American Medical Association’s recommended 6th-grade level. Creators should maintain a high standard of quality and comprehensiveness; prior studies note no inverse correlation between readability and quality.⁵ In the age of multimedia presentation, non–print-based materials can be explored, such as audio or video for online content, podcasts, and webinars. Providers also should take the opportunity to be mindful of health literacy in clinic. Beyond assessing the readability of written resources for a patient, assessing that patient’s health literacy and tailoring one’s language will maximize engagement.

Systemic Change Is Needed

Ultimately, systemic change is needed to address the root causes of health literacy disparity, requiring advocacy for social welfare, public health, and public policy initiatives. In recognizing existing efforts, such as community outreach teams and hospital committees to evaluate health literacy materials, numerous barriers remain. Despite the notable impact of health literacy on health outcomes, there is a lack of advocacy and funds to conduct health literacy–related work.⁷ Because dermatologists provide holistic care and remain mindful of patients’ health literacy in the clinic, they should continue to advocate for increased awareness, improved funding, and support for local and federal initiatives.

Final Thoughts

With more opportunities to narrow gaps in care, it is more pertinent than ever to acknowledge the impact of health literacy on dermatology outcomes. Leveling the playing field begins with (1) an awareness of health literacy and (2) creating readable and comprehensible patient education content. Greater advocacy from community and professional organizations; increased funding from nonprofit organizations, industry, and federal institutions; and increased involvement by dermatologists in bringing greater attention to health literacy will improve outcomes in dermatology.

Health literacy is a multifaceted construct that encompasses the knowledge of health and health systems, utilization of information related to health, and ability to maintain health.¹ Low health literacy impairs health outcomes, disproportionately affecting socioeconomically disadvantaged populations, including racial minorities and the older population. Consistently, it is associated with fewer vaccinations and screenings, higher health care utilization, and poorer ability to take medications or interpret health information.²

With growing utilization of the Internet for health information,³ much patient education now occurs outside the clinic. Differential utilization of the Internet can exacerbate disparities in health outcomes: people with a lower family income more frequently engage in health information and dialogue online.³ Despite opportunities to improve literacy and narrow gaps in care, a lack of awareness, advocacy, and funding limit patient- and community-based initiatives. Herein, we discuss health literacy challenges in dermatology, offer potential solutions, and propose ways that stakeholders can prioritize health literacy advocacy to improve outcomes.

The Importance of Health Literacy in Dermatology

Dermatology patients often face challenges that demand greater health literacy. Active participation in health promotion, protection, and maintenance can remarkably improve outcomes. When patients understand disease pathogenesis and the rationale behind treatment choices, adherence to a treatment regimen might improve.

However, understanding dermatologic diseases and disorders can be challenging. First, many are chronic inflammatory conditions that require intricate treatment regimens. Second, the complexity of those diseases and disorders continues to grow in the era of new research and unprecedented expansion of treatment options.

For chronic conditions that require ongoing complex management, researchers have developed advanced patient tools. For instance, the eczema action plan helps atopic dermatitis patients manage conditions from home.⁴ However, patients with greater literacy and the ability to participate will better utilize such tools and have fewer uncontrolled flares. Patient tools meant to improve outcomes might, instead, widen gaps in care. Even with nonchronic conditions, such as nonmelanoma skin cancer, continued awareness and the need for preventive care, timely diagnosis, and appropriate intervention remain critical.

Limited Accessibility of Patient Education Materials

Patient education in dermatology occurs through several formats. Because online health resources are more readily available to those with less access to health care, the potential for such resources to narrow health disparities is immense. However, online resources have not adequately taken advantage of the opportunity to make health information openly accessible to its users. The readability of online patient education materials on a large expanse of dermatologic conditions is far too advanced.⁵ The readability level of some resources is as high as 17th grade (graduate school), which is much higher than the American Medical Association recommendation⁶ that patient education materials be presented at a 6th-grade level or less. Furthermore, the quality and comprehensiveness of content is highly variable. Rather than serving as an equalizer, the Internet may widen the gap as low health literacy continues to impair the accessibility of health information.

Solutions to Level the Playing Field

What can be done to increase the readability of patient education materials? Leveling the playing field begins with creating materials at an appropriate readability level, including online content, printed handouts, and after-visit summaries in the clinic. Writers of patient education materials should be cognizant of their choice of language and routinely use a free readability checker (https://readabilityformulas.com). Patient education materials should reflect the American Medical Association’s recommended 6th-grade level. Creators should maintain a high standard of quality and comprehensiveness; prior studies note no inverse correlation between readability and quality.⁵ In the age of multimedia presentation, non–print-based materials can be explored, such as audio or video for online content, podcasts, and webinars. Providers also should take the opportunity to be mindful of health literacy in clinic. Beyond assessing the readability of written resources for a patient, assessing that patient’s health literacy and tailoring one’s language will maximize engagement.

Systemic Change Is Needed

Ultimately, systemic change is needed to address the root causes of health literacy disparity, requiring advocacy for social welfare, public health, and public policy initiatives. In recognizing existing efforts, such as community outreach teams and hospital committees to evaluate health literacy materials, numerous barriers remain. Despite the notable impact of health literacy on health outcomes, there is a lack of advocacy and funds to conduct health literacy–related work.⁷ Because dermatologists provide holistic care and remain mindful of patients’ health literacy in the clinic, they should continue to advocate for increased awareness, improved funding, and support for local and federal initiatives.

Final Thoughts

With more opportunities to narrow gaps in care, it is more pertinent than ever to acknowledge the impact of health literacy on dermatology outcomes. Leveling the playing field begins with (1) an awareness of health literacy and (2) creating readable and comprehensible patient education content. Greater advocacy from community and professional organizations; increased funding from nonprofit organizations, industry, and federal institutions; and increased involvement by dermatologists in bringing greater attention to health literacy will improve outcomes in dermatology.

Health literacy is a multifaceted construct that encompasses the knowledge of health and health systems, utilization of information related to health, and ability to maintain health.¹ Low health literacy impairs health outcomes, disproportionately affecting socioeconomically disadvantaged populations, including racial minorities and the older population. Consistently, it is associated with fewer vaccinations and screenings, higher health care utilization, and poorer ability to take medications or interpret health information.²

With growing utilization of the Internet for health information,³ much patient education now occurs outside the clinic. Differential utilization of the Internet can exacerbate disparities in health outcomes: people with a lower family income more frequently engage in health information and dialogue online.³ Despite opportunities to improve literacy and narrow gaps in care, a lack of awareness, advocacy, and funding limit patient- and community-based initiatives. Herein, we discuss health literacy challenges in dermatology, offer potential solutions, and propose ways that stakeholders can prioritize health literacy advocacy to improve outcomes.

The Importance of Health Literacy in Dermatology

Dermatology patients often face challenges that demand greater health literacy. Active participation in health promotion, protection, and maintenance can remarkably improve outcomes. When patients understand disease pathogenesis and the rationale behind treatment choices, adherence to a treatment regimen might improve.

However, understanding dermatologic diseases and disorders can be challenging. First, many are chronic inflammatory conditions that require intricate treatment regimens. Second, the complexity of those diseases and disorders continues to grow in the era of new research and unprecedented expansion of treatment options.

For chronic conditions that require ongoing complex management, researchers have developed advanced patient tools. For instance, the eczema action plan helps atopic dermatitis patients manage conditions from home.⁴ However, patients with greater literacy and the ability to participate will better utilize such tools and have fewer uncontrolled flares. Patient tools meant to improve outcomes might, instead, widen gaps in care. Even with nonchronic conditions, such as nonmelanoma skin cancer, continued awareness and the need for preventive care, timely diagnosis, and appropriate intervention remain critical.

Limited Accessibility of Patient Education Materials

Patient education in dermatology occurs through several formats. Because online health resources are more readily available to those with less access to health care, the potential for such resources to narrow health disparities is immense. However, online resources have not adequately taken advantage of the opportunity to make health information openly accessible to its users. The readability of online patient education materials on a large expanse of dermatologic conditions is far too advanced.⁵ The readability level of some resources is as high as 17th grade (graduate school), which is much higher than the American Medical Association recommendation⁶ that patient education materials be presented at a 6th-grade level or less. Furthermore, the quality and comprehensiveness of content is highly variable. Rather than serving as an equalizer, the Internet may widen the gap as low health literacy continues to impair the accessibility of health information.

Solutions to Level the Playing Field

What can be done to increase the readability of patient education materials? Leveling the playing field begins with creating materials at an appropriate readability level, including online content, printed handouts, and after-visit summaries in the clinic. Writers of patient education materials should be cognizant of their choice of language and routinely use a free readability checker (https://readabilityformulas.com). Patient education materials should reflect the American Medical Association’s recommended 6th-grade level. Creators should maintain a high standard of quality and comprehensiveness; prior studies note no inverse correlation between readability and quality.⁵ In the age of multimedia presentation, non–print-based materials can be explored, such as audio or video for online content, podcasts, and webinars. Providers also should take the opportunity to be mindful of health literacy in clinic. Beyond assessing the readability of written resources for a patient, assessing that patient’s health literacy and tailoring one’s language will maximize engagement.

Systemic Change Is Needed

Ultimately, systemic change is needed to address the root causes of health literacy disparity, requiring advocacy for social welfare, public health, and public policy initiatives. In recognizing existing efforts, such as community outreach teams and hospital committees to evaluate health literacy materials, numerous barriers remain. Despite the notable impact of health literacy on health outcomes, there is a lack of advocacy and funds to conduct health literacy–related work.⁷ Because dermatologists provide holistic care and remain mindful of patients’ health literacy in the clinic, they should continue to advocate for increased awareness, improved funding, and support for local and federal initiatives.

Final Thoughts

With more opportunities to narrow gaps in care, it is more pertinent than ever to acknowledge the impact of health literacy on dermatology outcomes. Leveling the playing field begins with (1) an awareness of health literacy and (2) creating readable and comprehensible patient education content. Greater advocacy from community and professional organizations; increased funding from nonprofit organizations, industry, and federal institutions; and increased involvement by dermatologists in bringing greater attention to health literacy will improve outcomes in dermatology.

The unfortunate death of Lori McClintock, wife of northern California congressman Tom McClintock, shortly after consuming the herbal remedy white mulberry leaf on Dec. 15, 2021, gives us the opportunity to discuss how to better protect the American public from nutritional supplements with claims to aid health. Mulberry leaf has been purported to lower blood glucose levels, cholesterol, and inflammation as well as promote weight loss.

Many people desire to improve their health with concoctions purported to be “natural” or “from nature” instead of seeing a doctor and taking a medication or other therapy that is evidenced-based and backed by approval from the Food and Drug Administration. With the burgeoning prevalence of obesity and type 2 diabetes in this country (and worldwide) and the lack of a magic bullet that can stop the progression of these life-threatening diseases, many Americans turn to herbal and nutritional supplements that claim to promote weight loss and improve health.

Passed in 1994, the Dietary Supplement Health and Education Act (DSHEA) has allowed manufacturers of herbal and nutritional supplements to be “off the radar” of government regulators, unless their products have been shown to do harm – which is the government’s burden to prove.

A dietary supplement is defined as a product containing one or more vitamin, mineral, herb, or other botanical; amino acid; or other substance that would increase the total dietary intake of that product.

DSHEA exempted dietary supplements from the rigorous safety and efficacy testing that medications must undergo for various disease states, which is regulated by the FDA.
 

People with obesity may fall prey to dietary supplements’ claims

Persons suffering from obesity and its metabolic sequelae may be susceptible to the claims of dietary supplements because:

• The stigma associated with obesity, including the lack of understanding that obesity is a disease not under a person’s control, may make those with the disease wish to remedy it on their own out of shame and peer pressure.
• Clinicians and doctors traditionally have not been trained in obesity medicine so they aren’t comfortable treating obesity.
• It’s only fairly recently that obesity was recognized as a disease, so many insurance companies still don’t reimburse for obesity treatments, including the agents that can suppress appetite and result in weight loss.

For all of these reasons and more, only 2% or less of the millions of Americans suffering from obesity are treated with an antiobesity agent each year.

This has paved the way for the dietary supplement industry to prey on a desperate population, in much the same way that fad diets continue to attract multitudes of Americans. These supplements, however, carry much more risk than fad diets.

The solution, of course, is better regulation of the supplement industry, but it’s also improvement of how obesity is treated by the medical community.
 

How can clinicians and the community help?

Government, academic, community, clinical, and lay persons are more frequently recognizing obesity as a disease. Stigma will slowly come to a halt, as it has for other diseases such as depression and addiction to alcohol and drugs. Medications that have undergone rigorous testing for safety and efficacy eventually will be prescribed more and covered by healthcare insurance. Clinicians, and specifically physicians, are the most trusted persons in terms of giving medical advice. We need to ask patients whether they are taking supplements and be vocal about their lack of protection against harm, as allowed by DSHEA.

It would not be overkill to add prompts to the medical record to ask patients not only about smoking, alcohol, and drug use but also about supplements of all kinds. Some medical records do use these prompts but they are not as ubiquitous as those for smoking, alcohol, and drug use.

The supplement industry is powerful, but so is the medical industry when it comes to lobbying for change. It is ironic that Lori McClintock was the wife of a congressman. Perhaps the silver lining is future work toward legislation advocating for an end to these tragic deaths from poorly regulated supplements. Alignment with government in pushing for stricter regulations could save lives in the future.

Dr. Apovian is a faculty member, department of medicine, division of endocrinology, diabetes, and hypertension; and codirector, Center for Weight Management and Wellness, Boston. She disclosed ties with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.



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

The unfortunate death of Lori McClintock, wife of northern California congressman Tom McClintock, shortly after consuming the herbal remedy white mulberry leaf on Dec. 15, 2021, gives us the opportunity to discuss how to better protect the American public from nutritional supplements with claims to aid health. Mulberry leaf has been purported to lower blood glucose levels, cholesterol, and inflammation as well as promote weight loss.

Many people desire to improve their health with concoctions purported to be “natural” or “from nature” instead of seeing a doctor and taking a medication or other therapy that is evidenced-based and backed by approval from the Food and Drug Administration. With the burgeoning prevalence of obesity and type 2 diabetes in this country (and worldwide) and the lack of a magic bullet that can stop the progression of these life-threatening diseases, many Americans turn to herbal and nutritional supplements that claim to promote weight loss and improve health.

Passed in 1994, the Dietary Supplement Health and Education Act (DSHEA) has allowed manufacturers of herbal and nutritional supplements to be “off the radar” of government regulators, unless their products have been shown to do harm – which is the government’s burden to prove.

A dietary supplement is defined as a product containing one or more vitamin, mineral, herb, or other botanical; amino acid; or other substance that would increase the total dietary intake of that product.

DSHEA exempted dietary supplements from the rigorous safety and efficacy testing that medications must undergo for various disease states, which is regulated by the FDA.
 

People with obesity may fall prey to dietary supplements’ claims

Persons suffering from obesity and its metabolic sequelae may be susceptible to the claims of dietary supplements because:

• The stigma associated with obesity, including the lack of understanding that obesity is a disease not under a person’s control, may make those with the disease wish to remedy it on their own out of shame and peer pressure.
• Clinicians and doctors traditionally have not been trained in obesity medicine so they aren’t comfortable treating obesity.
• It’s only fairly recently that obesity was recognized as a disease, so many insurance companies still don’t reimburse for obesity treatments, including the agents that can suppress appetite and result in weight loss.

For all of these reasons and more, only 2% or less of the millions of Americans suffering from obesity are treated with an antiobesity agent each year.

This has paved the way for the dietary supplement industry to prey on a desperate population, in much the same way that fad diets continue to attract multitudes of Americans. These supplements, however, carry much more risk than fad diets.

The solution, of course, is better regulation of the supplement industry, but it’s also improvement of how obesity is treated by the medical community.
 

How can clinicians and the community help?

Government, academic, community, clinical, and lay persons are more frequently recognizing obesity as a disease. Stigma will slowly come to a halt, as it has for other diseases such as depression and addiction to alcohol and drugs. Medications that have undergone rigorous testing for safety and efficacy eventually will be prescribed more and covered by healthcare insurance. Clinicians, and specifically physicians, are the most trusted persons in terms of giving medical advice. We need to ask patients whether they are taking supplements and be vocal about their lack of protection against harm, as allowed by DSHEA.

It would not be overkill to add prompts to the medical record to ask patients not only about smoking, alcohol, and drug use but also about supplements of all kinds. Some medical records do use these prompts but they are not as ubiquitous as those for smoking, alcohol, and drug use.

The supplement industry is powerful, but so is the medical industry when it comes to lobbying for change. It is ironic that Lori McClintock was the wife of a congressman. Perhaps the silver lining is future work toward legislation advocating for an end to these tragic deaths from poorly regulated supplements. Alignment with government in pushing for stricter regulations could save lives in the future.

Dr. Apovian is a faculty member, department of medicine, division of endocrinology, diabetes, and hypertension; and codirector, Center for Weight Management and Wellness, Boston. She disclosed ties with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.



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

The unfortunate death of Lori McClintock, wife of northern California congressman Tom McClintock, shortly after consuming the herbal remedy white mulberry leaf on Dec. 15, 2021, gives us the opportunity to discuss how to better protect the American public from nutritional supplements with claims to aid health. Mulberry leaf has been purported to lower blood glucose levels, cholesterol, and inflammation as well as promote weight loss.

Many people desire to improve their health with concoctions purported to be “natural” or “from nature” instead of seeing a doctor and taking a medication or other therapy that is evidenced-based and backed by approval from the Food and Drug Administration. With the burgeoning prevalence of obesity and type 2 diabetes in this country (and worldwide) and the lack of a magic bullet that can stop the progression of these life-threatening diseases, many Americans turn to herbal and nutritional supplements that claim to promote weight loss and improve health.

Passed in 1994, the Dietary Supplement Health and Education Act (DSHEA) has allowed manufacturers of herbal and nutritional supplements to be “off the radar” of government regulators, unless their products have been shown to do harm – which is the government’s burden to prove.

A dietary supplement is defined as a product containing one or more vitamin, mineral, herb, or other botanical; amino acid; or other substance that would increase the total dietary intake of that product.

DSHEA exempted dietary supplements from the rigorous safety and efficacy testing that medications must undergo for various disease states, which is regulated by the FDA.
 

People with obesity may fall prey to dietary supplements’ claims

Persons suffering from obesity and its metabolic sequelae may be susceptible to the claims of dietary supplements because:

• The stigma associated with obesity, including the lack of understanding that obesity is a disease not under a person’s control, may make those with the disease wish to remedy it on their own out of shame and peer pressure.
• Clinicians and doctors traditionally have not been trained in obesity medicine so they aren’t comfortable treating obesity.
• It’s only fairly recently that obesity was recognized as a disease, so many insurance companies still don’t reimburse for obesity treatments, including the agents that can suppress appetite and result in weight loss.

For all of these reasons and more, only 2% or less of the millions of Americans suffering from obesity are treated with an antiobesity agent each year.

This has paved the way for the dietary supplement industry to prey on a desperate population, in much the same way that fad diets continue to attract multitudes of Americans. These supplements, however, carry much more risk than fad diets.

The solution, of course, is better regulation of the supplement industry, but it’s also improvement of how obesity is treated by the medical community.
 

How can clinicians and the community help?

Government, academic, community, clinical, and lay persons are more frequently recognizing obesity as a disease. Stigma will slowly come to a halt, as it has for other diseases such as depression and addiction to alcohol and drugs. Medications that have undergone rigorous testing for safety and efficacy eventually will be prescribed more and covered by healthcare insurance. Clinicians, and specifically physicians, are the most trusted persons in terms of giving medical advice. We need to ask patients whether they are taking supplements and be vocal about their lack of protection against harm, as allowed by DSHEA.

It would not be overkill to add prompts to the medical record to ask patients not only about smoking, alcohol, and drug use but also about supplements of all kinds. Some medical records do use these prompts but they are not as ubiquitous as those for smoking, alcohol, and drug use.

The supplement industry is powerful, but so is the medical industry when it comes to lobbying for change. It is ironic that Lori McClintock was the wife of a congressman. Perhaps the silver lining is future work toward legislation advocating for an end to these tragic deaths from poorly regulated supplements. Alignment with government in pushing for stricter regulations could save lives in the future.

Dr. Apovian is a faculty member, department of medicine, division of endocrinology, diabetes, and hypertension; and codirector, Center for Weight Management and Wellness, Boston. She disclosed ties with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.



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

One of psychiatry’s long-standing dogmas is that personality disorders are enduring, unchangeable, and not amenable to treatment with potent psychotropics or intensive psychotherapy. I propose that this dogma may soon be shattered.

Several other dogmas in psychiatry have been demolished over the past several decades:

• that “insanity” is completely irreversible and requires lifetime institutionalization. The serendipitous discovery of chlorpromazine¹ annihilated this centuries-old dogma
• that chronic, severe, refractory depression (with ongoing suicidal urges) that fails to improve with pharmacotherapy or electroconvulsive therapy (ECT) is hopeless and untreatable, until ketamine not only pulverized this dogma, but did it with lightning speed, dazzling us all²
• that dissociative agents such as ketamine are dangerous and condemnable drugs of abuse, until the therapeutic effect of ketamine slayed that dragon³
• that ECT “fries” the brain (as malevolently propagated by antipsychiatry cults), which was completely disproven by neuroimaging studies that show the hippocampus (which shrinks during depression) actually grows by >10% after a few ECT sessions⁴
• that psychotherapy is not a “real” treatment because talking cannot reverse a psychiatric brain disorder, until studies showed significant neuroplasticity with psychotherapy and decrease in inflammatory biomarkers with cognitive-behavioral therapy (CBT)⁵
• that persons with refractory hallucinations and delusions are doomed to a life of disability, until clozapine torpedoed that pessimistic dogma⁶
• that hallucinogens/psychedelics are dangerous and should be banned, until a jarring paradigm shift occurred with the discovery of psilocybin’s transformative effects, and the remarkable therapeutic effects of its mystical trips.⁷

Psilocybin’s therapeutic effects

Psilocybin has already proved to have a strong and lasting effect on depression and promises to have therapeutic benefits for patients with substance use disorders, posttraumatic stress disorder (PTSD), and anxiety.⁸ In addition, when the multiple psychological and neuro­biological effects of psilocybin (and of other psychedelics) are examined, I see a very promising path to amelioration of severe personality disorders such as psychopathy, antisocial behavior, and narcissism. The mechanism(s) of action of psilocybin on the human brain are drastically different from any man-made psychotropic agent. As a psychiatric neuroscientist, I envision the neurologic impact of psilocybin to be conducive to a complete transformation of a patient’s view of themself, other people, and the meaning of life. It is reminiscent of religious conversion.

The psychological effects of psilocybin in humans have been described as follows:

• emotional breakthrough⁹
• increased psychological flexibility,^10,11 a very cortical effect
• mystical experience,¹² which results in sudden and significant changes in behavior and perception and includes the following dimensions: sacredness, noetic quality, deeply felt positive mood, ineffability, paradoxicality, and transcendence of time and space¹³
• oceanic boundlessness, feeling “one with the universe”¹⁴
• universal interconnectedness, insightfulness, blissful state, spiritual experience¹⁴
• ego dissolution,¹⁵ with loss of one’s personal identity
• increased neuroplasticity¹⁶
• changes in cognition and increase in insight.¹⁷

The neurobiological effects of psilocybin are mediated by serotonin 5HT2A agonism and include the following¹⁸:

• reduction in the activity of the medial prefrontal cortex, which regulates memory, attention, inhibitory control, and habit
• a decrease in the connectivity between the medial prefrontal cortex and the posterior cingulate cortex, which regulates memory and emotions
• reducing the default mode network, which is active during rest, stimulating internal thoughts and reminiscing about previous feelings and events, sometimes including ruminations. Psilocybin reverses those processes to thinking about others, not just the self, and becoming more open-minded about the world and other people. This can be therapeutic for depression, which is often associated with negative ruminations but also with entrenched habits (addictive behaviors), anxiety, PTSD, and obsessive-compulsive disorders
• increased global functional connectivity among various brain networks, leading to stronger functional integration of behavior
• collapse of major cortical oscillatory rhythms such as alpha and others that perpetuate “prior” beliefs
• extensive neuroplasticity and recalibration of thought processes and decomposition of pathological beliefs, referred to as REBUS (relaxed beliefs under psychedelics).

The bottom line is psilocybin and other psychedelics can dramatically alter, reshape, and relax rigid beliefs and personality traits by decreasing “neuroticism” and increasing “extraversion,” insightfulness, openness, and possibly conscientiousness.¹⁹ Although no studies of psychedelics in psychopathic, antisocial, or narcissistic personality disorders have been conducted, it is very reasonable to speculate that psilocybin may reverse traits of these disorders such as callousness, lack of empathy, and pathological self-centeredness.

Going further, a preliminary report suggests psilocybin can modify political views by decreasing authoritarianism and increasing libertarianism.^20,21 In the current political zeitgeist, could psychedelics such as psilocybin reduce or even eliminate political extremism and visceral hatred on all sides? It would be remarkable research to carry out to heal a politically divided populace.The dogma of untreatable personality disorders or hopelessly entrenched political extremism is on the chopping block, and psychedelics offer hope to splinter those beliefs by concurrently remodeling brain tissue (neuroplasticity) and rectifying the mindset (psychoplasticity).

One of psychiatry’s long-standing dogmas is that personality disorders are enduring, unchangeable, and not amenable to treatment with potent psychotropics or intensive psychotherapy. I propose that this dogma may soon be shattered.

Several other dogmas in psychiatry have been demolished over the past several decades:

• that “insanity” is completely irreversible and requires lifetime institutionalization. The serendipitous discovery of chlorpromazine¹ annihilated this centuries-old dogma
• that chronic, severe, refractory depression (with ongoing suicidal urges) that fails to improve with pharmacotherapy or electroconvulsive therapy (ECT) is hopeless and untreatable, until ketamine not only pulverized this dogma, but did it with lightning speed, dazzling us all²
• that dissociative agents such as ketamine are dangerous and condemnable drugs of abuse, until the therapeutic effect of ketamine slayed that dragon³
• that ECT “fries” the brain (as malevolently propagated by antipsychiatry cults), which was completely disproven by neuroimaging studies that show the hippocampus (which shrinks during depression) actually grows by >10% after a few ECT sessions⁴
• that psychotherapy is not a “real” treatment because talking cannot reverse a psychiatric brain disorder, until studies showed significant neuroplasticity with psychotherapy and decrease in inflammatory biomarkers with cognitive-behavioral therapy (CBT)⁵
• that persons with refractory hallucinations and delusions are doomed to a life of disability, until clozapine torpedoed that pessimistic dogma⁶
• that hallucinogens/psychedelics are dangerous and should be banned, until a jarring paradigm shift occurred with the discovery of psilocybin’s transformative effects, and the remarkable therapeutic effects of its mystical trips.⁷

Psilocybin’s therapeutic effects

Psilocybin has already proved to have a strong and lasting effect on depression and promises to have therapeutic benefits for patients with substance use disorders, posttraumatic stress disorder (PTSD), and anxiety.⁸ In addition, when the multiple psychological and neuro­biological effects of psilocybin (and of other psychedelics) are examined, I see a very promising path to amelioration of severe personality disorders such as psychopathy, antisocial behavior, and narcissism. The mechanism(s) of action of psilocybin on the human brain are drastically different from any man-made psychotropic agent. As a psychiatric neuroscientist, I envision the neurologic impact of psilocybin to be conducive to a complete transformation of a patient’s view of themself, other people, and the meaning of life. It is reminiscent of religious conversion.

The psychological effects of psilocybin in humans have been described as follows:

• emotional breakthrough⁹
• increased psychological flexibility,^10,11 a very cortical effect
• mystical experience,¹² which results in sudden and significant changes in behavior and perception and includes the following dimensions: sacredness, noetic quality, deeply felt positive mood, ineffability, paradoxicality, and transcendence of time and space¹³
• oceanic boundlessness, feeling “one with the universe”¹⁴
• universal interconnectedness, insightfulness, blissful state, spiritual experience¹⁴
• ego dissolution,¹⁵ with loss of one’s personal identity
• increased neuroplasticity¹⁶
• changes in cognition and increase in insight.¹⁷

The neurobiological effects of psilocybin are mediated by serotonin 5HT2A agonism and include the following¹⁸:

• reduction in the activity of the medial prefrontal cortex, which regulates memory, attention, inhibitory control, and habit
• a decrease in the connectivity between the medial prefrontal cortex and the posterior cingulate cortex, which regulates memory and emotions
• reducing the default mode network, which is active during rest, stimulating internal thoughts and reminiscing about previous feelings and events, sometimes including ruminations. Psilocybin reverses those processes to thinking about others, not just the self, and becoming more open-minded about the world and other people. This can be therapeutic for depression, which is often associated with negative ruminations but also with entrenched habits (addictive behaviors), anxiety, PTSD, and obsessive-compulsive disorders
• increased global functional connectivity among various brain networks, leading to stronger functional integration of behavior
• collapse of major cortical oscillatory rhythms such as alpha and others that perpetuate “prior” beliefs
• extensive neuroplasticity and recalibration of thought processes and decomposition of pathological beliefs, referred to as REBUS (relaxed beliefs under psychedelics).

The bottom line is psilocybin and other psychedelics can dramatically alter, reshape, and relax rigid beliefs and personality traits by decreasing “neuroticism” and increasing “extraversion,” insightfulness, openness, and possibly conscientiousness.¹⁹ Although no studies of psychedelics in psychopathic, antisocial, or narcissistic personality disorders have been conducted, it is very reasonable to speculate that psilocybin may reverse traits of these disorders such as callousness, lack of empathy, and pathological self-centeredness.

Going further, a preliminary report suggests psilocybin can modify political views by decreasing authoritarianism and increasing libertarianism.^20,21 In the current political zeitgeist, could psychedelics such as psilocybin reduce or even eliminate political extremism and visceral hatred on all sides? It would be remarkable research to carry out to heal a politically divided populace.The dogma of untreatable personality disorders or hopelessly entrenched political extremism is on the chopping block, and psychedelics offer hope to splinter those beliefs by concurrently remodeling brain tissue (neuroplasticity) and rectifying the mindset (psychoplasticity).

One of psychiatry’s long-standing dogmas is that personality disorders are enduring, unchangeable, and not amenable to treatment with potent psychotropics or intensive psychotherapy. I propose that this dogma may soon be shattered.

Several other dogmas in psychiatry have been demolished over the past several decades:

• that “insanity” is completely irreversible and requires lifetime institutionalization. The serendipitous discovery of chlorpromazine¹ annihilated this centuries-old dogma
• that chronic, severe, refractory depression (with ongoing suicidal urges) that fails to improve with pharmacotherapy or electroconvulsive therapy (ECT) is hopeless and untreatable, until ketamine not only pulverized this dogma, but did it with lightning speed, dazzling us all²
• that dissociative agents such as ketamine are dangerous and condemnable drugs of abuse, until the therapeutic effect of ketamine slayed that dragon³
• that ECT “fries” the brain (as malevolently propagated by antipsychiatry cults), which was completely disproven by neuroimaging studies that show the hippocampus (which shrinks during depression) actually grows by >10% after a few ECT sessions⁴
• that psychotherapy is not a “real” treatment because talking cannot reverse a psychiatric brain disorder, until studies showed significant neuroplasticity with psychotherapy and decrease in inflammatory biomarkers with cognitive-behavioral therapy (CBT)⁵
• that persons with refractory hallucinations and delusions are doomed to a life of disability, until clozapine torpedoed that pessimistic dogma⁶
• that hallucinogens/psychedelics are dangerous and should be banned, until a jarring paradigm shift occurred with the discovery of psilocybin’s transformative effects, and the remarkable therapeutic effects of its mystical trips.⁷

Psilocybin’s therapeutic effects

Psilocybin has already proved to have a strong and lasting effect on depression and promises to have therapeutic benefits for patients with substance use disorders, posttraumatic stress disorder (PTSD), and anxiety.⁸ In addition, when the multiple psychological and neuro­biological effects of psilocybin (and of other psychedelics) are examined, I see a very promising path to amelioration of severe personality disorders such as psychopathy, antisocial behavior, and narcissism. The mechanism(s) of action of psilocybin on the human brain are drastically different from any man-made psychotropic agent. As a psychiatric neuroscientist, I envision the neurologic impact of psilocybin to be conducive to a complete transformation of a patient’s view of themself, other people, and the meaning of life. It is reminiscent of religious conversion.

The psychological effects of psilocybin in humans have been described as follows:

• emotional breakthrough⁹
• increased psychological flexibility,^10,11 a very cortical effect
• mystical experience,¹² which results in sudden and significant changes in behavior and perception and includes the following dimensions: sacredness, noetic quality, deeply felt positive mood, ineffability, paradoxicality, and transcendence of time and space¹³
• oceanic boundlessness, feeling “one with the universe”¹⁴
• universal interconnectedness, insightfulness, blissful state, spiritual experience¹⁴
• ego dissolution,¹⁵ with loss of one’s personal identity
• increased neuroplasticity¹⁶
• changes in cognition and increase in insight.¹⁷

The neurobiological effects of psilocybin are mediated by serotonin 5HT2A agonism and include the following¹⁸:

• reduction in the activity of the medial prefrontal cortex, which regulates memory, attention, inhibitory control, and habit
• a decrease in the connectivity between the medial prefrontal cortex and the posterior cingulate cortex, which regulates memory and emotions
• reducing the default mode network, which is active during rest, stimulating internal thoughts and reminiscing about previous feelings and events, sometimes including ruminations. Psilocybin reverses those processes to thinking about others, not just the self, and becoming more open-minded about the world and other people. This can be therapeutic for depression, which is often associated with negative ruminations but also with entrenched habits (addictive behaviors), anxiety, PTSD, and obsessive-compulsive disorders
• increased global functional connectivity among various brain networks, leading to stronger functional integration of behavior
• collapse of major cortical oscillatory rhythms such as alpha and others that perpetuate “prior” beliefs
• extensive neuroplasticity and recalibration of thought processes and decomposition of pathological beliefs, referred to as REBUS (relaxed beliefs under psychedelics).

The bottom line is psilocybin and other psychedelics can dramatically alter, reshape, and relax rigid beliefs and personality traits by decreasing “neuroticism” and increasing “extraversion,” insightfulness, openness, and possibly conscientiousness.¹⁹ Although no studies of psychedelics in psychopathic, antisocial, or narcissistic personality disorders have been conducted, it is very reasonable to speculate that psilocybin may reverse traits of these disorders such as callousness, lack of empathy, and pathological self-centeredness.

Going further, a preliminary report suggests psilocybin can modify political views by decreasing authoritarianism and increasing libertarianism.^20,21 In the current political zeitgeist, could psychedelics such as psilocybin reduce or even eliminate political extremism and visceral hatred on all sides? It would be remarkable research to carry out to heal a politically divided populace.The dogma of untreatable personality disorders or hopelessly entrenched political extremism is on the chopping block, and psychedelics offer hope to splinter those beliefs by concurrently remodeling brain tissue (neuroplasticity) and rectifying the mindset (psychoplasticity).

The series “Neurotransmitter-based diagnosis and treatment: A hypothesis” (Part 1: Current Psychiatry, May 2022, p. 30-36, doi:10.12788/cp.0242; Part 2: Current Psychiatry, June 2022, p. 28-33, doi:10.12788/cp.0253; and Part 3: Current Psychiatry, July 2022, p. 34-40, doi:10.12788/cp.0260) translated biological psychiatry’s working causal theory into actionable clinical ideas.

The presentation of abnormal neuro­transmission may occur along a continuum. For example, extreme dopamine deficiency can present as catatonia, moderate deficiency may present with inattention, normal activity permits adaptive functioning, and excitatory delirium and sudden death may be at the extreme end of dopa­minergic excess.¹

The amplitude, rate of change, and location of neurotransmitter dysfunction may determine which specialty takes the primary treatment role. Fatigue, pain, sleep difficulty, and emotional distress require clinicians to understand the whole patient, which is why health care professionals need cross training in psychiatry, and psychiatry recognizes multisystem pathology.

The recognition and treatment of substance use disorders requires an understanding of neurotransmitter symptoms, in terms of both acute drug effects and withdrawal. Fallows² provides this information in an accessible chart. Discussions of neurotransmitters also have value in managing psychotropic medication withdrawal.³

Acetylcholine is another neuro­transmitter of importance; it is essential to normal motor, cognitive, and emotional function. Extreme cholinergic deficiency or anticholinergic crisis has symptoms of pupillary dilation, psychosis, and delirium.^4-6 The progressive decline seen in certain dementias is related in part to cholinergic deficit. Dominance of cholinergic activity is associated with depression and biomarkers such as increased rapid eye movement (REM) density, a measure of the frequency of rapid eye movements during REM sleep.⁷ Cholinergic excess or cholinergic crisis may present with symptoms of salivation, lacrimation, muscle weakness, delirium, or paralysis.⁸

The articles alluded to the interaction of neurotransmitter systems (eg, “dopamine blockade helps with endorphin suppression”). Isolating the effects of a single neurotransmitter is useful, but covariance of neurotransmitter activity also has diagnostic and treatment implications.^9-11 Abnormalities in these interactions may be part of the causal process in fundamental cognitive functions.¹² If endorphin suppression is insensitive to dopamine blockade, a relative endorphin excess may create symptoms. If acetylcholine changes are normally balanced by a relative increase in dopamine and norepinephrine, then a weak catecholamine response would fit the catecholamine-cholinergic balance hypothesis of depression. Neurotransmitter interactions are well worked out in the neurology of the basal ganglia but less clear in the frontal and limbic systems.¹³

Quantification has been applied in some areas of clinical care. Morphine equivalents are used to express opiate potency, and there are algorithms to summarize multiple medication effects on respiratory depression/overdose risk.^14,15 Chlorpromazine equivalents were used to translate a range of antipsychotic potencies in the early days of antipsychotic treatment. Adverse effects and some treatment responses partially corresponded to the level of dopamine blockade, but not without noise. There is a wide range of variance as antipsychotic potency is assessed for clinical efficacy.¹⁶ We are still working on the array of medication potency and selectivity across neurotransmitter systems.^17,18 For example, paroxetine is a potent serotonin reuptake blocker but less selective than citalopram, particularly antagonizing cholinergic muscarinic receptors.

The authors noted their hypothesis needs further elaboration and quantification as psychiatry moves from impressionistic practice to firmer science. Measurement of neuro­transmitter activity is an area of intense research. Biomeasures have yet to add much value to the clinical practice of psychiatry, but we hope for progress. Functional neuroimaging with sophisticated algorithms is beginning to detail neocortical activity.¹⁹ CSF measurement of dopamine and serotonin metabolites seem to correlate with severe depression and suicidal behavior. Noninvasive, wearable technologies to measure galvanic skin response, oxygenation, and neurotransmitter metabolic products may add to neuro-transmitter-based assessment and treatment.

Neurotransmitters are one aspect of brain function. Other processes, such as hormonal neuromodulation²⁰ and ion channels, may be over- or underactive. Channelopathies are of particular interest in cardiology and neurology but are also notable in pain and emotional disorders.^21-26 Voltage-gated sodium channels are thought to be involved in general anesthesia.²⁷ Adverse effects of some psychotropic medications are best understood as ion channel dysfunction.²⁸ Using the strategy of this hypothesis applied to activation or inactivation of sodium, potassium, and calcium channels can guide useful diagnostic and treatment ideas for further study.

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

Disclosures

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

References

1. Mash DC. Excited delirium and sudden death: a syndromal disorder at the extreme end of the neuropsychiatric continuum. Front Physiol. 2016;7:435.

2. Fallows Z. MIT MedLinks. Accessed August 8, 2022. http://web.mit.edu/zakf/www/drugchart/drugchart11.html

3. Groot PC, van Os J. How user knowledge of psychotropic drug withdrawal resulted in the development of person-specific tapering medication. Ther Adv Psychopharmacol. 2020;10:2045125320932452. doi:10.1177/2045125320932452

4. Picciotto MR, Higley MJ, Mineur YS. Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior. Neuron. 2012;76(1):116-129.

5. Nair VP, Hunter JM. Anticholinesterases and anticholinergic drugs. Continuing Education in Anaesthesia Critical Care & Pain. 2004;4(5):164-168.

6. Dawson AH, Buckley NA. Pharmacological management of anticholinergic delirium--theory, evidence and practice. Br J Clin Pharmacol. 2016;81(3):516-524.

7. Dulawa SC, Janowsky DS. Cholinergic regulation of mood: from basic and clinical studies to emerging therapeutics. Mol Psychiatry. 2019;24(5):694-709.

8. Adeyinka A, Kondamudi NP. Cholinergic Crisis. StatPearls Publishing; 2022.

9. El Mansari M, Guiard BP, Chernoloz O, et al. Relevance of norepinephrine-dopamine interactions in the treatment of major depressive disorder. CNS Neurosci Ther. 2010;16(3):e1-e17.

10. Esposito E. Serotonin-dopamine interaction as a focus of novel antidepressant drugs. Curr Drug Targets. 2006;7(2):177-185.

11. Kringelbach ML, Cruzat J, Cabral J, et al. Dynamic coupling of whole-brain neuronal and neurotransmitter systems. Proc Natl Acad Sci U S A. 2020;117(17):9566-9576.

12. Thiele A, Bellgrove MA. Neuromodulation of attention. Neuron. 2018;97(4):769-785.

13. Muñoz A, Lopez-Lopez A, Labandeira CM, et al. Interactions between the serotonergic and other neurotransmitter systems in the basal ganglia: role in Parkinson’s disease and adverse effects of L-DOPA. Front Neuroanat. 2020;14:26.

14. Nielsen S, Degenhardt L, Hoban B, et al. A synthesis of oral morphine equivalents (OME) for opioid utilisation studies. Pharmacoepidemiol Drug Saf. 2016;25(6):733-737.

15. Lo-Ciganic WH, Huang JL, Zhang HH, et al. Evaluation of machine-learning algorithms for predicting opioid overdose risk among Medicare beneficiaries with opioid prescriptions. JAMA Netw Open. 2019;2(3):e190968. doi:10.1001/jamanetworkopen.2019.0968

16. Dewan MJ, Koss M. The clinical impact of reported variance in potency of antipsychotic agents. Acta Psychiatr Scand. 1995;91(4):229-232.

17. Woods SW. Chlorpromazine equivalent doses for the newer atypical antipsychotics. J Clin Psychiatry. 2003;64(6):663-667.

18. Hayasaka Y, Purgato M, Magni LR, et al. Dose equivalents of antidepressants: evidence-based recommendations from randomized controlled trials. J Affect Disord. 2015;180:179-184.

19. Hansen JY, Shafiei G, Markello RD, et al. Mapping neurotransmitter systems to the structural and functional organization of the human neocortex. bioRxiv. 2021. https://doi.org/10.1101/2021.10.28.466336

20. Hwang WJ, Lee TY, Kim NS, et al. The role of estrogen receptors and their signaling across psychiatric disorders. Int J Mol Sci. 2020;22(1):373.

21. Lawrence JH, Tomaselli GF, Marban E. Ion channels: structure and function. Heart Dis Stroke. 1993;2(1):75-80.

22. Fedele F, Severino P, Bruno N, et al. Role of ion channels in coronary microcirculation: a review of the literature. Future Cardiol. 2013;9(6):897-905.

23. Kumar P, Kumar D, Jha SK, et al. Ion channels in neurological disorders. Adv Protein Chem Struct Biol. 2016;103:97-136.

24. Quagliato LA, Nardi AE. The role of convergent ion channel pathways in microglial phenotypes: a systematic review of the implications for neurological and psychiatric disorders. Transl Psychiatry. 2018;8(1):259.

25. Bianchi MT, Botzolakis EJ. Targeting ligand-gated ion channels in neurology and psychiatry: is pharmacological promiscuity an obstacle or an opportunity? BMC Pharmacol. 2010;10:3.

26. Imbrici P, Camerino DC, Tricarico D. Major channels involved in neuropsychiatric disorders and therapeutic perspectives. Front Genet. 2013;4:76.

27. Xiao J, Chen Z, Yu B. A potential mechanism of sodium channel mediating the general anesthesia induced by propofol. Front Cell Neurosci. 2020;14:593050. doi:10.3389/fncel.2020.593050

28. Kamei S, Sato N, Harayama Y, et al. Molecular analysis of potassium ion channel genes in sudden death cases among patients administered psychotropic drug therapy: are polymorphisms in LQT genes a potential risk factor? J Hum Genet. 2014;59(2):95-99.

The authors respond

Thank you for your thoughtful commen­tary. Our conceptual article was not designed to cover enough ground to be completely thorough. Everything you wrote adds to what we wanted to bring to the reader’s attention. The mechanisms of disease in psychiatry are numerous and still elusive, and the brain’s complexity is staggering. Our main goal was to point out possible correlations between specific symptoms and specific neurotransmitter activity. We had to oversimplify to make the article concise enough for publication. Neurotransmitter effects are based on their synthesis, storage, release, reuptake, and degradation. A receptor’s quantity and quality of function, inhibitors, inducers, and many other factors are involved in neurotransmitter performance. And, of course, there are additional fundamental neurotransmitters beyond the 6 we touched on. Our ability to sort through all of this is still rudimentary. You also reflect on the emerging methods to objectively measure neuro­transmitter activity, which will eventually find their way to clinical practice and become invaluable. Still, we treat people, not tests or pictures, so diagnostic thinking based on clinical presentation will forever remain a cornerstone of dealing with individual patients.

We hope scientists and clinicians such as yourself will improve our concept and make it truly practical.

Dmitry M. Arbuck, MD
Clinical Assistant Professor of Psychiatry and Medicine
Indiana University School of Medicine
Indianapolis, Indiana
President and Medical Director
Indiana Polyclinic
Carmel, Indiana

José Miguel Salmerón, MD
Professor
Department of Psychiatry
Universidad del Valle School of Medicine/Hospital
Universitario del Valle
Cali, Colombia

Disclosures

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

The series “Neurotransmitter-based diagnosis and treatment: A hypothesis” (Part 1: Current Psychiatry, May 2022, p. 30-36, doi:10.12788/cp.0242; Part 2: Current Psychiatry, June 2022, p. 28-33, doi:10.12788/cp.0253; and Part 3: Current Psychiatry, July 2022, p. 34-40, doi:10.12788/cp.0260) translated biological psychiatry’s working causal theory into actionable clinical ideas.

The presentation of abnormal neuro­transmission may occur along a continuum. For example, extreme dopamine deficiency can present as catatonia, moderate deficiency may present with inattention, normal activity permits adaptive functioning, and excitatory delirium and sudden death may be at the extreme end of dopa­minergic excess.¹

The amplitude, rate of change, and location of neurotransmitter dysfunction may determine which specialty takes the primary treatment role. Fatigue, pain, sleep difficulty, and emotional distress require clinicians to understand the whole patient, which is why health care professionals need cross training in psychiatry, and psychiatry recognizes multisystem pathology.

The recognition and treatment of substance use disorders requires an understanding of neurotransmitter symptoms, in terms of both acute drug effects and withdrawal. Fallows² provides this information in an accessible chart. Discussions of neurotransmitters also have value in managing psychotropic medication withdrawal.³

Acetylcholine is another neuro­transmitter of importance; it is essential to normal motor, cognitive, and emotional function. Extreme cholinergic deficiency or anticholinergic crisis has symptoms of pupillary dilation, psychosis, and delirium.^4-6 The progressive decline seen in certain dementias is related in part to cholinergic deficit. Dominance of cholinergic activity is associated with depression and biomarkers such as increased rapid eye movement (REM) density, a measure of the frequency of rapid eye movements during REM sleep.⁷ Cholinergic excess or cholinergic crisis may present with symptoms of salivation, lacrimation, muscle weakness, delirium, or paralysis.⁸

The articles alluded to the interaction of neurotransmitter systems (eg, “dopamine blockade helps with endorphin suppression”). Isolating the effects of a single neurotransmitter is useful, but covariance of neurotransmitter activity also has diagnostic and treatment implications.^9-11 Abnormalities in these interactions may be part of the causal process in fundamental cognitive functions.¹² If endorphin suppression is insensitive to dopamine blockade, a relative endorphin excess may create symptoms. If acetylcholine changes are normally balanced by a relative increase in dopamine and norepinephrine, then a weak catecholamine response would fit the catecholamine-cholinergic balance hypothesis of depression. Neurotransmitter interactions are well worked out in the neurology of the basal ganglia but less clear in the frontal and limbic systems.¹³

Quantification has been applied in some areas of clinical care. Morphine equivalents are used to express opiate potency, and there are algorithms to summarize multiple medication effects on respiratory depression/overdose risk.^14,15 Chlorpromazine equivalents were used to translate a range of antipsychotic potencies in the early days of antipsychotic treatment. Adverse effects and some treatment responses partially corresponded to the level of dopamine blockade, but not without noise. There is a wide range of variance as antipsychotic potency is assessed for clinical efficacy.¹⁶ We are still working on the array of medication potency and selectivity across neurotransmitter systems.^17,18 For example, paroxetine is a potent serotonin reuptake blocker but less selective than citalopram, particularly antagonizing cholinergic muscarinic receptors.

The authors noted their hypothesis needs further elaboration and quantification as psychiatry moves from impressionistic practice to firmer science. Measurement of neuro­transmitter activity is an area of intense research. Biomeasures have yet to add much value to the clinical practice of psychiatry, but we hope for progress. Functional neuroimaging with sophisticated algorithms is beginning to detail neocortical activity.¹⁹ CSF measurement of dopamine and serotonin metabolites seem to correlate with severe depression and suicidal behavior. Noninvasive, wearable technologies to measure galvanic skin response, oxygenation, and neurotransmitter metabolic products may add to neuro-transmitter-based assessment and treatment.

Neurotransmitters are one aspect of brain function. Other processes, such as hormonal neuromodulation²⁰ and ion channels, may be over- or underactive. Channelopathies are of particular interest in cardiology and neurology but are also notable in pain and emotional disorders.^21-26 Voltage-gated sodium channels are thought to be involved in general anesthesia.²⁷ Adverse effects of some psychotropic medications are best understood as ion channel dysfunction.²⁸ Using the strategy of this hypothesis applied to activation or inactivation of sodium, potassium, and calcium channels can guide useful diagnostic and treatment ideas for further study.

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

Disclosures

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

References

1. Mash DC. Excited delirium and sudden death: a syndromal disorder at the extreme end of the neuropsychiatric continuum. Front Physiol. 2016;7:435.

2. Fallows Z. MIT MedLinks. Accessed August 8, 2022. http://web.mit.edu/zakf/www/drugchart/drugchart11.html

3. Groot PC, van Os J. How user knowledge of psychotropic drug withdrawal resulted in the development of person-specific tapering medication. Ther Adv Psychopharmacol. 2020;10:2045125320932452. doi:10.1177/2045125320932452

4. Picciotto MR, Higley MJ, Mineur YS. Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior. Neuron. 2012;76(1):116-129.

5. Nair VP, Hunter JM. Anticholinesterases and anticholinergic drugs. Continuing Education in Anaesthesia Critical Care & Pain. 2004;4(5):164-168.

6. Dawson AH, Buckley NA. Pharmacological management of anticholinergic delirium--theory, evidence and practice. Br J Clin Pharmacol. 2016;81(3):516-524.

7. Dulawa SC, Janowsky DS. Cholinergic regulation of mood: from basic and clinical studies to emerging therapeutics. Mol Psychiatry. 2019;24(5):694-709.

8. Adeyinka A, Kondamudi NP. Cholinergic Crisis. StatPearls Publishing; 2022.

9. El Mansari M, Guiard BP, Chernoloz O, et al. Relevance of norepinephrine-dopamine interactions in the treatment of major depressive disorder. CNS Neurosci Ther. 2010;16(3):e1-e17.

10. Esposito E. Serotonin-dopamine interaction as a focus of novel antidepressant drugs. Curr Drug Targets. 2006;7(2):177-185.

11. Kringelbach ML, Cruzat J, Cabral J, et al. Dynamic coupling of whole-brain neuronal and neurotransmitter systems. Proc Natl Acad Sci U S A. 2020;117(17):9566-9576.

12. Thiele A, Bellgrove MA. Neuromodulation of attention. Neuron. 2018;97(4):769-785.

13. Muñoz A, Lopez-Lopez A, Labandeira CM, et al. Interactions between the serotonergic and other neurotransmitter systems in the basal ganglia: role in Parkinson’s disease and adverse effects of L-DOPA. Front Neuroanat. 2020;14:26.

14. Nielsen S, Degenhardt L, Hoban B, et al. A synthesis of oral morphine equivalents (OME) for opioid utilisation studies. Pharmacoepidemiol Drug Saf. 2016;25(6):733-737.

15. Lo-Ciganic WH, Huang JL, Zhang HH, et al. Evaluation of machine-learning algorithms for predicting opioid overdose risk among Medicare beneficiaries with opioid prescriptions. JAMA Netw Open. 2019;2(3):e190968. doi:10.1001/jamanetworkopen.2019.0968

16. Dewan MJ, Koss M. The clinical impact of reported variance in potency of antipsychotic agents. Acta Psychiatr Scand. 1995;91(4):229-232.

17. Woods SW. Chlorpromazine equivalent doses for the newer atypical antipsychotics. J Clin Psychiatry. 2003;64(6):663-667.

18. Hayasaka Y, Purgato M, Magni LR, et al. Dose equivalents of antidepressants: evidence-based recommendations from randomized controlled trials. J Affect Disord. 2015;180:179-184.

19. Hansen JY, Shafiei G, Markello RD, et al. Mapping neurotransmitter systems to the structural and functional organization of the human neocortex. bioRxiv. 2021. https://doi.org/10.1101/2021.10.28.466336

20. Hwang WJ, Lee TY, Kim NS, et al. The role of estrogen receptors and their signaling across psychiatric disorders. Int J Mol Sci. 2020;22(1):373.

21. Lawrence JH, Tomaselli GF, Marban E. Ion channels: structure and function. Heart Dis Stroke. 1993;2(1):75-80.

22. Fedele F, Severino P, Bruno N, et al. Role of ion channels in coronary microcirculation: a review of the literature. Future Cardiol. 2013;9(6):897-905.

23. Kumar P, Kumar D, Jha SK, et al. Ion channels in neurological disorders. Adv Protein Chem Struct Biol. 2016;103:97-136.

24. Quagliato LA, Nardi AE. The role of convergent ion channel pathways in microglial phenotypes: a systematic review of the implications for neurological and psychiatric disorders. Transl Psychiatry. 2018;8(1):259.

25. Bianchi MT, Botzolakis EJ. Targeting ligand-gated ion channels in neurology and psychiatry: is pharmacological promiscuity an obstacle or an opportunity? BMC Pharmacol. 2010;10:3.

26. Imbrici P, Camerino DC, Tricarico D. Major channels involved in neuropsychiatric disorders and therapeutic perspectives. Front Genet. 2013;4:76.

27. Xiao J, Chen Z, Yu B. A potential mechanism of sodium channel mediating the general anesthesia induced by propofol. Front Cell Neurosci. 2020;14:593050. doi:10.3389/fncel.2020.593050

28. Kamei S, Sato N, Harayama Y, et al. Molecular analysis of potassium ion channel genes in sudden death cases among patients administered psychotropic drug therapy: are polymorphisms in LQT genes a potential risk factor? J Hum Genet. 2014;59(2):95-99.

The authors respond

Thank you for your thoughtful commen­tary. Our conceptual article was not designed to cover enough ground to be completely thorough. Everything you wrote adds to what we wanted to bring to the reader’s attention. The mechanisms of disease in psychiatry are numerous and still elusive, and the brain’s complexity is staggering. Our main goal was to point out possible correlations between specific symptoms and specific neurotransmitter activity. We had to oversimplify to make the article concise enough for publication. Neurotransmitter effects are based on their synthesis, storage, release, reuptake, and degradation. A receptor’s quantity and quality of function, inhibitors, inducers, and many other factors are involved in neurotransmitter performance. And, of course, there are additional fundamental neurotransmitters beyond the 6 we touched on. Our ability to sort through all of this is still rudimentary. You also reflect on the emerging methods to objectively measure neuro­transmitter activity, which will eventually find their way to clinical practice and become invaluable. Still, we treat people, not tests or pictures, so diagnostic thinking based on clinical presentation will forever remain a cornerstone of dealing with individual patients.

We hope scientists and clinicians such as yourself will improve our concept and make it truly practical.

Dmitry M. Arbuck, MD
Clinical Assistant Professor of Psychiatry and Medicine
Indiana University School of Medicine
Indianapolis, Indiana
President and Medical Director
Indiana Polyclinic
Carmel, Indiana

José Miguel Salmerón, MD
Professor
Department of Psychiatry
Universidad del Valle School of Medicine/Hospital
Universitario del Valle
Cali, Colombia

Disclosures

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

The series “Neurotransmitter-based diagnosis and treatment: A hypothesis” (Part 1: Current Psychiatry, May 2022, p. 30-36, doi:10.12788/cp.0242; Part 2: Current Psychiatry, June 2022, p. 28-33, doi:10.12788/cp.0253; and Part 3: Current Psychiatry, July 2022, p. 34-40, doi:10.12788/cp.0260) translated biological psychiatry’s working causal theory into actionable clinical ideas.

The presentation of abnormal neuro­transmission may occur along a continuum. For example, extreme dopamine deficiency can present as catatonia, moderate deficiency may present with inattention, normal activity permits adaptive functioning, and excitatory delirium and sudden death may be at the extreme end of dopa­minergic excess.¹

The amplitude, rate of change, and location of neurotransmitter dysfunction may determine which specialty takes the primary treatment role. Fatigue, pain, sleep difficulty, and emotional distress require clinicians to understand the whole patient, which is why health care professionals need cross training in psychiatry, and psychiatry recognizes multisystem pathology.

The recognition and treatment of substance use disorders requires an understanding of neurotransmitter symptoms, in terms of both acute drug effects and withdrawal. Fallows² provides this information in an accessible chart. Discussions of neurotransmitters also have value in managing psychotropic medication withdrawal.³

Acetylcholine is another neuro­transmitter of importance; it is essential to normal motor, cognitive, and emotional function. Extreme cholinergic deficiency or anticholinergic crisis has symptoms of pupillary dilation, psychosis, and delirium.^4-6 The progressive decline seen in certain dementias is related in part to cholinergic deficit. Dominance of cholinergic activity is associated with depression and biomarkers such as increased rapid eye movement (REM) density, a measure of the frequency of rapid eye movements during REM sleep.⁷ Cholinergic excess or cholinergic crisis may present with symptoms of salivation, lacrimation, muscle weakness, delirium, or paralysis.⁸

The articles alluded to the interaction of neurotransmitter systems (eg, “dopamine blockade helps with endorphin suppression”). Isolating the effects of a single neurotransmitter is useful, but covariance of neurotransmitter activity also has diagnostic and treatment implications.^9-11 Abnormalities in these interactions may be part of the causal process in fundamental cognitive functions.¹² If endorphin suppression is insensitive to dopamine blockade, a relative endorphin excess may create symptoms. If acetylcholine changes are normally balanced by a relative increase in dopamine and norepinephrine, then a weak catecholamine response would fit the catecholamine-cholinergic balance hypothesis of depression. Neurotransmitter interactions are well worked out in the neurology of the basal ganglia but less clear in the frontal and limbic systems.¹³

Quantification has been applied in some areas of clinical care. Morphine equivalents are used to express opiate potency, and there are algorithms to summarize multiple medication effects on respiratory depression/overdose risk.^14,15 Chlorpromazine equivalents were used to translate a range of antipsychotic potencies in the early days of antipsychotic treatment. Adverse effects and some treatment responses partially corresponded to the level of dopamine blockade, but not without noise. There is a wide range of variance as antipsychotic potency is assessed for clinical efficacy.¹⁶ We are still working on the array of medication potency and selectivity across neurotransmitter systems.^17,18 For example, paroxetine is a potent serotonin reuptake blocker but less selective than citalopram, particularly antagonizing cholinergic muscarinic receptors.

The authors noted their hypothesis needs further elaboration and quantification as psychiatry moves from impressionistic practice to firmer science. Measurement of neuro­transmitter activity is an area of intense research. Biomeasures have yet to add much value to the clinical practice of psychiatry, but we hope for progress. Functional neuroimaging with sophisticated algorithms is beginning to detail neocortical activity.¹⁹ CSF measurement of dopamine and serotonin metabolites seem to correlate with severe depression and suicidal behavior. Noninvasive, wearable technologies to measure galvanic skin response, oxygenation, and neurotransmitter metabolic products may add to neuro-transmitter-based assessment and treatment.

Neurotransmitters are one aspect of brain function. Other processes, such as hormonal neuromodulation²⁰ and ion channels, may be over- or underactive. Channelopathies are of particular interest in cardiology and neurology but are also notable in pain and emotional disorders.^21-26 Voltage-gated sodium channels are thought to be involved in general anesthesia.²⁷ Adverse effects of some psychotropic medications are best understood as ion channel dysfunction.²⁸ Using the strategy of this hypothesis applied to activation or inactivation of sodium, potassium, and calcium channels can guide useful diagnostic and treatment ideas for further study.

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

Disclosures

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

References

1. Mash DC. Excited delirium and sudden death: a syndromal disorder at the extreme end of the neuropsychiatric continuum. Front Physiol. 2016;7:435.

2. Fallows Z. MIT MedLinks. Accessed August 8, 2022. http://web.mit.edu/zakf/www/drugchart/drugchart11.html

3. Groot PC, van Os J. How user knowledge of psychotropic drug withdrawal resulted in the development of person-specific tapering medication. Ther Adv Psychopharmacol. 2020;10:2045125320932452. doi:10.1177/2045125320932452

4. Picciotto MR, Higley MJ, Mineur YS. Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior. Neuron. 2012;76(1):116-129.

5. Nair VP, Hunter JM. Anticholinesterases and anticholinergic drugs. Continuing Education in Anaesthesia Critical Care & Pain. 2004;4(5):164-168.

6. Dawson AH, Buckley NA. Pharmacological management of anticholinergic delirium--theory, evidence and practice. Br J Clin Pharmacol. 2016;81(3):516-524.

7. Dulawa SC, Janowsky DS. Cholinergic regulation of mood: from basic and clinical studies to emerging therapeutics. Mol Psychiatry. 2019;24(5):694-709.

8. Adeyinka A, Kondamudi NP. Cholinergic Crisis. StatPearls Publishing; 2022.

9. El Mansari M, Guiard BP, Chernoloz O, et al. Relevance of norepinephrine-dopamine interactions in the treatment of major depressive disorder. CNS Neurosci Ther. 2010;16(3):e1-e17.

10. Esposito E. Serotonin-dopamine interaction as a focus of novel antidepressant drugs. Curr Drug Targets. 2006;7(2):177-185.

11. Kringelbach ML, Cruzat J, Cabral J, et al. Dynamic coupling of whole-brain neuronal and neurotransmitter systems. Proc Natl Acad Sci U S A. 2020;117(17):9566-9576.

12. Thiele A, Bellgrove MA. Neuromodulation of attention. Neuron. 2018;97(4):769-785.

13. Muñoz A, Lopez-Lopez A, Labandeira CM, et al. Interactions between the serotonergic and other neurotransmitter systems in the basal ganglia: role in Parkinson’s disease and adverse effects of L-DOPA. Front Neuroanat. 2020;14:26.

14. Nielsen S, Degenhardt L, Hoban B, et al. A synthesis of oral morphine equivalents (OME) for opioid utilisation studies. Pharmacoepidemiol Drug Saf. 2016;25(6):733-737.

15. Lo-Ciganic WH, Huang JL, Zhang HH, et al. Evaluation of machine-learning algorithms for predicting opioid overdose risk among Medicare beneficiaries with opioid prescriptions. JAMA Netw Open. 2019;2(3):e190968. doi:10.1001/jamanetworkopen.2019.0968

16. Dewan MJ, Koss M. The clinical impact of reported variance in potency of antipsychotic agents. Acta Psychiatr Scand. 1995;91(4):229-232.

17. Woods SW. Chlorpromazine equivalent doses for the newer atypical antipsychotics. J Clin Psychiatry. 2003;64(6):663-667.

18. Hayasaka Y, Purgato M, Magni LR, et al. Dose equivalents of antidepressants: evidence-based recommendations from randomized controlled trials. J Affect Disord. 2015;180:179-184.

19. Hansen JY, Shafiei G, Markello RD, et al. Mapping neurotransmitter systems to the structural and functional organization of the human neocortex. bioRxiv. 2021. https://doi.org/10.1101/2021.10.28.466336

20. Hwang WJ, Lee TY, Kim NS, et al. The role of estrogen receptors and their signaling across psychiatric disorders. Int J Mol Sci. 2020;22(1):373.

21. Lawrence JH, Tomaselli GF, Marban E. Ion channels: structure and function. Heart Dis Stroke. 1993;2(1):75-80.

22. Fedele F, Severino P, Bruno N, et al. Role of ion channels in coronary microcirculation: a review of the literature. Future Cardiol. 2013;9(6):897-905.

23. Kumar P, Kumar D, Jha SK, et al. Ion channels in neurological disorders. Adv Protein Chem Struct Biol. 2016;103:97-136.

24. Quagliato LA, Nardi AE. The role of convergent ion channel pathways in microglial phenotypes: a systematic review of the implications for neurological and psychiatric disorders. Transl Psychiatry. 2018;8(1):259.

25. Bianchi MT, Botzolakis EJ. Targeting ligand-gated ion channels in neurology and psychiatry: is pharmacological promiscuity an obstacle or an opportunity? BMC Pharmacol. 2010;10:3.

26. Imbrici P, Camerino DC, Tricarico D. Major channels involved in neuropsychiatric disorders and therapeutic perspectives. Front Genet. 2013;4:76.

27. Xiao J, Chen Z, Yu B. A potential mechanism of sodium channel mediating the general anesthesia induced by propofol. Front Cell Neurosci. 2020;14:593050. doi:10.3389/fncel.2020.593050

28. Kamei S, Sato N, Harayama Y, et al. Molecular analysis of potassium ion channel genes in sudden death cases among patients administered psychotropic drug therapy: are polymorphisms in LQT genes a potential risk factor? J Hum Genet. 2014;59(2):95-99.

The authors respond

Thank you for your thoughtful commen­tary. Our conceptual article was not designed to cover enough ground to be completely thorough. Everything you wrote adds to what we wanted to bring to the reader’s attention. The mechanisms of disease in psychiatry are numerous and still elusive, and the brain’s complexity is staggering. Our main goal was to point out possible correlations between specific symptoms and specific neurotransmitter activity. We had to oversimplify to make the article concise enough for publication. Neurotransmitter effects are based on their synthesis, storage, release, reuptake, and degradation. A receptor’s quantity and quality of function, inhibitors, inducers, and many other factors are involved in neurotransmitter performance. And, of course, there are additional fundamental neurotransmitters beyond the 6 we touched on. Our ability to sort through all of this is still rudimentary. You also reflect on the emerging methods to objectively measure neuro­transmitter activity, which will eventually find their way to clinical practice and become invaluable. Still, we treat people, not tests or pictures, so diagnostic thinking based on clinical presentation will forever remain a cornerstone of dealing with individual patients.

We hope scientists and clinicians such as yourself will improve our concept and make it truly practical.

Dmitry M. Arbuck, MD
Clinical Assistant Professor of Psychiatry and Medicine
Indiana University School of Medicine
Indianapolis, Indiana
President and Medical Director
Indiana Polyclinic
Carmel, Indiana

José Miguel Salmerón, MD
Professor
Department of Psychiatry
Universidad del Valle School of Medicine/Hospital
Universitario del Valle
Cali, Colombia

Disclosures

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

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.com.

Mr. F, age 42, says he has always been a very anxious person and has chronically found his worrying to negatively affect his life. He says that over the last month his anxiety has been “off the charts” and he is worrying “24/7” due to taking on new responsibilities at his job and his son being diagnosed with lupus. He says his constant worrying is significantly impairing his ability to focus at his job, and he is considering taking a mental health leave from work. His wife reports that she is extremely frustrated because Mr. F has been isolating himself from family and friends; he admits this is true and attributes it to being preoccupied by his worries.

Mr. F endorses chronic insomnia, muscle tension, and irritability associated with anxiety; these have all substantially worsened over the last month. He admits that recently he has occasionally thought it would be easier if he weren’t alive. Mr. F denies having problems with his energy or motivation levels and insists that he generally feels very anxious, but not depressed. He says he drinks 1 alcoholic drink per week and denies any other substance use. Mr. F is overweight and has slightly elevated cholesterol but denies any other health conditions. He takes melatonin to help him sleep but does not take any prescribed medications.

Although this vignette provides limited details, on the surface it appears that Mr. F is experiencing an exacerbation of chronic generalized anxiety disorder (GAD). However, in this article, I propose establishing a new diagnosis: “acute anxiety disorder,” which would encapsulate severe exacerbations of a pre-existing anxiety disorder. Among the patients I have encountered for whom this diagnosis would fit, most have pre-existing GAD or panic disorder.

A look at the differential diagnosis

It is important to determine whether Mr. F is using any substances or has a medical condition that could be contributing to his anxiety. Other psychiatric diagnoses that could be considered include:

Adjustment disorder. This diagnosis would make sense if Mr. F didn’t have an apparent chronic history of symptoms that meet criteria for GAD.

Major depressive disorder with anxious distress. Many patients experiencing a major depressive episode meet the criteria for the specifier “with anxious distress,” even those who do not have a comorbid anxiety disorder.¹ However, it is not evident from this vignette that Mr. F is experiencing a major depressive episode.

Continue to: Panic disorder and GAD...

Panic disorder and GAD. It is possible for a patient with GAD to develop panic disorder, which, at times, occurs after experiencing significant life stressors. Panic disorder requires the presence of recurrent panic attacks. Mr. F describes experiencing chronic, intense symptoms of anxiety rather than the discreet episodes of acute symptoms that characterize panic attacks.

Acute stress disorder. This diagnosis involves psychological symptoms that occur in response to exposure to actual or threatened death, serious injury, or sexual violation. Mr. F was not exposed to any of these stressors.

Why this new diagnosis would be helpful

A new diagnosis, acute anxiety disorder, would indicate that a patient is currently experiencing an acute exacerbation of a chronic anxiety disorder that is leading to a significant decrease in their baseline functioning. My proposed criteria for acute anxiety disorder appear in the Table. Here are some reasons this diagnosis would be helpful:

Signifier of severity. Anxiety disorders such as GAD are generally not considered severe conditions and not considered to fall under the rubric of SPMI (severe and persistent mental illness).² Posttraumatic stress disorder is the anxiety disorder–like condition most often found in the SPMI category. A diagnosis of acute anxiety disorder would indicate a patient is experiencing an episode of anxiety that is distinct from their chronic anxiety condition due to its severe impact on functional capabilities. Acute anxiety disorder would certainly not qualify as a “SPMI diagnosis” that would facilitate someone being considered eligible for supplemental security income, but it might be a legitimate justification for someone to receive short-term disability.

Treatment approach. The pharmacologic treatment of anxiety disorders usually involves a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI). However, these medications can sometimes briefly increase anxiety when they are started. Individuals with acute anxiety are the most vulnerable to the possibility of experiencing increased anxiety when starting an SSRI or SNRI and may benefit from a slower titration of these medications. In light of this and the length of time required for SSRIs or SNRIs to exert a positive effect (typically a few weeks), patients with acute anxiety are best served by treatment with a medication with an immediate onset of action, such as a benzodiazepine or a sleep medication (eg, zolpidem). Benzodiazepines and hypnotics such as zolpidem are best prescribed for as-needed use because they carry a risk of dependence. One might consider prescribing mirtazapine or pregabalin (both of which are used off-label to treat anxiety) because these medications also have a relatively rapid onset of action and can treat both anxiety and insomnia (particularly mirtazapine).

Research considerations. It would be helpful to study which treatments are most effective for the subset of patients who experience acute anxiety disorder as I define it. Perhaps psychotherapy treatment protocols could be adapted or created. Treatment with esketamine or IV ketamine might be further studied as a treatment for acute anxiety because some evidence suggests ketamine is efficacious for this indication.³

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.com.

Mr. F, age 42, says he has always been a very anxious person and has chronically found his worrying to negatively affect his life. He says that over the last month his anxiety has been “off the charts” and he is worrying “24/7” due to taking on new responsibilities at his job and his son being diagnosed with lupus. He says his constant worrying is significantly impairing his ability to focus at his job, and he is considering taking a mental health leave from work. His wife reports that she is extremely frustrated because Mr. F has been isolating himself from family and friends; he admits this is true and attributes it to being preoccupied by his worries.

Mr. F endorses chronic insomnia, muscle tension, and irritability associated with anxiety; these have all substantially worsened over the last month. He admits that recently he has occasionally thought it would be easier if he weren’t alive. Mr. F denies having problems with his energy or motivation levels and insists that he generally feels very anxious, but not depressed. He says he drinks 1 alcoholic drink per week and denies any other substance use. Mr. F is overweight and has slightly elevated cholesterol but denies any other health conditions. He takes melatonin to help him sleep but does not take any prescribed medications.

Although this vignette provides limited details, on the surface it appears that Mr. F is experiencing an exacerbation of chronic generalized anxiety disorder (GAD). However, in this article, I propose establishing a new diagnosis: “acute anxiety disorder,” which would encapsulate severe exacerbations of a pre-existing anxiety disorder. Among the patients I have encountered for whom this diagnosis would fit, most have pre-existing GAD or panic disorder.

A look at the differential diagnosis

It is important to determine whether Mr. F is using any substances or has a medical condition that could be contributing to his anxiety. Other psychiatric diagnoses that could be considered include:

Adjustment disorder. This diagnosis would make sense if Mr. F didn’t have an apparent chronic history of symptoms that meet criteria for GAD.

Major depressive disorder with anxious distress. Many patients experiencing a major depressive episode meet the criteria for the specifier “with anxious distress,” even those who do not have a comorbid anxiety disorder.¹ However, it is not evident from this vignette that Mr. F is experiencing a major depressive episode.

Continue to: Panic disorder and GAD...

Panic disorder and GAD. It is possible for a patient with GAD to develop panic disorder, which, at times, occurs after experiencing significant life stressors. Panic disorder requires the presence of recurrent panic attacks. Mr. F describes experiencing chronic, intense symptoms of anxiety rather than the discreet episodes of acute symptoms that characterize panic attacks.

Acute stress disorder. This diagnosis involves psychological symptoms that occur in response to exposure to actual or threatened death, serious injury, or sexual violation. Mr. F was not exposed to any of these stressors.

Why this new diagnosis would be helpful

A new diagnosis, acute anxiety disorder, would indicate that a patient is currently experiencing an acute exacerbation of a chronic anxiety disorder that is leading to a significant decrease in their baseline functioning. My proposed criteria for acute anxiety disorder appear in the Table. Here are some reasons this diagnosis would be helpful:

Signifier of severity. Anxiety disorders such as GAD are generally not considered severe conditions and not considered to fall under the rubric of SPMI (severe and persistent mental illness).² Posttraumatic stress disorder is the anxiety disorder–like condition most often found in the SPMI category. A diagnosis of acute anxiety disorder would indicate a patient is experiencing an episode of anxiety that is distinct from their chronic anxiety condition due to its severe impact on functional capabilities. Acute anxiety disorder would certainly not qualify as a “SPMI diagnosis” that would facilitate someone being considered eligible for supplemental security income, but it might be a legitimate justification for someone to receive short-term disability.

Treatment approach. The pharmacologic treatment of anxiety disorders usually involves a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI). However, these medications can sometimes briefly increase anxiety when they are started. Individuals with acute anxiety are the most vulnerable to the possibility of experiencing increased anxiety when starting an SSRI or SNRI and may benefit from a slower titration of these medications. In light of this and the length of time required for SSRIs or SNRIs to exert a positive effect (typically a few weeks), patients with acute anxiety are best served by treatment with a medication with an immediate onset of action, such as a benzodiazepine or a sleep medication (eg, zolpidem). Benzodiazepines and hypnotics such as zolpidem are best prescribed for as-needed use because they carry a risk of dependence. One might consider prescribing mirtazapine or pregabalin (both of which are used off-label to treat anxiety) because these medications also have a relatively rapid onset of action and can treat both anxiety and insomnia (particularly mirtazapine).

Research considerations. It would be helpful to study which treatments are most effective for the subset of patients who experience acute anxiety disorder as I define it. Perhaps psychotherapy treatment protocols could be adapted or created. Treatment with esketamine or IV ketamine might be further studied as a treatment for acute anxiety because some evidence suggests ketamine is efficacious for this indication.³

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.com.

Mr. F, age 42, says he has always been a very anxious person and has chronically found his worrying to negatively affect his life. He says that over the last month his anxiety has been “off the charts” and he is worrying “24/7” due to taking on new responsibilities at his job and his son being diagnosed with lupus. He says his constant worrying is significantly impairing his ability to focus at his job, and he is considering taking a mental health leave from work. His wife reports that she is extremely frustrated because Mr. F has been isolating himself from family and friends; he admits this is true and attributes it to being preoccupied by his worries.

Mr. F endorses chronic insomnia, muscle tension, and irritability associated with anxiety; these have all substantially worsened over the last month. He admits that recently he has occasionally thought it would be easier if he weren’t alive. Mr. F denies having problems with his energy or motivation levels and insists that he generally feels very anxious, but not depressed. He says he drinks 1 alcoholic drink per week and denies any other substance use. Mr. F is overweight and has slightly elevated cholesterol but denies any other health conditions. He takes melatonin to help him sleep but does not take any prescribed medications.

Although this vignette provides limited details, on the surface it appears that Mr. F is experiencing an exacerbation of chronic generalized anxiety disorder (GAD). However, in this article, I propose establishing a new diagnosis: “acute anxiety disorder,” which would encapsulate severe exacerbations of a pre-existing anxiety disorder. Among the patients I have encountered for whom this diagnosis would fit, most have pre-existing GAD or panic disorder.

A look at the differential diagnosis

It is important to determine whether Mr. F is using any substances or has a medical condition that could be contributing to his anxiety. Other psychiatric diagnoses that could be considered include:

Adjustment disorder. This diagnosis would make sense if Mr. F didn’t have an apparent chronic history of symptoms that meet criteria for GAD.

Major depressive disorder with anxious distress. Many patients experiencing a major depressive episode meet the criteria for the specifier “with anxious distress,” even those who do not have a comorbid anxiety disorder.¹ However, it is not evident from this vignette that Mr. F is experiencing a major depressive episode.

Continue to: Panic disorder and GAD...

Panic disorder and GAD. It is possible for a patient with GAD to develop panic disorder, which, at times, occurs after experiencing significant life stressors. Panic disorder requires the presence of recurrent panic attacks. Mr. F describes experiencing chronic, intense symptoms of anxiety rather than the discreet episodes of acute symptoms that characterize panic attacks.

Acute stress disorder. This diagnosis involves psychological symptoms that occur in response to exposure to actual or threatened death, serious injury, or sexual violation. Mr. F was not exposed to any of these stressors.

Why this new diagnosis would be helpful

A new diagnosis, acute anxiety disorder, would indicate that a patient is currently experiencing an acute exacerbation of a chronic anxiety disorder that is leading to a significant decrease in their baseline functioning. My proposed criteria for acute anxiety disorder appear in the Table. Here are some reasons this diagnosis would be helpful:

Signifier of severity. Anxiety disorders such as GAD are generally not considered severe conditions and not considered to fall under the rubric of SPMI (severe and persistent mental illness).² Posttraumatic stress disorder is the anxiety disorder–like condition most often found in the SPMI category. A diagnosis of acute anxiety disorder would indicate a patient is experiencing an episode of anxiety that is distinct from their chronic anxiety condition due to its severe impact on functional capabilities. Acute anxiety disorder would certainly not qualify as a “SPMI diagnosis” that would facilitate someone being considered eligible for supplemental security income, but it might be a legitimate justification for someone to receive short-term disability.

Treatment approach. The pharmacologic treatment of anxiety disorders usually involves a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI). However, these medications can sometimes briefly increase anxiety when they are started. Individuals with acute anxiety are the most vulnerable to the possibility of experiencing increased anxiety when starting an SSRI or SNRI and may benefit from a slower titration of these medications. In light of this and the length of time required for SSRIs or SNRIs to exert a positive effect (typically a few weeks), patients with acute anxiety are best served by treatment with a medication with an immediate onset of action, such as a benzodiazepine or a sleep medication (eg, zolpidem). Benzodiazepines and hypnotics such as zolpidem are best prescribed for as-needed use because they carry a risk of dependence. One might consider prescribing mirtazapine or pregabalin (both of which are used off-label to treat anxiety) because these medications also have a relatively rapid onset of action and can treat both anxiety and insomnia (particularly mirtazapine).

Research considerations. It would be helpful to study which treatments are most effective for the subset of patients who experience acute anxiety disorder as I define it. Perhaps psychotherapy treatment protocols could be adapted or created. Treatment with esketamine or IV ketamine might be further studied as a treatment for acute anxiety because some evidence suggests ketamine is efficacious for this indication.³