MDedge Psychiatry

This transcript has been edited for clarity.

Recently, the Supreme Court of the United States struck down the use of affirmative action in admissions to colleges, universities, medical schools, and nursing schools. This has led to an enormous amount of worry and concern, particularly in medical school admissions in the world I’m in, where people start to say that diversity matters. Diversity is important.

I know many deans of medical schools immediately sent out messages of reassurance to their students, saying New York University or Stanford or Harvard or Minnesota or Case Western is still deeply concerned about diversity, and we’re going to do what we can to preserve attention to diversity.

I’ve served on admissions at a number of schools over the years for med school. I understand – and have been told – that diversity is important, and according to the Supreme Court, not explicitly by race. There are obviously many variables to take into account when trying to keep diversity at the forefront of admissions.

At the schools I’ve been at, including Columbia, NYU, University of Pittsburgh, University of Minnesota, and University of Pennsylvania, there are plenty of qualified students. Happily, we’ve always been engaged in some effort to try and whittle down the class to the size that we can manage and accept, and many qualified students don’t get admitted.

The first order of business for me is not to worry about how to maintain diversity. It’s to recognize that we need more doctors, nurses, and mental health care providers. I will, in a second, say a few words about diversity and where it fits into admissions, but I want to make the point clearly that what we should be doing is trying to expand the pool of students who are going to become doctors, nurses, mental health care providers, and social workers.

There are too many early retirements. We don’t have the person power we need to manage the health care challenges of an aging population. Let’s not get lost in arguing about what characteristics ought to get you into the finest medical schools. Let’s realize that we have to expand the number of schools we have.

We better be working pretty hard to expand our physician assistant programs, to make sure that we give full authority to qualified dentists and nurses who can help deliver some clinical care. We need more folks. That’s really where the battle ought to be: How do we get that done and how do we get it done quickly, not arguing about who’s in, who’s out, and why.

That said, diversity to me has never meant just race. I’m always interested in gender orientation, disability, and geographic input. Sometimes in decisions that you’re looking at, when I have students in front of me, they tell me they play a musical instrument or about the obstacles they had to overcome to get to medical school. Some of them will say they were involved in 4-H and did rodeo in high school or junior high school, which makes them a diverse potential student with characteristics that maybe some others don’t bring.

I’m not against diversity. I think having a rich set of experiences in any class – medicine, nursing, whatever it’s going to be – is beneficial to the students. They learn from each other. It is sometimes said that it’s also good for patients. I’m a little less excited about that, because I think our training goal should be to make every medical student and nursing student qualified to treat anybody.

I don’t think that, just because you’re Latinx or gay, that’s going to make a gay patient feel better. I think we should teach our students how to give care to everybody that they encounter. They shouldn’t have to match up characteristics to feel like they’re going to get quality care. That isn’t the right reason.

Diversity is important, I think, to teach our students, to broaden our research, and to make sure that bias doesn’t creep in to how we teach, learn, or behave. When you have a diverse set of providers, they can call that out and be on the alert for it, and that’s very important.

I also believe that we should think widely and broadly about diversity. Maybe race is out, but certainly other experiences related to income, background, struggle that got you to the point where you’re applying to medical school, motivation, the kinds of experiences you might have had caring for an elderly person, dealing with a disability or learning disability, and trying to overcome, let’s say, going to school in a poor area with not such a wonderful school, really help in terms of forming professionalism, empathy, and a caring point of view.

To me, the main goal is to expand our workforce. The secondary goal is to stay diverse, because we get better providers when we do so.

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

This transcript has been edited for clarity.

Recently, the Supreme Court of the United States struck down the use of affirmative action in admissions to colleges, universities, medical schools, and nursing schools. This has led to an enormous amount of worry and concern, particularly in medical school admissions in the world I’m in, where people start to say that diversity matters. Diversity is important.

I know many deans of medical schools immediately sent out messages of reassurance to their students, saying New York University or Stanford or Harvard or Minnesota or Case Western is still deeply concerned about diversity, and we’re going to do what we can to preserve attention to diversity.

I’ve served on admissions at a number of schools over the years for med school. I understand – and have been told – that diversity is important, and according to the Supreme Court, not explicitly by race. There are obviously many variables to take into account when trying to keep diversity at the forefront of admissions.

At the schools I’ve been at, including Columbia, NYU, University of Pittsburgh, University of Minnesota, and University of Pennsylvania, there are plenty of qualified students. Happily, we’ve always been engaged in some effort to try and whittle down the class to the size that we can manage and accept, and many qualified students don’t get admitted.

The first order of business for me is not to worry about how to maintain diversity. It’s to recognize that we need more doctors, nurses, and mental health care providers. I will, in a second, say a few words about diversity and where it fits into admissions, but I want to make the point clearly that what we should be doing is trying to expand the pool of students who are going to become doctors, nurses, mental health care providers, and social workers.

There are too many early retirements. We don’t have the person power we need to manage the health care challenges of an aging population. Let’s not get lost in arguing about what characteristics ought to get you into the finest medical schools. Let’s realize that we have to expand the number of schools we have.

We better be working pretty hard to expand our physician assistant programs, to make sure that we give full authority to qualified dentists and nurses who can help deliver some clinical care. We need more folks. That’s really where the battle ought to be: How do we get that done and how do we get it done quickly, not arguing about who’s in, who’s out, and why.

That said, diversity to me has never meant just race. I’m always interested in gender orientation, disability, and geographic input. Sometimes in decisions that you’re looking at, when I have students in front of me, they tell me they play a musical instrument or about the obstacles they had to overcome to get to medical school. Some of them will say they were involved in 4-H and did rodeo in high school or junior high school, which makes them a diverse potential student with characteristics that maybe some others don’t bring.

I’m not against diversity. I think having a rich set of experiences in any class – medicine, nursing, whatever it’s going to be – is beneficial to the students. They learn from each other. It is sometimes said that it’s also good for patients. I’m a little less excited about that, because I think our training goal should be to make every medical student and nursing student qualified to treat anybody.

I don’t think that, just because you’re Latinx or gay, that’s going to make a gay patient feel better. I think we should teach our students how to give care to everybody that they encounter. They shouldn’t have to match up characteristics to feel like they’re going to get quality care. That isn’t the right reason.

Diversity is important, I think, to teach our students, to broaden our research, and to make sure that bias doesn’t creep in to how we teach, learn, or behave. When you have a diverse set of providers, they can call that out and be on the alert for it, and that’s very important.

I also believe that we should think widely and broadly about diversity. Maybe race is out, but certainly other experiences related to income, background, struggle that got you to the point where you’re applying to medical school, motivation, the kinds of experiences you might have had caring for an elderly person, dealing with a disability or learning disability, and trying to overcome, let’s say, going to school in a poor area with not such a wonderful school, really help in terms of forming professionalism, empathy, and a caring point of view.

To me, the main goal is to expand our workforce. The secondary goal is to stay diverse, because we get better providers when we do so.

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

This transcript has been edited for clarity.

Recently, the Supreme Court of the United States struck down the use of affirmative action in admissions to colleges, universities, medical schools, and nursing schools. This has led to an enormous amount of worry and concern, particularly in medical school admissions in the world I’m in, where people start to say that diversity matters. Diversity is important.

I know many deans of medical schools immediately sent out messages of reassurance to their students, saying New York University or Stanford or Harvard or Minnesota or Case Western is still deeply concerned about diversity, and we’re going to do what we can to preserve attention to diversity.

I’ve served on admissions at a number of schools over the years for med school. I understand – and have been told – that diversity is important, and according to the Supreme Court, not explicitly by race. There are obviously many variables to take into account when trying to keep diversity at the forefront of admissions.

At the schools I’ve been at, including Columbia, NYU, University of Pittsburgh, University of Minnesota, and University of Pennsylvania, there are plenty of qualified students. Happily, we’ve always been engaged in some effort to try and whittle down the class to the size that we can manage and accept, and many qualified students don’t get admitted.

The first order of business for me is not to worry about how to maintain diversity. It’s to recognize that we need more doctors, nurses, and mental health care providers. I will, in a second, say a few words about diversity and where it fits into admissions, but I want to make the point clearly that what we should be doing is trying to expand the pool of students who are going to become doctors, nurses, mental health care providers, and social workers.

There are too many early retirements. We don’t have the person power we need to manage the health care challenges of an aging population. Let’s not get lost in arguing about what characteristics ought to get you into the finest medical schools. Let’s realize that we have to expand the number of schools we have.

We better be working pretty hard to expand our physician assistant programs, to make sure that we give full authority to qualified dentists and nurses who can help deliver some clinical care. We need more folks. That’s really where the battle ought to be: How do we get that done and how do we get it done quickly, not arguing about who’s in, who’s out, and why.

That said, diversity to me has never meant just race. I’m always interested in gender orientation, disability, and geographic input. Sometimes in decisions that you’re looking at, when I have students in front of me, they tell me they play a musical instrument or about the obstacles they had to overcome to get to medical school. Some of them will say they were involved in 4-H and did rodeo in high school or junior high school, which makes them a diverse potential student with characteristics that maybe some others don’t bring.

I’m not against diversity. I think having a rich set of experiences in any class – medicine, nursing, whatever it’s going to be – is beneficial to the students. They learn from each other. It is sometimes said that it’s also good for patients. I’m a little less excited about that, because I think our training goal should be to make every medical student and nursing student qualified to treat anybody.

I don’t think that, just because you’re Latinx or gay, that’s going to make a gay patient feel better. I think we should teach our students how to give care to everybody that they encounter. They shouldn’t have to match up characteristics to feel like they’re going to get quality care. That isn’t the right reason.

Diversity is important, I think, to teach our students, to broaden our research, and to make sure that bias doesn’t creep in to how we teach, learn, or behave. When you have a diverse set of providers, they can call that out and be on the alert for it, and that’s very important.

I also believe that we should think widely and broadly about diversity. Maybe race is out, but certainly other experiences related to income, background, struggle that got you to the point where you’re applying to medical school, motivation, the kinds of experiences you might have had caring for an elderly person, dealing with a disability or learning disability, and trying to overcome, let’s say, going to school in a poor area with not such a wonderful school, really help in terms of forming professionalism, empathy, and a caring point of view.

To me, the main goal is to expand our workforce. The secondary goal is to stay diverse, because we get better providers when we do so.

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

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

This transcript has been edited for clarity.

On May 3, 2023, Surgeon General Vivek Murthy issued an advisory raising an alarm about what he called an “epidemic of loneliness” in the United States.

Now, I am not saying that Vivek Murthy read my book, “How Medicine Works and When It Doesn’t” – released in January and available in bookstores now – where, in chapter 11, I call attention to the problem of loneliness and its relationship to the exponential rise in deaths of despair. But Vivek, if you did, let me know. I could use the publicity.

No, of course the idea that loneliness is a public health issue is not new, but I’m glad to see it finally getting attention. At this point, studies have linked loneliness to heart disease, stroke, dementia, and premature death. And now, according to a new study, loneliness may be linked to Parkinson’s disease.

The UK Biobank is really a treasure trove of data for epidemiologists. I must see three to four studies a week coming out of this mega-dataset. This one, appearing in JAMA Neurology, caught my eye for its focus specifically on loneliness as a risk factor – something I’m hoping to see more of in the future.

The study examines data from just under 500,000 individuals in the United Kingdom who answered a survey including the question “Do you often feel lonely?” between 2006 and 2010; 18.4% of people answered yes. Individuals’ electronic health record data were then monitored over time to see who would get a new diagnosis code consistent with Parkinson’s disease. Through 2021, 2822 people did – that’s just over half a percent.

So, now we do the statistics thing. Of the nonlonely folks, 2,273 went on to develop Parkinson’s disease. Of those who said they often feel lonely, 549 people did. The raw numbers here, to be honest, aren’t that compelling. Lonely people had an absolute risk for Parkinson’s disease about 0.03% higher than that of nonlonely people. Put another way, you’d need to take over 3,000 lonely souls and make them not lonely to prevent 1 case of Parkinson’s disease.

Still, the costs of loneliness are not measured exclusively in Parkinson’s disease, and I would argue that the real risks here come from other sources: alcohol abuse, drug abuse, and suicide. Nevertheless, the weak but significant association with Parkinson’s disease reminds us that loneliness is a neurologic phenomenon. There is something about social connection that affects our brain in a way that is not just spiritual; it is actually biological.

Of course, people who say they are often lonely are different in other ways from people who report not being lonely. Lonely people, in this dataset, were younger, more likely to be female, less likely to have a college degree, in worse physical health, and engaged in more high-risk health behaviors like smoking.

The authors adjusted for all of these factors and found that, on the relative scale, lonely people were still about 20%-30% more likely to develop Parkinson’s disease.

courtesy JAMA Neurology

F. Perry Wilson, MD, MSCE, is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no relevant conflicts of interest.
 

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

This transcript has been edited for clarity.

On May 3, 2023, Surgeon General Vivek Murthy issued an advisory raising an alarm about what he called an “epidemic of loneliness” in the United States.

Now, I am not saying that Vivek Murthy read my book, “How Medicine Works and When It Doesn’t” – released in January and available in bookstores now – where, in chapter 11, I call attention to the problem of loneliness and its relationship to the exponential rise in deaths of despair. But Vivek, if you did, let me know. I could use the publicity.

No, of course the idea that loneliness is a public health issue is not new, but I’m glad to see it finally getting attention. At this point, studies have linked loneliness to heart disease, stroke, dementia, and premature death. And now, according to a new study, loneliness may be linked to Parkinson’s disease.

The UK Biobank is really a treasure trove of data for epidemiologists. I must see three to four studies a week coming out of this mega-dataset. This one, appearing in JAMA Neurology, caught my eye for its focus specifically on loneliness as a risk factor – something I’m hoping to see more of in the future.

The study examines data from just under 500,000 individuals in the United Kingdom who answered a survey including the question “Do you often feel lonely?” between 2006 and 2010; 18.4% of people answered yes. Individuals’ electronic health record data were then monitored over time to see who would get a new diagnosis code consistent with Parkinson’s disease. Through 2021, 2822 people did – that’s just over half a percent.

So, now we do the statistics thing. Of the nonlonely folks, 2,273 went on to develop Parkinson’s disease. Of those who said they often feel lonely, 549 people did. The raw numbers here, to be honest, aren’t that compelling. Lonely people had an absolute risk for Parkinson’s disease about 0.03% higher than that of nonlonely people. Put another way, you’d need to take over 3,000 lonely souls and make them not lonely to prevent 1 case of Parkinson’s disease.

Still, the costs of loneliness are not measured exclusively in Parkinson’s disease, and I would argue that the real risks here come from other sources: alcohol abuse, drug abuse, and suicide. Nevertheless, the weak but significant association with Parkinson’s disease reminds us that loneliness is a neurologic phenomenon. There is something about social connection that affects our brain in a way that is not just spiritual; it is actually biological.

Of course, people who say they are often lonely are different in other ways from people who report not being lonely. Lonely people, in this dataset, were younger, more likely to be female, less likely to have a college degree, in worse physical health, and engaged in more high-risk health behaviors like smoking.

The authors adjusted for all of these factors and found that, on the relative scale, lonely people were still about 20%-30% more likely to develop Parkinson’s disease.

courtesy JAMA Neurology

F. Perry Wilson, MD, MSCE, is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no relevant conflicts of interest.
 

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

This transcript has been edited for clarity.

On May 3, 2023, Surgeon General Vivek Murthy issued an advisory raising an alarm about what he called an “epidemic of loneliness” in the United States.

Now, I am not saying that Vivek Murthy read my book, “How Medicine Works and When It Doesn’t” – released in January and available in bookstores now – where, in chapter 11, I call attention to the problem of loneliness and its relationship to the exponential rise in deaths of despair. But Vivek, if you did, let me know. I could use the publicity.

No, of course the idea that loneliness is a public health issue is not new, but I’m glad to see it finally getting attention. At this point, studies have linked loneliness to heart disease, stroke, dementia, and premature death. And now, according to a new study, loneliness may be linked to Parkinson’s disease.

The UK Biobank is really a treasure trove of data for epidemiologists. I must see three to four studies a week coming out of this mega-dataset. This one, appearing in JAMA Neurology, caught my eye for its focus specifically on loneliness as a risk factor – something I’m hoping to see more of in the future.

The study examines data from just under 500,000 individuals in the United Kingdom who answered a survey including the question “Do you often feel lonely?” between 2006 and 2010; 18.4% of people answered yes. Individuals’ electronic health record data were then monitored over time to see who would get a new diagnosis code consistent with Parkinson’s disease. Through 2021, 2822 people did – that’s just over half a percent.

So, now we do the statistics thing. Of the nonlonely folks, 2,273 went on to develop Parkinson’s disease. Of those who said they often feel lonely, 549 people did. The raw numbers here, to be honest, aren’t that compelling. Lonely people had an absolute risk for Parkinson’s disease about 0.03% higher than that of nonlonely people. Put another way, you’d need to take over 3,000 lonely souls and make them not lonely to prevent 1 case of Parkinson’s disease.

Still, the costs of loneliness are not measured exclusively in Parkinson’s disease, and I would argue that the real risks here come from other sources: alcohol abuse, drug abuse, and suicide. Nevertheless, the weak but significant association with Parkinson’s disease reminds us that loneliness is a neurologic phenomenon. There is something about social connection that affects our brain in a way that is not just spiritual; it is actually biological.

Of course, people who say they are often lonely are different in other ways from people who report not being lonely. Lonely people, in this dataset, were younger, more likely to be female, less likely to have a college degree, in worse physical health, and engaged in more high-risk health behaviors like smoking.

The authors adjusted for all of these factors and found that, on the relative scale, lonely people were still about 20%-30% more likely to develop Parkinson’s disease.

courtesy JAMA Neurology

F. Perry Wilson, MD, MSCE, is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no relevant conflicts of interest.
 

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

With physicians under increasing pressure to see more patients in shorter office visits, developing a social media presence may offer valuable opportunities to connect with patients, explain procedures, combat misinformation, talk through a published article, and even share a joke or meme.

But there are caveats for doctors posting on social media platforms. This news organization spoke to four doctors who successfully use social media. Here is what they want you to know before you post – and how to make your posts personable and helpful to patients and your practice simultaneously.
 

Use social media for the right reasons

While you’re under no obligation to build a social media presence, if you’re going to do it, be sure your intentions are solid, said Don S. Dizon, MD, professor of medicine and professor of surgery at Brown University, Providence, R.I. Dr. Dizon, as @DoctorDon, has 44,700 TikTok followers and uses the platform to answer cancer-related questions.

“It should be your altruism that motivates you to post,” said Dr. Dizon, who is also associate director of community outreach and engagement at the Legorreta Cancer Center in Providence, R.I., and director of medical oncology at Rhode Island Hospital. “What we can do for society at large is to provide our input into issues, add informed opinions where there’s controversy, and address misinformation.”

If you don’t know where to start, consider seeking a digital mentor to talk through your options.

“You may never meet this person, but you should choose them if you like their style, their content, their delivery, and their perspective,” Dr. Dizon said. “Find another doctor out there on social media whom you feel you can emulate. Take your time, too. Soon enough, you’ll develop your own style and your own online persona.”
 

Post clear, accurate information

If you want to be lighthearted on social media, that’s your choice. But Jennifer Trachtenberg, a pediatrician with nearly 7,000 Instagram followers in New York who posts as @askdrjen, prefers to offer vaccine scheduling tips, alert parents about COVID-19 rates, and offer advice on cold and flu prevention.

“Right now, I’m mainly doing this to educate patients and make them aware of topics that I think are important and that I see my patients needing more information on,” she said. “We have to be clear: People take what we say seriously. So, while it’s important to be relatable, it’s even more important to share evidence-based information.”
 

Many patients get their information on social media

While patients once came to the doctor armed with information sourced via “Doctor Google,” today, just as many patients use social media to learn about their condition or the medications they’re taking.

Unfortunately, a recent Ohio State University, Columbus, study found that the majority of gynecologic cancer advice on TikTok, for example, was either misleading or inaccurate.

“This misinformation should be a motivator for physicians to explore the social media space,” Dr. Dizon said. “Our voices need to be on there.”
 

Break down barriers – and make connections

Mike Natter, MD, an endocrinologist in New York, has type 1 diabetes. This informs his work – and his life – and he’s passionate about sharing it with his 117,000 followers as @mike.natter on Instagram.

“A lot of type 1s follow me, so there’s an advocacy component to what I do,” he said. “I enjoy being able to raise awareness and keep people up to date on the newest research and treatment.”

But that’s not all: Dr. Natter is also an artist who went to art school before he went to medical school, and his account is rife with his cartoons and illustrations about everything from valvular disease to diabetic ketoacidosis.

“I found that I was drawing a lot of my notes in medical school,” he said. “When I drew my notes, I did quite well, and I think that using art and illustration is a great tool. It breaks down barriers and makes health information all the more accessible to everyone.”
 

Share your expertise as a doctor – and a person

As a mom and pediatrician, Krupa Playforth, MD, who practices in Vienna, Va., knows that what she posts carries weight. So, whether she’s writing about backpack safety tips, choking hazards, or separation anxiety, her followers can rest assured that she’s posting responsibly.

“Pediatricians often underestimate how smart parents are,” said Dr. Playforth, who has three kids, ages 8, 5, and 2, and has 137,000 followers on @thepediatricianmom, her Instagram account. “Their anxiety comes from an understandable place, which is why I see my role as that of a parent and pediatrician who can translate the knowledge pediatricians have into something parents can understand.”

Dr. Playforth, who jumped on social media during COVID-19 and experienced a positive response in her local community, said being on social media is imperative if you’re a pediatrician.

“This is the future of pediatric medicine in particular,” she said. “A lot of pediatricians don’t want to embrace social media, but I think that’s a mistake. After all, while parents think pediatricians have all the answers, when we think of our own children, most doctors are like other parents – we can’t think objectively about our kids. It’s helpful for me to share that and to help parents feel less alone.”

If you’re not yet using social media to the best of your physician abilities, you might take a shot at becoming widely recognizable. Pick a preferred platform, answer common patient questions, dispel medical myths, provide pertinent information, and let your personality shine.

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

With physicians under increasing pressure to see more patients in shorter office visits, developing a social media presence may offer valuable opportunities to connect with patients, explain procedures, combat misinformation, talk through a published article, and even share a joke or meme.

But there are caveats for doctors posting on social media platforms. This news organization spoke to four doctors who successfully use social media. Here is what they want you to know before you post – and how to make your posts personable and helpful to patients and your practice simultaneously.
 

Use social media for the right reasons

While you’re under no obligation to build a social media presence, if you’re going to do it, be sure your intentions are solid, said Don S. Dizon, MD, professor of medicine and professor of surgery at Brown University, Providence, R.I. Dr. Dizon, as @DoctorDon, has 44,700 TikTok followers and uses the platform to answer cancer-related questions.

“It should be your altruism that motivates you to post,” said Dr. Dizon, who is also associate director of community outreach and engagement at the Legorreta Cancer Center in Providence, R.I., and director of medical oncology at Rhode Island Hospital. “What we can do for society at large is to provide our input into issues, add informed opinions where there’s controversy, and address misinformation.”

If you don’t know where to start, consider seeking a digital mentor to talk through your options.

“You may never meet this person, but you should choose them if you like their style, their content, their delivery, and their perspective,” Dr. Dizon said. “Find another doctor out there on social media whom you feel you can emulate. Take your time, too. Soon enough, you’ll develop your own style and your own online persona.”
 

Post clear, accurate information

If you want to be lighthearted on social media, that’s your choice. But Jennifer Trachtenberg, a pediatrician with nearly 7,000 Instagram followers in New York who posts as @askdrjen, prefers to offer vaccine scheduling tips, alert parents about COVID-19 rates, and offer advice on cold and flu prevention.

“Right now, I’m mainly doing this to educate patients and make them aware of topics that I think are important and that I see my patients needing more information on,” she said. “We have to be clear: People take what we say seriously. So, while it’s important to be relatable, it’s even more important to share evidence-based information.”
 

Many patients get their information on social media

While patients once came to the doctor armed with information sourced via “Doctor Google,” today, just as many patients use social media to learn about their condition or the medications they’re taking.

Unfortunately, a recent Ohio State University, Columbus, study found that the majority of gynecologic cancer advice on TikTok, for example, was either misleading or inaccurate.

“This misinformation should be a motivator for physicians to explore the social media space,” Dr. Dizon said. “Our voices need to be on there.”
 

Break down barriers – and make connections

Mike Natter, MD, an endocrinologist in New York, has type 1 diabetes. This informs his work – and his life – and he’s passionate about sharing it with his 117,000 followers as @mike.natter on Instagram.

“A lot of type 1s follow me, so there’s an advocacy component to what I do,” he said. “I enjoy being able to raise awareness and keep people up to date on the newest research and treatment.”

But that’s not all: Dr. Natter is also an artist who went to art school before he went to medical school, and his account is rife with his cartoons and illustrations about everything from valvular disease to diabetic ketoacidosis.

“I found that I was drawing a lot of my notes in medical school,” he said. “When I drew my notes, I did quite well, and I think that using art and illustration is a great tool. It breaks down barriers and makes health information all the more accessible to everyone.”
 

Share your expertise as a doctor – and a person

As a mom and pediatrician, Krupa Playforth, MD, who practices in Vienna, Va., knows that what she posts carries weight. So, whether she’s writing about backpack safety tips, choking hazards, or separation anxiety, her followers can rest assured that she’s posting responsibly.

“Pediatricians often underestimate how smart parents are,” said Dr. Playforth, who has three kids, ages 8, 5, and 2, and has 137,000 followers on @thepediatricianmom, her Instagram account. “Their anxiety comes from an understandable place, which is why I see my role as that of a parent and pediatrician who can translate the knowledge pediatricians have into something parents can understand.”

Dr. Playforth, who jumped on social media during COVID-19 and experienced a positive response in her local community, said being on social media is imperative if you’re a pediatrician.

“This is the future of pediatric medicine in particular,” she said. “A lot of pediatricians don’t want to embrace social media, but I think that’s a mistake. After all, while parents think pediatricians have all the answers, when we think of our own children, most doctors are like other parents – we can’t think objectively about our kids. It’s helpful for me to share that and to help parents feel less alone.”

If you’re not yet using social media to the best of your physician abilities, you might take a shot at becoming widely recognizable. Pick a preferred platform, answer common patient questions, dispel medical myths, provide pertinent information, and let your personality shine.

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

With physicians under increasing pressure to see more patients in shorter office visits, developing a social media presence may offer valuable opportunities to connect with patients, explain procedures, combat misinformation, talk through a published article, and even share a joke or meme.

But there are caveats for doctors posting on social media platforms. This news organization spoke to four doctors who successfully use social media. Here is what they want you to know before you post – and how to make your posts personable and helpful to patients and your practice simultaneously.
 

Use social media for the right reasons

While you’re under no obligation to build a social media presence, if you’re going to do it, be sure your intentions are solid, said Don S. Dizon, MD, professor of medicine and professor of surgery at Brown University, Providence, R.I. Dr. Dizon, as @DoctorDon, has 44,700 TikTok followers and uses the platform to answer cancer-related questions.

“It should be your altruism that motivates you to post,” said Dr. Dizon, who is also associate director of community outreach and engagement at the Legorreta Cancer Center in Providence, R.I., and director of medical oncology at Rhode Island Hospital. “What we can do for society at large is to provide our input into issues, add informed opinions where there’s controversy, and address misinformation.”

If you don’t know where to start, consider seeking a digital mentor to talk through your options.

“You may never meet this person, but you should choose them if you like their style, their content, their delivery, and their perspective,” Dr. Dizon said. “Find another doctor out there on social media whom you feel you can emulate. Take your time, too. Soon enough, you’ll develop your own style and your own online persona.”
 

Post clear, accurate information

If you want to be lighthearted on social media, that’s your choice. But Jennifer Trachtenberg, a pediatrician with nearly 7,000 Instagram followers in New York who posts as @askdrjen, prefers to offer vaccine scheduling tips, alert parents about COVID-19 rates, and offer advice on cold and flu prevention.

“Right now, I’m mainly doing this to educate patients and make them aware of topics that I think are important and that I see my patients needing more information on,” she said. “We have to be clear: People take what we say seriously. So, while it’s important to be relatable, it’s even more important to share evidence-based information.”
 

Many patients get their information on social media

While patients once came to the doctor armed with information sourced via “Doctor Google,” today, just as many patients use social media to learn about their condition or the medications they’re taking.

Unfortunately, a recent Ohio State University, Columbus, study found that the majority of gynecologic cancer advice on TikTok, for example, was either misleading or inaccurate.

“This misinformation should be a motivator for physicians to explore the social media space,” Dr. Dizon said. “Our voices need to be on there.”
 

Break down barriers – and make connections

Mike Natter, MD, an endocrinologist in New York, has type 1 diabetes. This informs his work – and his life – and he’s passionate about sharing it with his 117,000 followers as @mike.natter on Instagram.

“A lot of type 1s follow me, so there’s an advocacy component to what I do,” he said. “I enjoy being able to raise awareness and keep people up to date on the newest research and treatment.”

But that’s not all: Dr. Natter is also an artist who went to art school before he went to medical school, and his account is rife with his cartoons and illustrations about everything from valvular disease to diabetic ketoacidosis.

“I found that I was drawing a lot of my notes in medical school,” he said. “When I drew my notes, I did quite well, and I think that using art and illustration is a great tool. It breaks down barriers and makes health information all the more accessible to everyone.”
 

Share your expertise as a doctor – and a person

As a mom and pediatrician, Krupa Playforth, MD, who practices in Vienna, Va., knows that what she posts carries weight. So, whether she’s writing about backpack safety tips, choking hazards, or separation anxiety, her followers can rest assured that she’s posting responsibly.

“Pediatricians often underestimate how smart parents are,” said Dr. Playforth, who has three kids, ages 8, 5, and 2, and has 137,000 followers on @thepediatricianmom, her Instagram account. “Their anxiety comes from an understandable place, which is why I see my role as that of a parent and pediatrician who can translate the knowledge pediatricians have into something parents can understand.”

Dr. Playforth, who jumped on social media during COVID-19 and experienced a positive response in her local community, said being on social media is imperative if you’re a pediatrician.

“This is the future of pediatric medicine in particular,” she said. “A lot of pediatricians don’t want to embrace social media, but I think that’s a mistake. After all, while parents think pediatricians have all the answers, when we think of our own children, most doctors are like other parents – we can’t think objectively about our kids. It’s helpful for me to share that and to help parents feel less alone.”

If you’re not yet using social media to the best of your physician abilities, you might take a shot at becoming widely recognizable. Pick a preferred platform, answer common patient questions, dispel medical myths, provide pertinent information, and let your personality shine.

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

PHILADELPHIA – Cognitive behavioral therapy (CBT) was effective in addressing peri- and postmenopausal women’s sexual concerns, according to a small study presented at the annual meeting of the Menopause Society (formerly The North American Menopause Society). Four CBT sessions specifically focused on sexual concerns resulted in decreased sexual distress and concern, reduced depressive and menopausal symptoms, and increased sexual desire and functioning, as well as improved body image and relationship satisfaction.

An estimated 68%-87% of perimenopausal and postmenopausal women report sexual concerns, Sheryl Green, PhD, CPsych, an associate professor of psychiatry and behavioral neurosciences at McMaster University and a psychologist at St. Joseph’s Healthcare’s Women’s Health Concerns Clinic, both in Hamilton, Ont., told attendees at the meeting.

“Sexual concerns over the menopausal transition are not just physical, but they’re also psychological and emotional,” Dr. Green said. “Three common challenges include decreased sexual desire, a reduction in physical arousal and ability to achieve an orgasm, and sexual pain and discomfort during intercourse.”

The reasons for these concerns are multifactorial, she said. Decreased sexual desire can stem from stress, medical problems, their relationship with their partner, or other causes. A woman’s difficulty with reduced physical arousal or ability to have an orgasm can result from changes in hormone levels and vaginal changes, such as vaginal atrophy, which can also contribute to the sexual pain or discomfort reported by 17%-45% of postmenopausal women.

Two pharmacologic treatments exist for sexual concerns: oral flibanserin (Addyi) and injectable bremelanotide (Vyleesi). But many women may be unable or unwilling to take medication for their concerns. Previous research from Lori Brotto has found cognitive behavioral therapy and mindfulness interventions to effectively improve sexual functioning in women treated for gynecologic cancer and in women without a history of cancer.

“Sexual function needs to be understood from a bio-psychosocial model, looking at the biologic factors, the psychological factors, the sociocultural factors, and the interpersonal factors,” Sheryl Kingsberg, PhD, a professor of psychiatry and reproductive biology at Case Western Reserve University and a psychologist at University Hospitals in Cleveland, said in an interview.

“They can all overlap, and the clinician can ask a few pointed questions that help identify what the source of the problem is,” said Dr. Kingsberg, who was not involved in this study. She noted that the International Society for the Study of Women’s Sexual Health has an algorithm that can help in determining the source of the problems.

“Sometimes it’s going to be a biologic condition for which pharmacologic options are nice, but even if it is primarily pharmacologic, psychotherapy is always useful,” Dr. Kingsberg said. “Once the problem is there, even if it’s biologically based, then you have all the things in terms of the cognitive distortion, anxiety,” and other issues that a cognitive behavioral approach can help address. “And access is now much wider because of telehealth,” she added.
 

‘Psychology of menopause’

The study led by Dr. Green focused on peri- and postmenopausal women, with an average age of 50, who were experiencing primary sexual concerns based on a score of at least 26 on the Female Sexual Function Index (FSFI). Among the 20 women recruited for the study, 6 had already been prescribed hormone therapy for sexual concerns.

All reported decreased sexual desire, 17 reported decreased sexual arousal, 14 had body image dissatisfaction related to sexual concerns, and 6 reported urogenital problems. Nine of the women were in full remission from major depressive disorder, one had post-traumatic stress syndrome, and one had subclinical generalized anxiety disorder.

After spending 4 weeks on a wait list as self-control group for the study, the 15 women who completed the trial underwent four individual CBT sessions focusing on sexual concerns. The first session focused on psychoeducation and thought monitoring, and the second focused on cognitive distortions, cognitive strategies, and unhelpful beliefs or expectations related to sexual concerns. The third session looked at the role of problematic behaviors and behavioral experiments, and the fourth focused on continuation of strategies, long-term goals, and maintaining gains.

The participants completed eight measures at baseline, after the 4 weeks on the wait list, and after the four CBT sessions to assess the following:

• Sexual satisfaction, distress, and desire, using the FSFI, the Female Sexual Distress Scale-Revised (FSDS-R), and the Female Sexual Desire Questionnaire (FSDQ).
• Menopause symptoms, using the Greene Climacteric Scale (GCS).
• Body image, using the Dresden Body Image Questionnaire (DBIQ).
• Relationship satisfaction, using the Couples Satisfaction Index (CSI).
• Depression, using the Beck Depression Inventory-II (BDI-II).
• Anxiety, using the Hamilton Anxiety Rating Scale (HAM-A).

The women did not experience any significant changes while on the wait list except a slight decrease on the FSDQ concern subscale. Following the CBT sessions, however, the women experienced a significant decrease in sexual distress and concern as well as an increase in sexual dyadic desire and sexual functioning (P = .003 for FSFI, P = .002 for FSDS-R, and P = .003 for FSDQ).

Participants also experienced a decrease in depression (P < .0001) and menopausal symptoms (P = .001) and an increase in body-image satisfaction (P = .018) and relationship satisfaction (P = .0011) after the CBT sessions. The researchers assessed participants’ satisfaction with the Client Satisfaction Questionnaire after the CBT sessions and reported some of the qualitative findings.

“The treatment program was able to assist me with recognizing that some of my sexual concerns were normal, emotional as well as physical and hormonal, and provided me the ability to delve more deeply into the psychology of menopause and how to work through symptoms and concerns in more manageable pieces,” one participant wrote. Another found helpful the “homework exercises of recognizing a thought/feeling/emotion surrounding how I feel about myself/body and working through. More positive thought pattern/restructuring a response the most helpful.”

The main complaint about the program was that it was too short, with women wanting more sessions to help continue their progress.
 

Not an ‘either-or’ approach

Dr. Kingsberg said ISSWSH has a variety of sexual medicine practitioners, including providers who can provide CBT for sexual concerns, and the American Association of Sexuality Educators, Counselors and Therapists has a referral directory.

“Keeping in mind the bio-psychosocial model, sometimes psychotherapy is going to be a really effective treatment for sexual concerns,” Dr. Kingsberg said. “Sometimes the pharmacologic option is going to be a really effective treatment for some concerns, and sometimes the combination is going to have a really nice treatment effect. So it’s not a one-size-fits-all, and it doesn’t have to be an either-or.”

The sexual concerns of women still do not get adequately addressed in medical schools and residencies, Dr. Kingsberg said, which is distinctly different from how male sexual concerns are addressed in health care.

“Erectile dysfunction is kind of in the norm, and women are still a little hesitant to bring up their sexual concerns,” Dr. Kingsberg said. “They don’t know if it’s appropriate and they’re hoping that their clinician will ask.”

One way clinicians can do that is with a global question for all their patients: “Most of my patients have sexual questions or concerns; what concerns do you have?”

“They don’t have to go through a checklist of 10 things,” Dr. Kingsberg said. If the patient does not bring anything up, providers can then ask a single follow up question: “Do you have any concerns with desire, arousal, orgasm, or pain?” That question, Dr. Kingsberg said, covers the four main areas of concern.

The study was funded by the Canadian Institute of Health Research. Dr. Green reported no disclosures. Dr. Kingsberg has consulted for or served on the advisory board for Alloy, Astellas, Bayer, Dare Bioscience, Freya, Reunion Neuroscience, Materna Medical, Madorra, Palatin, Pfizer, ReJoy, Sprout, Strategic Science Technologies, and MsMedicine.

PHILADELPHIA – Cognitive behavioral therapy (CBT) was effective in addressing peri- and postmenopausal women’s sexual concerns, according to a small study presented at the annual meeting of the Menopause Society (formerly The North American Menopause Society). Four CBT sessions specifically focused on sexual concerns resulted in decreased sexual distress and concern, reduced depressive and menopausal symptoms, and increased sexual desire and functioning, as well as improved body image and relationship satisfaction.

An estimated 68%-87% of perimenopausal and postmenopausal women report sexual concerns, Sheryl Green, PhD, CPsych, an associate professor of psychiatry and behavioral neurosciences at McMaster University and a psychologist at St. Joseph’s Healthcare’s Women’s Health Concerns Clinic, both in Hamilton, Ont., told attendees at the meeting.

“Sexual concerns over the menopausal transition are not just physical, but they’re also psychological and emotional,” Dr. Green said. “Three common challenges include decreased sexual desire, a reduction in physical arousal and ability to achieve an orgasm, and sexual pain and discomfort during intercourse.”

The reasons for these concerns are multifactorial, she said. Decreased sexual desire can stem from stress, medical problems, their relationship with their partner, or other causes. A woman’s difficulty with reduced physical arousal or ability to have an orgasm can result from changes in hormone levels and vaginal changes, such as vaginal atrophy, which can also contribute to the sexual pain or discomfort reported by 17%-45% of postmenopausal women.

Two pharmacologic treatments exist for sexual concerns: oral flibanserin (Addyi) and injectable bremelanotide (Vyleesi). But many women may be unable or unwilling to take medication for their concerns. Previous research from Lori Brotto has found cognitive behavioral therapy and mindfulness interventions to effectively improve sexual functioning in women treated for gynecologic cancer and in women without a history of cancer.

“Sexual function needs to be understood from a bio-psychosocial model, looking at the biologic factors, the psychological factors, the sociocultural factors, and the interpersonal factors,” Sheryl Kingsberg, PhD, a professor of psychiatry and reproductive biology at Case Western Reserve University and a psychologist at University Hospitals in Cleveland, said in an interview.

“They can all overlap, and the clinician can ask a few pointed questions that help identify what the source of the problem is,” said Dr. Kingsberg, who was not involved in this study. She noted that the International Society for the Study of Women’s Sexual Health has an algorithm that can help in determining the source of the problems.

“Sometimes it’s going to be a biologic condition for which pharmacologic options are nice, but even if it is primarily pharmacologic, psychotherapy is always useful,” Dr. Kingsberg said. “Once the problem is there, even if it’s biologically based, then you have all the things in terms of the cognitive distortion, anxiety,” and other issues that a cognitive behavioral approach can help address. “And access is now much wider because of telehealth,” she added.
 

‘Psychology of menopause’

The study led by Dr. Green focused on peri- and postmenopausal women, with an average age of 50, who were experiencing primary sexual concerns based on a score of at least 26 on the Female Sexual Function Index (FSFI). Among the 20 women recruited for the study, 6 had already been prescribed hormone therapy for sexual concerns.

All reported decreased sexual desire, 17 reported decreased sexual arousal, 14 had body image dissatisfaction related to sexual concerns, and 6 reported urogenital problems. Nine of the women were in full remission from major depressive disorder, one had post-traumatic stress syndrome, and one had subclinical generalized anxiety disorder.

After spending 4 weeks on a wait list as self-control group for the study, the 15 women who completed the trial underwent four individual CBT sessions focusing on sexual concerns. The first session focused on psychoeducation and thought monitoring, and the second focused on cognitive distortions, cognitive strategies, and unhelpful beliefs or expectations related to sexual concerns. The third session looked at the role of problematic behaviors and behavioral experiments, and the fourth focused on continuation of strategies, long-term goals, and maintaining gains.

The participants completed eight measures at baseline, after the 4 weeks on the wait list, and after the four CBT sessions to assess the following:

• Sexual satisfaction, distress, and desire, using the FSFI, the Female Sexual Distress Scale-Revised (FSDS-R), and the Female Sexual Desire Questionnaire (FSDQ).
• Menopause symptoms, using the Greene Climacteric Scale (GCS).
• Body image, using the Dresden Body Image Questionnaire (DBIQ).
• Relationship satisfaction, using the Couples Satisfaction Index (CSI).
• Depression, using the Beck Depression Inventory-II (BDI-II).
• Anxiety, using the Hamilton Anxiety Rating Scale (HAM-A).

The women did not experience any significant changes while on the wait list except a slight decrease on the FSDQ concern subscale. Following the CBT sessions, however, the women experienced a significant decrease in sexual distress and concern as well as an increase in sexual dyadic desire and sexual functioning (P = .003 for FSFI, P = .002 for FSDS-R, and P = .003 for FSDQ).

Participants also experienced a decrease in depression (P < .0001) and menopausal symptoms (P = .001) and an increase in body-image satisfaction (P = .018) and relationship satisfaction (P = .0011) after the CBT sessions. The researchers assessed participants’ satisfaction with the Client Satisfaction Questionnaire after the CBT sessions and reported some of the qualitative findings.

“The treatment program was able to assist me with recognizing that some of my sexual concerns were normal, emotional as well as physical and hormonal, and provided me the ability to delve more deeply into the psychology of menopause and how to work through symptoms and concerns in more manageable pieces,” one participant wrote. Another found helpful the “homework exercises of recognizing a thought/feeling/emotion surrounding how I feel about myself/body and working through. More positive thought pattern/restructuring a response the most helpful.”

The main complaint about the program was that it was too short, with women wanting more sessions to help continue their progress.
 

Not an ‘either-or’ approach

Dr. Kingsberg said ISSWSH has a variety of sexual medicine practitioners, including providers who can provide CBT for sexual concerns, and the American Association of Sexuality Educators, Counselors and Therapists has a referral directory.

“Keeping in mind the bio-psychosocial model, sometimes psychotherapy is going to be a really effective treatment for sexual concerns,” Dr. Kingsberg said. “Sometimes the pharmacologic option is going to be a really effective treatment for some concerns, and sometimes the combination is going to have a really nice treatment effect. So it’s not a one-size-fits-all, and it doesn’t have to be an either-or.”

The sexual concerns of women still do not get adequately addressed in medical schools and residencies, Dr. Kingsberg said, which is distinctly different from how male sexual concerns are addressed in health care.

“Erectile dysfunction is kind of in the norm, and women are still a little hesitant to bring up their sexual concerns,” Dr. Kingsberg said. “They don’t know if it’s appropriate and they’re hoping that their clinician will ask.”

One way clinicians can do that is with a global question for all their patients: “Most of my patients have sexual questions or concerns; what concerns do you have?”

“They don’t have to go through a checklist of 10 things,” Dr. Kingsberg said. If the patient does not bring anything up, providers can then ask a single follow up question: “Do you have any concerns with desire, arousal, orgasm, or pain?” That question, Dr. Kingsberg said, covers the four main areas of concern.

The study was funded by the Canadian Institute of Health Research. Dr. Green reported no disclosures. Dr. Kingsberg has consulted for or served on the advisory board for Alloy, Astellas, Bayer, Dare Bioscience, Freya, Reunion Neuroscience, Materna Medical, Madorra, Palatin, Pfizer, ReJoy, Sprout, Strategic Science Technologies, and MsMedicine.

PHILADELPHIA – Cognitive behavioral therapy (CBT) was effective in addressing peri- and postmenopausal women’s sexual concerns, according to a small study presented at the annual meeting of the Menopause Society (formerly The North American Menopause Society). Four CBT sessions specifically focused on sexual concerns resulted in decreased sexual distress and concern, reduced depressive and menopausal symptoms, and increased sexual desire and functioning, as well as improved body image and relationship satisfaction.

An estimated 68%-87% of perimenopausal and postmenopausal women report sexual concerns, Sheryl Green, PhD, CPsych, an associate professor of psychiatry and behavioral neurosciences at McMaster University and a psychologist at St. Joseph’s Healthcare’s Women’s Health Concerns Clinic, both in Hamilton, Ont., told attendees at the meeting.

“Sexual concerns over the menopausal transition are not just physical, but they’re also psychological and emotional,” Dr. Green said. “Three common challenges include decreased sexual desire, a reduction in physical arousal and ability to achieve an orgasm, and sexual pain and discomfort during intercourse.”

The reasons for these concerns are multifactorial, she said. Decreased sexual desire can stem from stress, medical problems, their relationship with their partner, or other causes. A woman’s difficulty with reduced physical arousal or ability to have an orgasm can result from changes in hormone levels and vaginal changes, such as vaginal atrophy, which can also contribute to the sexual pain or discomfort reported by 17%-45% of postmenopausal women.

Two pharmacologic treatments exist for sexual concerns: oral flibanserin (Addyi) and injectable bremelanotide (Vyleesi). But many women may be unable or unwilling to take medication for their concerns. Previous research from Lori Brotto has found cognitive behavioral therapy and mindfulness interventions to effectively improve sexual functioning in women treated for gynecologic cancer and in women without a history of cancer.

“Sexual function needs to be understood from a bio-psychosocial model, looking at the biologic factors, the psychological factors, the sociocultural factors, and the interpersonal factors,” Sheryl Kingsberg, PhD, a professor of psychiatry and reproductive biology at Case Western Reserve University and a psychologist at University Hospitals in Cleveland, said in an interview.

“They can all overlap, and the clinician can ask a few pointed questions that help identify what the source of the problem is,” said Dr. Kingsberg, who was not involved in this study. She noted that the International Society for the Study of Women’s Sexual Health has an algorithm that can help in determining the source of the problems.

“Sometimes it’s going to be a biologic condition for which pharmacologic options are nice, but even if it is primarily pharmacologic, psychotherapy is always useful,” Dr. Kingsberg said. “Once the problem is there, even if it’s biologically based, then you have all the things in terms of the cognitive distortion, anxiety,” and other issues that a cognitive behavioral approach can help address. “And access is now much wider because of telehealth,” she added.
 

‘Psychology of menopause’

The study led by Dr. Green focused on peri- and postmenopausal women, with an average age of 50, who were experiencing primary sexual concerns based on a score of at least 26 on the Female Sexual Function Index (FSFI). Among the 20 women recruited for the study, 6 had already been prescribed hormone therapy for sexual concerns.

All reported decreased sexual desire, 17 reported decreased sexual arousal, 14 had body image dissatisfaction related to sexual concerns, and 6 reported urogenital problems. Nine of the women were in full remission from major depressive disorder, one had post-traumatic stress syndrome, and one had subclinical generalized anxiety disorder.

After spending 4 weeks on a wait list as self-control group for the study, the 15 women who completed the trial underwent four individual CBT sessions focusing on sexual concerns. The first session focused on psychoeducation and thought monitoring, and the second focused on cognitive distortions, cognitive strategies, and unhelpful beliefs or expectations related to sexual concerns. The third session looked at the role of problematic behaviors and behavioral experiments, and the fourth focused on continuation of strategies, long-term goals, and maintaining gains.

The participants completed eight measures at baseline, after the 4 weeks on the wait list, and after the four CBT sessions to assess the following:

• Sexual satisfaction, distress, and desire, using the FSFI, the Female Sexual Distress Scale-Revised (FSDS-R), and the Female Sexual Desire Questionnaire (FSDQ).
• Menopause symptoms, using the Greene Climacteric Scale (GCS).
• Body image, using the Dresden Body Image Questionnaire (DBIQ).
• Relationship satisfaction, using the Couples Satisfaction Index (CSI).
• Depression, using the Beck Depression Inventory-II (BDI-II).
• Anxiety, using the Hamilton Anxiety Rating Scale (HAM-A).

The women did not experience any significant changes while on the wait list except a slight decrease on the FSDQ concern subscale. Following the CBT sessions, however, the women experienced a significant decrease in sexual distress and concern as well as an increase in sexual dyadic desire and sexual functioning (P = .003 for FSFI, P = .002 for FSDS-R, and P = .003 for FSDQ).

Participants also experienced a decrease in depression (P < .0001) and menopausal symptoms (P = .001) and an increase in body-image satisfaction (P = .018) and relationship satisfaction (P = .0011) after the CBT sessions. The researchers assessed participants’ satisfaction with the Client Satisfaction Questionnaire after the CBT sessions and reported some of the qualitative findings.

“The treatment program was able to assist me with recognizing that some of my sexual concerns were normal, emotional as well as physical and hormonal, and provided me the ability to delve more deeply into the psychology of menopause and how to work through symptoms and concerns in more manageable pieces,” one participant wrote. Another found helpful the “homework exercises of recognizing a thought/feeling/emotion surrounding how I feel about myself/body and working through. More positive thought pattern/restructuring a response the most helpful.”

The main complaint about the program was that it was too short, with women wanting more sessions to help continue their progress.
 

Not an ‘either-or’ approach

Dr. Kingsberg said ISSWSH has a variety of sexual medicine practitioners, including providers who can provide CBT for sexual concerns, and the American Association of Sexuality Educators, Counselors and Therapists has a referral directory.

“Keeping in mind the bio-psychosocial model, sometimes psychotherapy is going to be a really effective treatment for sexual concerns,” Dr. Kingsberg said. “Sometimes the pharmacologic option is going to be a really effective treatment for some concerns, and sometimes the combination is going to have a really nice treatment effect. So it’s not a one-size-fits-all, and it doesn’t have to be an either-or.”

The sexual concerns of women still do not get adequately addressed in medical schools and residencies, Dr. Kingsberg said, which is distinctly different from how male sexual concerns are addressed in health care.

“Erectile dysfunction is kind of in the norm, and women are still a little hesitant to bring up their sexual concerns,” Dr. Kingsberg said. “They don’t know if it’s appropriate and they’re hoping that their clinician will ask.”

One way clinicians can do that is with a global question for all their patients: “Most of my patients have sexual questions or concerns; what concerns do you have?”

“They don’t have to go through a checklist of 10 things,” Dr. Kingsberg said. If the patient does not bring anything up, providers can then ask a single follow up question: “Do you have any concerns with desire, arousal, orgasm, or pain?” That question, Dr. Kingsberg said, covers the four main areas of concern.

The study was funded by the Canadian Institute of Health Research. Dr. Green reported no disclosures. Dr. Kingsberg has consulted for or served on the advisory board for Alloy, Astellas, Bayer, Dare Bioscience, Freya, Reunion Neuroscience, Materna Medical, Madorra, Palatin, Pfizer, ReJoy, Sprout, Strategic Science Technologies, and MsMedicine.

TOPLINE:

In patients with fibromyalgia, cognitive behavior therapy (CBT) can reduce pain through its effect on pain-related catastrophizing, which involves intensified cognitive and emotional responses to things like intrusive thoughts, a new study suggests.

METHODOLOGY:

• The study included 98 female patients with fibromyalgia (FM), mean age about 42 years, who underwent a baseline neuroimaging assessment and were randomly assigned to CBT (where patients learned to identify negative thoughts and use cognitive restructuring to diminish pain-related distress) or a matched educational intervention (where patients learned about fibromyalgia and chronic pain); both groups had eight weekly individual 60- to 75-minute visits.
• The primary outcome was the pain interference subscale of the Brief Pain Inventory (BPI); secondary outcomes included the BPI pain severity subscale, the Fibromyalgia Impact Questionnaire–Revised (FIQR), and the Pain Catastrophizing Scale (PCS), which includes subscales of rumination, magnification, and helplessness.
• Researchers used functional magnetic resonance imaging (fMRI)-adapted task to investigate the neural circuitry supporting pain catastrophizing.

TAKEAWAY:

• After controlling for baseline values, BPI pain interference scores were significantly reduced, with a larger reduction in the CBT group, compared with the education group (P = .03), which was also the case for FIQR scores (P = .05) and pain catastrophizing (P = .04).
• There were larger reductions in pain-related symptomatology in the CBT group, but they did not reach statistical significance.
• Following CBT treatment, the study showed reduced connectivity between regions of the brain associated with self-awareness, pain, and emotional processing.

IN PRACTICE:

The results “highlight the important role of targeting pain catastrophizing with psychotherapy, particularly for patients reporting high levels of catastrophizing cognitions” write the authors, adding that altered network connectivity identified by the study “may emerge as a valuable biomarker of catastrophizing-related cognitive and affective processes.”

SOURCE:

The study was carried out by Jeungchan Lee, PhD, department of radiology, center for biomedical imaging, Massachusetts General Hospital, Boston, and the Discovery Center for Recovery from Chronic Pain, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, and colleagues. It was published in Arthritis & Rheumatology.

LIMITATIONS:

Findings were limited to female participants. CBT for chronic pain includes different therapeutic modules, and the study can’t draw definitive conclusions regarding which CBT skills were most beneficial to patients in reducing catastrophizing. Baseline symptom severity was higher for the CBT group, which may complicate interpretation of the findings.

DISCLOSURES:

The study received support from the National Institutes of Health: National Center for Complementary and Integrative Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases, and the National Center for Research Resources. The authors have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

In patients with fibromyalgia, cognitive behavior therapy (CBT) can reduce pain through its effect on pain-related catastrophizing, which involves intensified cognitive and emotional responses to things like intrusive thoughts, a new study suggests.

METHODOLOGY:

• The study included 98 female patients with fibromyalgia (FM), mean age about 42 years, who underwent a baseline neuroimaging assessment and were randomly assigned to CBT (where patients learned to identify negative thoughts and use cognitive restructuring to diminish pain-related distress) or a matched educational intervention (where patients learned about fibromyalgia and chronic pain); both groups had eight weekly individual 60- to 75-minute visits.
• The primary outcome was the pain interference subscale of the Brief Pain Inventory (BPI); secondary outcomes included the BPI pain severity subscale, the Fibromyalgia Impact Questionnaire–Revised (FIQR), and the Pain Catastrophizing Scale (PCS), which includes subscales of rumination, magnification, and helplessness.
• Researchers used functional magnetic resonance imaging (fMRI)-adapted task to investigate the neural circuitry supporting pain catastrophizing.

TAKEAWAY:

• After controlling for baseline values, BPI pain interference scores were significantly reduced, with a larger reduction in the CBT group, compared with the education group (P = .03), which was also the case for FIQR scores (P = .05) and pain catastrophizing (P = .04).
• There were larger reductions in pain-related symptomatology in the CBT group, but they did not reach statistical significance.
• Following CBT treatment, the study showed reduced connectivity between regions of the brain associated with self-awareness, pain, and emotional processing.

IN PRACTICE:

The results “highlight the important role of targeting pain catastrophizing with psychotherapy, particularly for patients reporting high levels of catastrophizing cognitions” write the authors, adding that altered network connectivity identified by the study “may emerge as a valuable biomarker of catastrophizing-related cognitive and affective processes.”

SOURCE:

The study was carried out by Jeungchan Lee, PhD, department of radiology, center for biomedical imaging, Massachusetts General Hospital, Boston, and the Discovery Center for Recovery from Chronic Pain, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, and colleagues. It was published in Arthritis & Rheumatology.

LIMITATIONS:

Findings were limited to female participants. CBT for chronic pain includes different therapeutic modules, and the study can’t draw definitive conclusions regarding which CBT skills were most beneficial to patients in reducing catastrophizing. Baseline symptom severity was higher for the CBT group, which may complicate interpretation of the findings.

DISCLOSURES:

The study received support from the National Institutes of Health: National Center for Complementary and Integrative Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases, and the National Center for Research Resources. The authors have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

In patients with fibromyalgia, cognitive behavior therapy (CBT) can reduce pain through its effect on pain-related catastrophizing, which involves intensified cognitive and emotional responses to things like intrusive thoughts, a new study suggests.

METHODOLOGY:

• The study included 98 female patients with fibromyalgia (FM), mean age about 42 years, who underwent a baseline neuroimaging assessment and were randomly assigned to CBT (where patients learned to identify negative thoughts and use cognitive restructuring to diminish pain-related distress) or a matched educational intervention (where patients learned about fibromyalgia and chronic pain); both groups had eight weekly individual 60- to 75-minute visits.
• The primary outcome was the pain interference subscale of the Brief Pain Inventory (BPI); secondary outcomes included the BPI pain severity subscale, the Fibromyalgia Impact Questionnaire–Revised (FIQR), and the Pain Catastrophizing Scale (PCS), which includes subscales of rumination, magnification, and helplessness.
• Researchers used functional magnetic resonance imaging (fMRI)-adapted task to investigate the neural circuitry supporting pain catastrophizing.

TAKEAWAY:

• After controlling for baseline values, BPI pain interference scores were significantly reduced, with a larger reduction in the CBT group, compared with the education group (P = .03), which was also the case for FIQR scores (P = .05) and pain catastrophizing (P = .04).
• There were larger reductions in pain-related symptomatology in the CBT group, but they did not reach statistical significance.
• Following CBT treatment, the study showed reduced connectivity between regions of the brain associated with self-awareness, pain, and emotional processing.

IN PRACTICE:

The results “highlight the important role of targeting pain catastrophizing with psychotherapy, particularly for patients reporting high levels of catastrophizing cognitions” write the authors, adding that altered network connectivity identified by the study “may emerge as a valuable biomarker of catastrophizing-related cognitive and affective processes.”

SOURCE:

The study was carried out by Jeungchan Lee, PhD, department of radiology, center for biomedical imaging, Massachusetts General Hospital, Boston, and the Discovery Center for Recovery from Chronic Pain, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, and colleagues. It was published in Arthritis & Rheumatology.

LIMITATIONS:

Findings were limited to female participants. CBT for chronic pain includes different therapeutic modules, and the study can’t draw definitive conclusions regarding which CBT skills were most beneficial to patients in reducing catastrophizing. Baseline symptom severity was higher for the CBT group, which may complicate interpretation of the findings.

DISCLOSURES:

The study received support from the National Institutes of Health: National Center for Complementary and Integrative Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases, and the National Center for Research Resources. The authors have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

She went by the name “Dr. Roxy” on social media and became something of a sensation on TikTok, where she livestreamed her patients’ operations. Ultimately, however, plastic surgeon Katharine Roxanne Grawe, MD, lost her medical license based partly on her “life-altering, reckless treatment,” heightened by her social media fame. In July, the Ohio state medical board permanently revoked Dr. Grawe’s license after twice reprimanding her for her failure to meet the standard of care. The board also determined that, by livestreaming procedures, she placed her patients in danger of immediate and serious harm.

Although most doctors don’t use social media to the degree that Dr. Grawe did, using the various platforms – from X (formerly Twitter) to Facebook, Instagram, and TikTok – can be a slippery slope. Medscape’s Physician Behavior Report 2023 revealed that doctors have seen their share of unprofessional or offensive social media use from their peers. Nearly 7 in 10 said it is unethical for a doctor to act rudely, offensively, or unprofessionally on social media, even if their medical practice isn’t mentioned. As one physician put it: “Professional is not a 9-to-5 descriptor.”

In today’s world, social media use is almost a given. Doctors must tread cautiously when they approach it – maybe even more so. “There’s still a stigma attached,” said Liudmila Schafer, MD, an oncologist with The Doctor Connect, a career consulting firm. “Physicians face a tougher challenge due to societal expectations of perfection, with greater consequences for mistakes. We’re under constant ‘observation’ from peers, employers, and patients.”

Beverly Hills plastic surgeon Jay Calvert, MD, says he holds firm boundaries with how he uses social media. “I do comedy on the side, but it’s not acceptable for me as a doctor to share that on social media,” he said. “People want doctors who are professional, and I’m always concerned about how I present myself.”

Dr. Calvert said it is fairly easy to spot doctors who cross the line with social media. “You have to hold yourself back when posting. Doing things like dancing in the OR are out of whack with the profession.”

According to Dr. Schafer, a definite line to avoid crossing is offering medical advice or guidance on social media. “You also can’t discuss confidential practice details, respond to unfamiliar contacts, or discuss institutional policies without permission,” she said. “It’s important to add disclaimers if a personal scientific opinion is shared without reference [or] research or with unchecked sources.”
 

Navigating the many social media sites

Each social media platform has its pros and cons. Doctors need to determine why to use them and what the payback of each might be. Dr. Schafer uses multiple sites, including LinkedIn, Facebook, Instagram, X, Threads, YouTube, and, to a lesser degree, Clubhouse. How and what she posts on each varies. “I use them almost 95% professionally,” she said. “It’s challenging to meet and engage in person, so that is where social media helps.”

Stephen Pribut, MD, a Washington-based podiatrist, likes to use X as an information source. He follows pretty simple rules when it comes to what he tweets and shares on various sites: “I stay away from politics and religion,” he said. “I also avoid controversial topics online, such as vaccines.”

Joseph Daibes, DO, who specializes in cardiovascular medicine at New Jersey Heart and Vein, Clifton, said he has changed how he uses social media. “Initially, I was a passive consumer, but as I recognized the importance of accurate medical information online, I became more active in weighing in responsibly, occasionally sharing studies, debunking myths, and engaging in meaningful conversations,” he said. “Social media can get dangerous, so we have a duty to use it responsibly, and I cannot stress that enough.”

For plastic surgeons like Dr. Calvert, the visual platforms such as Instagram can prove invaluable for marketing purposes. “I’ve been using Instagram since 2012, and it’s been my most positive experience,” he said. “I don’t generate business from it, but I use it to back up my qualifications as a surgeon.”

Potential patients like to scroll through posts by plastic surgeons to learn what their finished product looks like, Dr. Calvert said. In many cases, plastic surgeons hire social media experts to cultivate their content. “I’ve hired and fired social media managers over the years, ultimately deciding I should develop my own content,” he said. “I want people to see the same doctor on social media that they will see in the office. I like an authentic presentation, not glitzy.”
 

Social media gone wrong

Dr. Calvert said that in the world of plastic surgery, some doctors use social media to present “before and after” compilations that in his opinion aren’t necessarily fully authentic, and this rubs him wrong. “There’s a bit of ‘cheating’ in some of these posts, using filters, making the ‘befores’ particularly bad, and other tricks,” he said.

Dr. Daibes has also seen his share of social media misuse: ”Red flags include oversharing personal indulgences, engaging in online spats, or making unfounded medical claims,” he said. “It’s essential to remember our role as educators and advocates, and to present ourselves in a way that upholds the dignity of our profession.”

At the end of the day, social media can have positive uses for physicians, and it is clearly here to stay. The onus for responsible use ultimately falls to the physicians using it.

Dr. Daibes emphasizes the fact that a doctor’s words carry weight – perhaps more so than those of other professionals. “The added scrutiny is good because it keeps us accountable; it’s crucial that our information is accurate,” he said. “The downside is that the scrutiny can be stifling at times and lead to self-censorship, even on nonmedical matters.”

Physicians have suggested eight guidelines for doctors to follow when using social media:

• Remember that you represent your profession, even if posting on personal accounts.
• Never post from the operating room, the emergency department, or any sort of medical space.
• If you’re employed, before you post, check with your employer to see whether they have any rules or guidance surrounding social media.
• Never use social media to badmouth colleagues, hospitals, or other healthcare organizations.
• Never use social media to dispense medical advice.
• Steer clear of the obvious hot-button issues, like religion and politics.
• Always protect patient privacy when posting.
• Be careful with how and whom you engage on social media.

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

She went by the name “Dr. Roxy” on social media and became something of a sensation on TikTok, where she livestreamed her patients’ operations. Ultimately, however, plastic surgeon Katharine Roxanne Grawe, MD, lost her medical license based partly on her “life-altering, reckless treatment,” heightened by her social media fame. In July, the Ohio state medical board permanently revoked Dr. Grawe’s license after twice reprimanding her for her failure to meet the standard of care. The board also determined that, by livestreaming procedures, she placed her patients in danger of immediate and serious harm.

Although most doctors don’t use social media to the degree that Dr. Grawe did, using the various platforms – from X (formerly Twitter) to Facebook, Instagram, and TikTok – can be a slippery slope. Medscape’s Physician Behavior Report 2023 revealed that doctors have seen their share of unprofessional or offensive social media use from their peers. Nearly 7 in 10 said it is unethical for a doctor to act rudely, offensively, or unprofessionally on social media, even if their medical practice isn’t mentioned. As one physician put it: “Professional is not a 9-to-5 descriptor.”

In today’s world, social media use is almost a given. Doctors must tread cautiously when they approach it – maybe even more so. “There’s still a stigma attached,” said Liudmila Schafer, MD, an oncologist with The Doctor Connect, a career consulting firm. “Physicians face a tougher challenge due to societal expectations of perfection, with greater consequences for mistakes. We’re under constant ‘observation’ from peers, employers, and patients.”

Beverly Hills plastic surgeon Jay Calvert, MD, says he holds firm boundaries with how he uses social media. “I do comedy on the side, but it’s not acceptable for me as a doctor to share that on social media,” he said. “People want doctors who are professional, and I’m always concerned about how I present myself.”

Dr. Calvert said it is fairly easy to spot doctors who cross the line with social media. “You have to hold yourself back when posting. Doing things like dancing in the OR are out of whack with the profession.”

According to Dr. Schafer, a definite line to avoid crossing is offering medical advice or guidance on social media. “You also can’t discuss confidential practice details, respond to unfamiliar contacts, or discuss institutional policies without permission,” she said. “It’s important to add disclaimers if a personal scientific opinion is shared without reference [or] research or with unchecked sources.”
 

Navigating the many social media sites

Each social media platform has its pros and cons. Doctors need to determine why to use them and what the payback of each might be. Dr. Schafer uses multiple sites, including LinkedIn, Facebook, Instagram, X, Threads, YouTube, and, to a lesser degree, Clubhouse. How and what she posts on each varies. “I use them almost 95% professionally,” she said. “It’s challenging to meet and engage in person, so that is where social media helps.”

Stephen Pribut, MD, a Washington-based podiatrist, likes to use X as an information source. He follows pretty simple rules when it comes to what he tweets and shares on various sites: “I stay away from politics and religion,” he said. “I also avoid controversial topics online, such as vaccines.”

Joseph Daibes, DO, who specializes in cardiovascular medicine at New Jersey Heart and Vein, Clifton, said he has changed how he uses social media. “Initially, I was a passive consumer, but as I recognized the importance of accurate medical information online, I became more active in weighing in responsibly, occasionally sharing studies, debunking myths, and engaging in meaningful conversations,” he said. “Social media can get dangerous, so we have a duty to use it responsibly, and I cannot stress that enough.”

For plastic surgeons like Dr. Calvert, the visual platforms such as Instagram can prove invaluable for marketing purposes. “I’ve been using Instagram since 2012, and it’s been my most positive experience,” he said. “I don’t generate business from it, but I use it to back up my qualifications as a surgeon.”

Potential patients like to scroll through posts by plastic surgeons to learn what their finished product looks like, Dr. Calvert said. In many cases, plastic surgeons hire social media experts to cultivate their content. “I’ve hired and fired social media managers over the years, ultimately deciding I should develop my own content,” he said. “I want people to see the same doctor on social media that they will see in the office. I like an authentic presentation, not glitzy.”
 

Social media gone wrong

Dr. Calvert said that in the world of plastic surgery, some doctors use social media to present “before and after” compilations that in his opinion aren’t necessarily fully authentic, and this rubs him wrong. “There’s a bit of ‘cheating’ in some of these posts, using filters, making the ‘befores’ particularly bad, and other tricks,” he said.

Dr. Daibes has also seen his share of social media misuse: ”Red flags include oversharing personal indulgences, engaging in online spats, or making unfounded medical claims,” he said. “It’s essential to remember our role as educators and advocates, and to present ourselves in a way that upholds the dignity of our profession.”

At the end of the day, social media can have positive uses for physicians, and it is clearly here to stay. The onus for responsible use ultimately falls to the physicians using it.

Dr. Daibes emphasizes the fact that a doctor’s words carry weight – perhaps more so than those of other professionals. “The added scrutiny is good because it keeps us accountable; it’s crucial that our information is accurate,” he said. “The downside is that the scrutiny can be stifling at times and lead to self-censorship, even on nonmedical matters.”

Physicians have suggested eight guidelines for doctors to follow when using social media:

• Remember that you represent your profession, even if posting on personal accounts.
• Never post from the operating room, the emergency department, or any sort of medical space.
• If you’re employed, before you post, check with your employer to see whether they have any rules or guidance surrounding social media.
• Never use social media to badmouth colleagues, hospitals, or other healthcare organizations.
• Never use social media to dispense medical advice.
• Steer clear of the obvious hot-button issues, like religion and politics.
• Always protect patient privacy when posting.
• Be careful with how and whom you engage on social media.

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

She went by the name “Dr. Roxy” on social media and became something of a sensation on TikTok, where she livestreamed her patients’ operations. Ultimately, however, plastic surgeon Katharine Roxanne Grawe, MD, lost her medical license based partly on her “life-altering, reckless treatment,” heightened by her social media fame. In July, the Ohio state medical board permanently revoked Dr. Grawe’s license after twice reprimanding her for her failure to meet the standard of care. The board also determined that, by livestreaming procedures, she placed her patients in danger of immediate and serious harm.

Although most doctors don’t use social media to the degree that Dr. Grawe did, using the various platforms – from X (formerly Twitter) to Facebook, Instagram, and TikTok – can be a slippery slope. Medscape’s Physician Behavior Report 2023 revealed that doctors have seen their share of unprofessional or offensive social media use from their peers. Nearly 7 in 10 said it is unethical for a doctor to act rudely, offensively, or unprofessionally on social media, even if their medical practice isn’t mentioned. As one physician put it: “Professional is not a 9-to-5 descriptor.”

In today’s world, social media use is almost a given. Doctors must tread cautiously when they approach it – maybe even more so. “There’s still a stigma attached,” said Liudmila Schafer, MD, an oncologist with The Doctor Connect, a career consulting firm. “Physicians face a tougher challenge due to societal expectations of perfection, with greater consequences for mistakes. We’re under constant ‘observation’ from peers, employers, and patients.”

Beverly Hills plastic surgeon Jay Calvert, MD, says he holds firm boundaries with how he uses social media. “I do comedy on the side, but it’s not acceptable for me as a doctor to share that on social media,” he said. “People want doctors who are professional, and I’m always concerned about how I present myself.”

Dr. Calvert said it is fairly easy to spot doctors who cross the line with social media. “You have to hold yourself back when posting. Doing things like dancing in the OR are out of whack with the profession.”

According to Dr. Schafer, a definite line to avoid crossing is offering medical advice or guidance on social media. “You also can’t discuss confidential practice details, respond to unfamiliar contacts, or discuss institutional policies without permission,” she said. “It’s important to add disclaimers if a personal scientific opinion is shared without reference [or] research or with unchecked sources.”
 

Navigating the many social media sites

Each social media platform has its pros and cons. Doctors need to determine why to use them and what the payback of each might be. Dr. Schafer uses multiple sites, including LinkedIn, Facebook, Instagram, X, Threads, YouTube, and, to a lesser degree, Clubhouse. How and what she posts on each varies. “I use them almost 95% professionally,” she said. “It’s challenging to meet and engage in person, so that is where social media helps.”

Stephen Pribut, MD, a Washington-based podiatrist, likes to use X as an information source. He follows pretty simple rules when it comes to what he tweets and shares on various sites: “I stay away from politics and religion,” he said. “I also avoid controversial topics online, such as vaccines.”

Joseph Daibes, DO, who specializes in cardiovascular medicine at New Jersey Heart and Vein, Clifton, said he has changed how he uses social media. “Initially, I was a passive consumer, but as I recognized the importance of accurate medical information online, I became more active in weighing in responsibly, occasionally sharing studies, debunking myths, and engaging in meaningful conversations,” he said. “Social media can get dangerous, so we have a duty to use it responsibly, and I cannot stress that enough.”

For plastic surgeons like Dr. Calvert, the visual platforms such as Instagram can prove invaluable for marketing purposes. “I’ve been using Instagram since 2012, and it’s been my most positive experience,” he said. “I don’t generate business from it, but I use it to back up my qualifications as a surgeon.”

Potential patients like to scroll through posts by plastic surgeons to learn what their finished product looks like, Dr. Calvert said. In many cases, plastic surgeons hire social media experts to cultivate their content. “I’ve hired and fired social media managers over the years, ultimately deciding I should develop my own content,” he said. “I want people to see the same doctor on social media that they will see in the office. I like an authentic presentation, not glitzy.”
 

Social media gone wrong

Dr. Calvert said that in the world of plastic surgery, some doctors use social media to present “before and after” compilations that in his opinion aren’t necessarily fully authentic, and this rubs him wrong. “There’s a bit of ‘cheating’ in some of these posts, using filters, making the ‘befores’ particularly bad, and other tricks,” he said.

Dr. Daibes has also seen his share of social media misuse: ”Red flags include oversharing personal indulgences, engaging in online spats, or making unfounded medical claims,” he said. “It’s essential to remember our role as educators and advocates, and to present ourselves in a way that upholds the dignity of our profession.”

At the end of the day, social media can have positive uses for physicians, and it is clearly here to stay. The onus for responsible use ultimately falls to the physicians using it.

Dr. Daibes emphasizes the fact that a doctor’s words carry weight – perhaps more so than those of other professionals. “The added scrutiny is good because it keeps us accountable; it’s crucial that our information is accurate,” he said. “The downside is that the scrutiny can be stifling at times and lead to self-censorship, even on nonmedical matters.”

Physicians have suggested eight guidelines for doctors to follow when using social media:

• Remember that you represent your profession, even if posting on personal accounts.
• Never post from the operating room, the emergency department, or any sort of medical space.
• If you’re employed, before you post, check with your employer to see whether they have any rules or guidance surrounding social media.
• Never use social media to badmouth colleagues, hospitals, or other healthcare organizations.
• Never use social media to dispense medical advice.
• Steer clear of the obvious hot-button issues, like religion and politics.
• Always protect patient privacy when posting.
• Be careful with how and whom you engage on social media.

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

I have written before about the COSMOS study and its finding that multivitamins (and chocolate) did not improve brain or cardiovascular health. So I was surprised to read that a “new” study found that vitamins can forestall dementia and age-related cognitive decline.

Upon closer look, the new data are neither new nor convincing, at least to me.

©Graça Victoria/iStockphoto.com

Chocolate and multivitamins for CVD and cancer prevention

The large randomized COSMOS trial was supposed to be the definitive study on chocolate that would establish its heart-health benefits without a doubt. Or, rather, the benefits of a cocoa bean extract in pill form given to healthy, older volunteers. The COSMOS study was negative. Chocolate, or the cocoa bean extract they used, did not reduce cardiovascular events.

And yet for all the prepublication importance attached to COSMOS, it is scarcely mentioned. Had it been positive, rest assured that Mars, the candy bar company that cofunded the research, and other interested parties would have been shouting it from the rooftops. As it is, they’re already spinning it.

Which brings us to the multivitamin component. COSMOS actually had a 2 × 2 design. In other words, there were four groups in this study: chocolate plus multivitamin, chocolate plus placebo, placebo plus multivitamin, and placebo plus placebo. This type of study design allows you to study two different interventions simultaneously, provided that they are independent and do not interact with each other. In addition to the primary cardiovascular endpoint, they also studied a cancer endpoint.

The multivitamin supplement didn’t reduce cardiovascular events either. Nor did it affect cancer outcomes. The main COSMOS study was negative and reinforced what countless other studies have proven: Taking a daily multivitamin does not reduce your risk of having a heart attack or developing cancer.
 

But wait, there’s more: COSMOS-Mind

But no researcher worth his salt studies just one or two endpoints in a study. The participants also underwent neurologic and memory testing. These results were reported separately in the COSMOS-Mind study.

COSMOS-Mind is often described as a separate (or “new”) study. In reality, it included the same participants from the original COSMOS trial and measured yet another primary outcome of cognitive performance on a series of tests administered by telephone. Although there is nothing inherently wrong with studying multiple outcomes in your patient population (after all, that salami isn’t going to slice itself), they cannot all be primary outcomes. Some, by necessity, must be secondary hypothesis–generating outcomes. If you test enough endpoints, multiple hypothesis testing dictates that eventually you will get a positive result simply by chance.

There was a time when the neurocognitive outcomes of COSMOS would have been reported in the same paper as the cardiovascular outcomes, but that time seems to have passed us by. Researchers live or die by the number of their publications, and there is an inherent advantage to squeezing as many publications as possible from the same dataset. Though, to be fair, the journal would probably have asked them to split up the paper as well.

In brief, the cocoa extract again fell short in COSMOS-Mind, but the multivitamin arm did better on the composite cognitive outcome. It was a fairly small difference – a 0.07-point improvement on the z-score at the 3-year mark (the z-score is the mean divided by the standard deviation). Much was also made of the fact that the improvement seemed to vary by prior history of cardiovascular disease (CVD). Those with a history of CVD had a 0.11-point improvement, whereas those without had a 0.06-point improvement. The authors couldn’t offer a definitive explanation for these findings. Any argument that multivitamins improve cardiovascular health and therefore prevent vascular dementia has to contend with the fact that the main COSMOS study didn’t show a cardiovascular benefit for vitamins. Speculation that you are treating nutritional deficiencies is exactly that: speculation.

A more salient question is: What does a 0.07-point improvement on the z-score mean clinically? This study didn’t assess whether a multivitamin supplement prevented dementia or allowed people to live independently for longer. In fairness, that would have been exceptionally difficult to do and would have required a much longer study.

Their one attempt to quantify the cognitive benefit clinically was a calculation about normal age-related decline. Test scores were 0.045 points lower for every 1-year increase in age among participants (their mean age was 73 years). So the authors contend that a 0.07-point increase, or the 0.083-point increase that they found at year 3, corresponds to 1.8 years of age-related decline forestalled. Whether this is an appropriate assumption, I leave for the reader to decide.
 

COSMOS-Web and replication

The results of COSMOS-Mind were seemingly bolstered by the recent publication of COSMOS-Web. Although I’ve seen this study described as having replicated the results of COSMOS-Mind, that description is a bit misleading. This was yet another ancillary COSMOS study; more than half of the 2,262 participants in COSMOS-Mind were also included in COSMOS-Web. Replicating results in the same people isn’t true replication.

The main difference between COSMOS-Mind and COSMOS-Web is that the former used a telephone interview to administer the cognitive tests and the latter used the Internet. They also had different endpoints, with COSMOS-Web looking at immediate recall rather than a global test composite.

COSMOS-Web was a positive study in that patients getting the multivitamin supplement did better on the test for immediate memory recall (remembering a list of 20 words), though they didn’t improve on tests of memory retention, executive function, or novel object recognition (basically a test where subjects have to identify matching geometric patterns and then recall them later). They were able to remember an additional 0.71 word on average, compared with 0.44 word in the placebo group. (For the record, it found no benefit for the cocoa extract).

Everybody does better on memory tests the second time around because practice makes perfect, hence the improvement in the placebo group. This benefit at 1 year did not survive to the end of follow-up at 3 years, in contrast to COSMOS-Mind, where the benefit was not apparent at 1 year and seen only at year 3. A history of cardiovascular disease didn’t seem to affect the results in COSMOS-Web as it did in COSMOS-Mind. As far as replications go, COSMOS-Web has some very non-negligible differences, compared with COSMOS-Mind. This incongruity, especially given the overlap in the patient populations is hard to reconcile. If COSMOS-Web was supposed to assuage any doubts that persisted after COSMOS-Mind, it hasn’t for me.
 

One of these studies is not like the others

Finally, although the COSMOS trial and all its ancillary study analyses suggest a neurocognitive benefit to multivitamin supplementation, it’s not the first study to test the matter. The Age-Related Eye Disease Study looked at vitamin C, vitamin E, beta-carotene, zinc, and copper. There was no benefit on any of the six cognitive tests administered to patients. The Women’s Health Study, the Women’s Antioxidant Cardiovascular Study and PREADViSE have all failed to show any benefit to the various vitamins and minerals they studied. A meta-analysis of 11 trials found no benefit to B vitamins in slowing cognitive aging.

The claim that COSMOS is the “first” study to test the hypothesis hinges on some careful wordplay. Prior studies tested specific vitamins, not a multivitamin. In the discussion of the paper, these other studies are critiqued for being short term. But the Physicians’ Health Study II did in fact study a multivitamin and assessed cognitive performance on average 2.5 years after randomization. It found no benefit. The authors of COSMOS-Web critiqued the 2.5-year wait to perform cognitive testing, saying it would have missed any short-term benefits. Although, given that they simultaneously praised their 3 years of follow-up, the criticism is hard to fully accept or even understand.

Whether follow-up is short or long, uses individual vitamins or a multivitamin, the results excluding COSMOS are uniformly negative. I for one am skeptical that a multivitamin or any individual vitamin can prevent dementia. Same goes for chocolate.

Do enough tests in the same population, and something will rise above the noise just by chance. When you get a positive result in your research, it’s always exciting. But when a slew of studies that came before you are negative, you aren’t groundbreaking. You’re an outlier.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

I have written before about the COSMOS study and its finding that multivitamins (and chocolate) did not improve brain or cardiovascular health. So I was surprised to read that a “new” study found that vitamins can forestall dementia and age-related cognitive decline.

Upon closer look, the new data are neither new nor convincing, at least to me.

©Graça Victoria/iStockphoto.com

Chocolate and multivitamins for CVD and cancer prevention

The large randomized COSMOS trial was supposed to be the definitive study on chocolate that would establish its heart-health benefits without a doubt. Or, rather, the benefits of a cocoa bean extract in pill form given to healthy, older volunteers. The COSMOS study was negative. Chocolate, or the cocoa bean extract they used, did not reduce cardiovascular events.

And yet for all the prepublication importance attached to COSMOS, it is scarcely mentioned. Had it been positive, rest assured that Mars, the candy bar company that cofunded the research, and other interested parties would have been shouting it from the rooftops. As it is, they’re already spinning it.

Which brings us to the multivitamin component. COSMOS actually had a 2 × 2 design. In other words, there were four groups in this study: chocolate plus multivitamin, chocolate plus placebo, placebo plus multivitamin, and placebo plus placebo. This type of study design allows you to study two different interventions simultaneously, provided that they are independent and do not interact with each other. In addition to the primary cardiovascular endpoint, they also studied a cancer endpoint.

The multivitamin supplement didn’t reduce cardiovascular events either. Nor did it affect cancer outcomes. The main COSMOS study was negative and reinforced what countless other studies have proven: Taking a daily multivitamin does not reduce your risk of having a heart attack or developing cancer.
 

But wait, there’s more: COSMOS-Mind

But no researcher worth his salt studies just one or two endpoints in a study. The participants also underwent neurologic and memory testing. These results were reported separately in the COSMOS-Mind study.

COSMOS-Mind is often described as a separate (or “new”) study. In reality, it included the same participants from the original COSMOS trial and measured yet another primary outcome of cognitive performance on a series of tests administered by telephone. Although there is nothing inherently wrong with studying multiple outcomes in your patient population (after all, that salami isn’t going to slice itself), they cannot all be primary outcomes. Some, by necessity, must be secondary hypothesis–generating outcomes. If you test enough endpoints, multiple hypothesis testing dictates that eventually you will get a positive result simply by chance.

There was a time when the neurocognitive outcomes of COSMOS would have been reported in the same paper as the cardiovascular outcomes, but that time seems to have passed us by. Researchers live or die by the number of their publications, and there is an inherent advantage to squeezing as many publications as possible from the same dataset. Though, to be fair, the journal would probably have asked them to split up the paper as well.

In brief, the cocoa extract again fell short in COSMOS-Mind, but the multivitamin arm did better on the composite cognitive outcome. It was a fairly small difference – a 0.07-point improvement on the z-score at the 3-year mark (the z-score is the mean divided by the standard deviation). Much was also made of the fact that the improvement seemed to vary by prior history of cardiovascular disease (CVD). Those with a history of CVD had a 0.11-point improvement, whereas those without had a 0.06-point improvement. The authors couldn’t offer a definitive explanation for these findings. Any argument that multivitamins improve cardiovascular health and therefore prevent vascular dementia has to contend with the fact that the main COSMOS study didn’t show a cardiovascular benefit for vitamins. Speculation that you are treating nutritional deficiencies is exactly that: speculation.

A more salient question is: What does a 0.07-point improvement on the z-score mean clinically? This study didn’t assess whether a multivitamin supplement prevented dementia or allowed people to live independently for longer. In fairness, that would have been exceptionally difficult to do and would have required a much longer study.

Their one attempt to quantify the cognitive benefit clinically was a calculation about normal age-related decline. Test scores were 0.045 points lower for every 1-year increase in age among participants (their mean age was 73 years). So the authors contend that a 0.07-point increase, or the 0.083-point increase that they found at year 3, corresponds to 1.8 years of age-related decline forestalled. Whether this is an appropriate assumption, I leave for the reader to decide.
 

COSMOS-Web and replication

The results of COSMOS-Mind were seemingly bolstered by the recent publication of COSMOS-Web. Although I’ve seen this study described as having replicated the results of COSMOS-Mind, that description is a bit misleading. This was yet another ancillary COSMOS study; more than half of the 2,262 participants in COSMOS-Mind were also included in COSMOS-Web. Replicating results in the same people isn’t true replication.

The main difference between COSMOS-Mind and COSMOS-Web is that the former used a telephone interview to administer the cognitive tests and the latter used the Internet. They also had different endpoints, with COSMOS-Web looking at immediate recall rather than a global test composite.

COSMOS-Web was a positive study in that patients getting the multivitamin supplement did better on the test for immediate memory recall (remembering a list of 20 words), though they didn’t improve on tests of memory retention, executive function, or novel object recognition (basically a test where subjects have to identify matching geometric patterns and then recall them later). They were able to remember an additional 0.71 word on average, compared with 0.44 word in the placebo group. (For the record, it found no benefit for the cocoa extract).

Everybody does better on memory tests the second time around because practice makes perfect, hence the improvement in the placebo group. This benefit at 1 year did not survive to the end of follow-up at 3 years, in contrast to COSMOS-Mind, where the benefit was not apparent at 1 year and seen only at year 3. A history of cardiovascular disease didn’t seem to affect the results in COSMOS-Web as it did in COSMOS-Mind. As far as replications go, COSMOS-Web has some very non-negligible differences, compared with COSMOS-Mind. This incongruity, especially given the overlap in the patient populations is hard to reconcile. If COSMOS-Web was supposed to assuage any doubts that persisted after COSMOS-Mind, it hasn’t for me.
 

One of these studies is not like the others

Finally, although the COSMOS trial and all its ancillary study analyses suggest a neurocognitive benefit to multivitamin supplementation, it’s not the first study to test the matter. The Age-Related Eye Disease Study looked at vitamin C, vitamin E, beta-carotene, zinc, and copper. There was no benefit on any of the six cognitive tests administered to patients. The Women’s Health Study, the Women’s Antioxidant Cardiovascular Study and PREADViSE have all failed to show any benefit to the various vitamins and minerals they studied. A meta-analysis of 11 trials found no benefit to B vitamins in slowing cognitive aging.

The claim that COSMOS is the “first” study to test the hypothesis hinges on some careful wordplay. Prior studies tested specific vitamins, not a multivitamin. In the discussion of the paper, these other studies are critiqued for being short term. But the Physicians’ Health Study II did in fact study a multivitamin and assessed cognitive performance on average 2.5 years after randomization. It found no benefit. The authors of COSMOS-Web critiqued the 2.5-year wait to perform cognitive testing, saying it would have missed any short-term benefits. Although, given that they simultaneously praised their 3 years of follow-up, the criticism is hard to fully accept or even understand.

Whether follow-up is short or long, uses individual vitamins or a multivitamin, the results excluding COSMOS are uniformly negative. I for one am skeptical that a multivitamin or any individual vitamin can prevent dementia. Same goes for chocolate.

Do enough tests in the same population, and something will rise above the noise just by chance. When you get a positive result in your research, it’s always exciting. But when a slew of studies that came before you are negative, you aren’t groundbreaking. You’re an outlier.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

I have written before about the COSMOS study and its finding that multivitamins (and chocolate) did not improve brain or cardiovascular health. So I was surprised to read that a “new” study found that vitamins can forestall dementia and age-related cognitive decline.

Upon closer look, the new data are neither new nor convincing, at least to me.

©Graça Victoria/iStockphoto.com

Chocolate and multivitamins for CVD and cancer prevention

The large randomized COSMOS trial was supposed to be the definitive study on chocolate that would establish its heart-health benefits without a doubt. Or, rather, the benefits of a cocoa bean extract in pill form given to healthy, older volunteers. The COSMOS study was negative. Chocolate, or the cocoa bean extract they used, did not reduce cardiovascular events.

And yet for all the prepublication importance attached to COSMOS, it is scarcely mentioned. Had it been positive, rest assured that Mars, the candy bar company that cofunded the research, and other interested parties would have been shouting it from the rooftops. As it is, they’re already spinning it.

Which brings us to the multivitamin component. COSMOS actually had a 2 × 2 design. In other words, there were four groups in this study: chocolate plus multivitamin, chocolate plus placebo, placebo plus multivitamin, and placebo plus placebo. This type of study design allows you to study two different interventions simultaneously, provided that they are independent and do not interact with each other. In addition to the primary cardiovascular endpoint, they also studied a cancer endpoint.

The multivitamin supplement didn’t reduce cardiovascular events either. Nor did it affect cancer outcomes. The main COSMOS study was negative and reinforced what countless other studies have proven: Taking a daily multivitamin does not reduce your risk of having a heart attack or developing cancer.
 

But wait, there’s more: COSMOS-Mind

But no researcher worth his salt studies just one or two endpoints in a study. The participants also underwent neurologic and memory testing. These results were reported separately in the COSMOS-Mind study.

COSMOS-Mind is often described as a separate (or “new”) study. In reality, it included the same participants from the original COSMOS trial and measured yet another primary outcome of cognitive performance on a series of tests administered by telephone. Although there is nothing inherently wrong with studying multiple outcomes in your patient population (after all, that salami isn’t going to slice itself), they cannot all be primary outcomes. Some, by necessity, must be secondary hypothesis–generating outcomes. If you test enough endpoints, multiple hypothesis testing dictates that eventually you will get a positive result simply by chance.

There was a time when the neurocognitive outcomes of COSMOS would have been reported in the same paper as the cardiovascular outcomes, but that time seems to have passed us by. Researchers live or die by the number of their publications, and there is an inherent advantage to squeezing as many publications as possible from the same dataset. Though, to be fair, the journal would probably have asked them to split up the paper as well.

In brief, the cocoa extract again fell short in COSMOS-Mind, but the multivitamin arm did better on the composite cognitive outcome. It was a fairly small difference – a 0.07-point improvement on the z-score at the 3-year mark (the z-score is the mean divided by the standard deviation). Much was also made of the fact that the improvement seemed to vary by prior history of cardiovascular disease (CVD). Those with a history of CVD had a 0.11-point improvement, whereas those without had a 0.06-point improvement. The authors couldn’t offer a definitive explanation for these findings. Any argument that multivitamins improve cardiovascular health and therefore prevent vascular dementia has to contend with the fact that the main COSMOS study didn’t show a cardiovascular benefit for vitamins. Speculation that you are treating nutritional deficiencies is exactly that: speculation.

A more salient question is: What does a 0.07-point improvement on the z-score mean clinically? This study didn’t assess whether a multivitamin supplement prevented dementia or allowed people to live independently for longer. In fairness, that would have been exceptionally difficult to do and would have required a much longer study.

Their one attempt to quantify the cognitive benefit clinically was a calculation about normal age-related decline. Test scores were 0.045 points lower for every 1-year increase in age among participants (their mean age was 73 years). So the authors contend that a 0.07-point increase, or the 0.083-point increase that they found at year 3, corresponds to 1.8 years of age-related decline forestalled. Whether this is an appropriate assumption, I leave for the reader to decide.
 

COSMOS-Web and replication

The results of COSMOS-Mind were seemingly bolstered by the recent publication of COSMOS-Web. Although I’ve seen this study described as having replicated the results of COSMOS-Mind, that description is a bit misleading. This was yet another ancillary COSMOS study; more than half of the 2,262 participants in COSMOS-Mind were also included in COSMOS-Web. Replicating results in the same people isn’t true replication.

The main difference between COSMOS-Mind and COSMOS-Web is that the former used a telephone interview to administer the cognitive tests and the latter used the Internet. They also had different endpoints, with COSMOS-Web looking at immediate recall rather than a global test composite.

COSMOS-Web was a positive study in that patients getting the multivitamin supplement did better on the test for immediate memory recall (remembering a list of 20 words), though they didn’t improve on tests of memory retention, executive function, or novel object recognition (basically a test where subjects have to identify matching geometric patterns and then recall them later). They were able to remember an additional 0.71 word on average, compared with 0.44 word in the placebo group. (For the record, it found no benefit for the cocoa extract).

Everybody does better on memory tests the second time around because practice makes perfect, hence the improvement in the placebo group. This benefit at 1 year did not survive to the end of follow-up at 3 years, in contrast to COSMOS-Mind, where the benefit was not apparent at 1 year and seen only at year 3. A history of cardiovascular disease didn’t seem to affect the results in COSMOS-Web as it did in COSMOS-Mind. As far as replications go, COSMOS-Web has some very non-negligible differences, compared with COSMOS-Mind. This incongruity, especially given the overlap in the patient populations is hard to reconcile. If COSMOS-Web was supposed to assuage any doubts that persisted after COSMOS-Mind, it hasn’t for me.
 

One of these studies is not like the others

Finally, although the COSMOS trial and all its ancillary study analyses suggest a neurocognitive benefit to multivitamin supplementation, it’s not the first study to test the matter. The Age-Related Eye Disease Study looked at vitamin C, vitamin E, beta-carotene, zinc, and copper. There was no benefit on any of the six cognitive tests administered to patients. The Women’s Health Study, the Women’s Antioxidant Cardiovascular Study and PREADViSE have all failed to show any benefit to the various vitamins and minerals they studied. A meta-analysis of 11 trials found no benefit to B vitamins in slowing cognitive aging.

The claim that COSMOS is the “first” study to test the hypothesis hinges on some careful wordplay. Prior studies tested specific vitamins, not a multivitamin. In the discussion of the paper, these other studies are critiqued for being short term. But the Physicians’ Health Study II did in fact study a multivitamin and assessed cognitive performance on average 2.5 years after randomization. It found no benefit. The authors of COSMOS-Web critiqued the 2.5-year wait to perform cognitive testing, saying it would have missed any short-term benefits. Although, given that they simultaneously praised their 3 years of follow-up, the criticism is hard to fully accept or even understand.

Whether follow-up is short or long, uses individual vitamins or a multivitamin, the results excluding COSMOS are uniformly negative. I for one am skeptical that a multivitamin or any individual vitamin can prevent dementia. Same goes for chocolate.

Do enough tests in the same population, and something will rise above the noise just by chance. When you get a positive result in your research, it’s always exciting. But when a slew of studies that came before you are negative, you aren’t groundbreaking. You’re an outlier.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Patients with chronic insomnia that does not improve with nonpharmacologic techniques often develop tolerance to sedative medications (benzodiazepines) prescribed for nightly use. When nonbenzodiazepine medications are used, tachyphylaxis can develop and these medications no longer initiate or maintain sleep. Strategies that alternate between these 2 types of agents are simple to follow and may allow patients to maintain sensitivity to both types of medications. In this article, I review the types, causes, evaluation, and treatment of insomnia; describe an alternating medication strategy to help patients avoid developing tolerance/tachyphylaxis; and present 3 fictional case vignettes to illustrate this approach.

A common, troubling condition

Insomnia is a common problem among psychiatric patients. Approximately 30% to 50% of adults experience occasional, short-term (<3 months) insomnia, and 5% to 10% experience chronic (≥3 months) insomnia,¹ with associated negative impacts on health and quality of life. Insomnia is sometimes primary and may have a hereditary component, but more often is associated with medical, neurologic, or psychiatric disorders.

Patterns of insomnia include difficulty falling asleep (initial or sleep-onset insomnia), remaining asleep (middle or sleep-maintenance insomnia), or falling back asleep after early awakening (late or sleep-offset insomnia). Sleep-onset insomnia correlates with high levels of anxiety and worrying, but once asleep, patients usually stay asleep. Sleep-maintenance problems involve multiple awakenings after falling asleep and taking hours to fall back to sleep. These patients experience inadequate sleep when they must wake up early for school or work. Early-awakening patients report feeling wide awake by 4 to 5 am and being unable to get back to sleep.

Caffeine is an important consideration for patients with sleep difficulties. Its use is widespread in much of the world, whether ingested as coffee, tea, in soft drinks, or in “energy” drinks that may contain as much as 200 mg of caffeine (twice the amount in a typical cup of brewed coffee). Caffeine may also be ingested as an ingredient of medications for headache or migraine. While some individuals maintain that they can fall asleep easily after drinking caffeinated coffee, many may not recognize the amount of caffeine they consume and its negative impact on sleep.² Author Michael Pollan stopped use of all caffeine and reported on the surprising positive effect on his sleep.³

Patients with mood, anxiety, or psychotic disorders are likely to experience insomnia intermittently or chronically, and insomnia predisposes some individuals to develop mood and anxiety symptoms.⁴ Patients with insomnia often experience anxiety focused on a fear of not getting adequate sleep, which creates a vicious cycle in which hyperarousal associated with fear of not sleeping complicates other causes of insomnia. A patient’s chronotype (preference for the time of day in which they carry out activities vs sleeping) also may play a role in sleep difficulties (Box⁵).

Box

Certain medications may contribute to insomnia, particularly stimulants. It is important to understand and explain to patients the time frame during which immediate-release or extended-release (ER) stimulants are active, which varies in individuals depending on liver enzyme activity. Other commonly used psychotropic medications—including bupropion, modafinil, armodafinil, atomoxetine, amphetamine salts, and methylphenidate—may interfere with sleep if used later in the day.⁶

Patients typically do not mention their use of alcohol and/or marijuana unless asked. Those who are binge drinkers or alcohol-dependent may expect alcohol to help them fall asleep, but usually find their sleep is disrupted and difficult to maintain. Patients may use marijuana to help them sleep, particularly marijuana high in tetrahydrocannabinol (THC). While it may help with sleep initiation, THC can disrupt sleep maintenance. Cannabidiol does not have intrinsic sedating effects and may even interfere with sleep.^7,8

Continue to: Women may be more likely...

Women may be more likely than men to experience insomnia.⁹ The onset of menopause can bring hot flashes that interfere with sleep.

Women with a history of mood disorders are more likely to have a history of premenstrual dysphoric disorder, postpartum depression, and unusual responses to oral contraceptives.¹⁰ These women are more likely to report problems with mood, energy, and sleep at perimenopause. Treatment with estrogen replacement may be an option for women without risk factors, such as clotting disorders, smoking history, or a personal or family history of breast or uterine cancer. For many who are not candidates for or who refuse estrogen replacement, use of a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor at low doses may help with vasomotor symptoms but not with insomnia.

Insomnia symptoms typically increase with age.¹¹ When sleep is adequate early in life but becomes a problem in midlife, an individual’s eating habits, obesity, and lack of exercise may be contributing factors. The typical American diet includes highly refined carbohydrates with excess salt; such foods are often readily available to the exclusion of healthy options. Overweight and obese patients may insist they eat a healthy diet with 3 meals per day, but a careful history often uncovers nighttime binge eating. Nighttime binge eating is rarely reported. This not only maintains obesity, but also interferes with sleep, since patients stay up late to avoid discovery by family members.¹² This lack of sleep can lead to an endless loop because insufficient sleep is a risk factor for obesity.¹³

Evaluating sleep difficulties

New patient evaluations should include a careful history beginning with childhood, including personal early childhood history and family psychiatric history. Patients often report the onset of sleep difficulty and anxiety during childhood, which should raise further questions about aspects of mood regulation from early life such as concentration, energy, motivation, appetite, and academic performance. While many children and adolescents are diagnosed with attention-deficit/hyperactivity disorder due to concentration problems that cause difficulties at school, be aware this might be part of a syndrome related to mood regulation.¹⁴ Unexpected responses to an SSRI—such as agitation, euphoria, or an immediate response with the first dose—should also raise suspicion of a mood disorder. Once the underlying mood disorder is stabilized, many patients report improved sleep.¹⁵

If a patient reports having difficulty falling and remaining asleep but is not sure if there is a pattern, keeping a sleep diary can help. Further questioning may uncover the cause. Does the patient have spontaneous jerks of lower extremities (restless leg syndrome) that interfere with falling asleep or wake them up? Have they noticed problems with dreams/nightmares that wake them, which could be associated with posttraumatic stress, anxiety, or depression? Have they been told by a partner that they act out dreams or are seemingly awake but not responsive, which could point to REM sleep behavior disorder or early Parkinson’s disease? Referral to a sleep laboratory and a neurologist can help establish the correct diagnosis and point to appropriate treatment.^16-18

Treatment options

Several cognitive-behavioral techniques, including cognitive-behavioral therapy for insomnia (CBT-I), yogic breathing, progressive relaxation, mindfulness meditation, and sleep hygiene techniques may help considerably,^19,20 but insomnia often remains difficult to treat. Pharmacotherapy is not necessarily more effective than nonpharmacologic approaches. Both options require the patient to take initiative to either find nonpharmacologic approaches or discuss the problem with a physician and agree to take medication.²¹ A trial comparing CBT-I to sedatives or the combination of CBT-I plus sedatives found higher rates of sleep with CBT-I for 3 months, after which improvement fluctuated; the combination showed sustained improvement for the entire 6-month trial.²² CBT-I has also been shown to be as effective with patients who do not have psychiatric illness as for those who are depressed, anxious, or stressed.²³ However, behavioral techniques that require regular practice may be difficult for individuals to maintain, particularly when they are depressed or anxious.

Continue to: Clinicians should understand...

Clinicians should understand the distinctions among the various types of pharmacotherapy for insomnia. Sedative-hypnotics include medications with varying half-lives and metabolic pathways. Short-acting benzodiazepines such as triazolam or alprazolam and the “z-drugs” zolpidem or zaleplon may help initiate sleep in patients with sleep-onset insomnia. Longer-acting benzodiazepines such as diazepam, clonazepam, or temazepam and the z-drug eszopiclone may also help with sleep maintenance.²³ Based on my clinical experience, individual patients may respond better to 1 type of medication over another, or even to different agents within the same class of sedative-hypnotics.

Some clinicians prescribe nonbenzodiazepine medications for sleep, such as doxepin (which is FDA-approved for treating insomnia) or off-label trazodone, mirtazapine, or quetiapine. Their antihistaminic properties confer sedating effects. Virtually all over-the-counter (OTC) medications for insomnia are antihistaminic. These OTC medications are not designed to treat insomnia, and the optimal dosage to maintain sleep without daytime sedation must be determined by trial and error. Sedating nonbenzodiazepine medications may be slowly absorbed if taken at bedtime (depending on whether they are taken with or without food) and cause daytime sedation and cognitive slowness in patients with sleep-onset and maintenance insomnia who must wake up early. Starting trazodone at 50 to 75 mg may cause slow metabolizers to wake up with considerable sedation, while fast metabolizers might never feel soundly asleep.²⁴

Patients with mood and anxiety disorders that complicate insomnia are often prescribed second-generation antipsychotics such as quetiapine, lurasidone, or olanzapine, which are sedating as well as mood-stabilizing. These approaches require careful attention to titrating doses and timing their use.

Problems with pharmacotherapy

When either benzodiazepines or nonbenzodiazepine medications are used on a long-standing, nightly basis, they often stop working well. It is not unusual that after days to weeks of taking a benzodiazepine, patients find they no longer stay asleep but can’t fall asleep if they don’t take them. Once tolerance develops, the individual experiences pharmacologic withdrawal with an inability to fall asleep or stay asleep. The medication becomes necessary but ineffective, and many patients increase their use to higher doses to fall asleep, and sometimes in early morning to maintain sleep. This leads to negative effects on cognition, coordination/balance, and mood during the day, especially in older patients.

Nonbenzodiazepine sedating medications do not lead to pharmacologic tolerance but do lead to tachyphylaxis as the CNS attempts to downregulate sedation to keep the organism safe. For some patients, this happens quickly, within a matter of days.²⁵ Others increase doses to stay asleep. For example, a patient with a starting dose of trazodone 75 mg/d might increase the dosage to 300 mg/d. While trazodone is approved in doses of 300 to 600 mg as an antidepressant, it is preferable to keep doses lower when used only for sedation.

Continue to: An alternating medication strategy

Alternating between medications from different classes can help patients avoid developing tolerance with benzodiazepines or tachyphylaxis as occurs with antihistaminic medications. It can be effective for patients with primary insomnia as well as for those whose sleep problems are associated with mood or anxiety disorders. Patients typically maintain sensitivity to any form of pharmacologic sedation for several nights without loss of effect but need to take a break to maintain the sedation effect. For example, in 1 case study, a 30-year-old female who rapidly developed tachyphylaxis to the sedative action of mirtazapine experienced a return of the medication’s sedative effects after taking a 3-day break.²⁵

To initiate an alternating strategy, the clinician must first help the patient establish a sedating dose of 2 medications from different classes, such as trazodone and zolpidem, and then instruct the patient to use each for 2 to 3 consecutive nights on an alternating basis. Patients can use calendars or pillboxes to avoid confusion about which medication to take on a given night. In many cases, this approach can work indefinitely.

The following 3 case vignettes illustrate how this alternating medication strategy can work.

CASE 1

Mr. B, age 58, is a married salesman whose territory includes 3 states. He drives from client to client from Monday through Thursday each week, staying overnight in hotels. He is comfortable talking to clients, has a close and supportive relationship with his wife, and enjoys socializing with friends. Mr. B has a high level of trait anxiety and perfectionism and is proud of his sales record throughout his career, but this leads to insomnia during his nights on the road, and often on Sunday night as he starts anticipating the week ahead. Mr. B denies having a depressed mood or cognitive problems. When on vacation with his wife he has no trouble sleeping. He has no psychiatric family history or any substantial medical problems. He simply wishes that he could sleep on work nights.

We set up an alternating medication approach. Mr. B takes trazodone 100 mg on the first night and 150 mg on the second and third nights. He then takes triazolam 0.25 mg for 2 nights; previously, he had found that zolpidem did not work as well for maintaining sleep. He can sleep adequately for the 2 weekend nights, then restarts the alternating pattern. Mr. B has done well with this regimen for >10 years.

Continue to: CASE 2

Ms. C, age 60, is widowed and has a successful career as a corporate attorney. She has been anxious since early childhood and has had trouble falling asleep for much of her life. Once she falls asleep on her sofa—often between 1 and 2 am—Ms. C can sleep soundly for 7 to 8 hours, but early morning work meetings require her to set an alarm for 6 am daily. Ms. C feels irritable and anxious on awakening but arrives at her office by 7:30 am, where she maintains a full schedule, with frequent 12-hour workdays. Ms. C did not experience significant insomnia or hot flashes with menopause at age 52 and does not use hormone replacement therapy.

Ms. C denies having depression, but experienced appropriate grief related to her husband’s illness and death from metastatic cancer 3 years ago. At the time, her internist prescribed escitalopram and zolpidem; escitalopram caused greater agitation and distress, so she stopped it after 10 days. Zolpidem 10 mg/d allowed her to sleep but she worried about taking it because her mother had long-standing sedative dependence. Ms. C lives alone, but her adult children live nearby, and she has a strong support system that includes colleagues at her firm, friends at her book club, and a support group for partners of cancer patients.

Ms. C tries trazodone, starting with 50 mg, but reports feeling agitated rather than sleepy and has cognitive fogginess in the morning. She is switched to quetiapine 50 mg, which she tolerates well and allows her to sleep soundly. To avoid developing tachyphylaxis with quetiapine, she takes eszopiclone 3 mg for 2 nights, alternating with quetiapine for 3 nights. This strategy allows her to reliably fall asleep by 11 pm, wake up at 6 am, and feel rested throughout the day.

CASE 3

Ms. D, age 55, is married with a long-standing diagnosis of generalized anxiety disorder (GAD), panic disorder, and depression so severe she is unable to work as a preschool teacher. She notes that past clinicians have prescribed a wide array of antidepressants and benzodiazepines but she remains anxious, agitated, and unable to sleep. She worries constantly about running out of benzodiazepines, which are “the only medication that helps me.” At the time of evaluation, her medications are venlafaxine ER 150 mg/d, lorazepam 1 mg 3 times daily and 2 mg at bedtime, and buspirone 15 mg 3 times daily, which she admits to not taking. She is overweight and does not exercise. She spends her days snacking and watching television. She can’t settle down enough to read and feels overwhelmed most of the time. Her adult children won’t allow her to babysit their young children because she dozes during the day.

Ms. D has a strong family history of psychiatric illness, including a father with bipolar I disorder and alcohol use disorder and a sister with schizoaffective disorder. Ms. D has never felt overtly manic, but has spent most of her life feeling depressed, anxious, and hopeless, and at times she has wished she was dead. She has had poor responses to many antidepressants, with transient euphoria followed by more anxiety.

Continue to: Rather than major depressive disorder...

Rather than major depressive disorder or GAD, Ms. D’s symptoms better meet the criteria for bipolar II disorder. She agrees to a slow taper of venlafaxine and a slow increase of divalproex, starting with 125 mg each evening. While taking venlafaxine 75 mg/d and divalproex 375 mg/d, she experiences distinct improvement in anxiety and agitation, which further improve after venlafaxine is stopped and divalproex is increased to 750 mg in the evening. She finds that she forgets daytime doses of lorazepam but depends on it to fall asleep. While taking quetiapine 50 mg and lorazepam 1 mg at bedtime, Ms. D reports sleeping soundly and feeling alert in the morning. Over several weeks, she tapers lorazepam slowly by 0.5 mg every 2 weeks. She finds she needs a higher dose of quetiapine to stay asleep, eventually requiring 400 mg each night. Ms. D says overall she feels better but is distressed because she has gained 25 lbs since starting divalproex and quetiapine.

To avoid further increases in quetiapine and maintain its sedating effect, Ms. D is switched to an alternating schedule of clonazepam 1.5 mg for 2 nights and quetiapine 300 mg for 3 nights. She agrees to begin exercising by walking in her neighborhood daily, and gradually increases this to 1 hour per day. After starting to exercise regularly, she finds she is oversedated by quetiapine at night, so she is gradually decreased to a dose of 150 mg, while still alternating with clonazepam 1.5 mg. Ms. D loses most of the weight she had gained and begins volunteering as a reading coach in the elementary school in her neighborhood.

Bottom Line

Patients with chronic insomnia can often maintain adequate sedation without developing tolerance to benzodiazepines or tachyphylaxis with nonsedating agents by using 2 sleep medications that have different mechanisms of action on an alternating schedule.

Related Resources

• Sateia MJ, Buysse DJ, Krystal AD, et al. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(2): 307-349. doi:10.5664/jcsm.6470
• Muppavarapu K, Muthukanagaraj M, Saeed SA. Cognitive-behavioral therapy for insomnia: a review of 8 studies. Current Psychiatry. 2020;19(9):40-46. doi:10.12788/cp.0040

Drug Brand Names

Alprazolam • Xanax
Armodafinil • Nuvigil
Atomoxetine • Strattera
Bupropion • Wellbutrin
Clonazepam • Klonopin
Diazepam • Valium
Divalproex • Depakote
Doxepin • Sinequan
Escitalopram • Lexapro
Eszopiclone • Lunesta
Lorazepam • Ativan
Lurasidone • Latuda
Methylphenidate • Concerta
Mirtazapine • Remeron
Modafinil • Provigil
Olanzapine • Zyprexa
Quetiapine • Seroquel
Temazepam • Restoril
Trazodone • Desyrel
Triazolam • Halcion
Venlafaxine • Effexor
Zaleplon • Sonata
Zolpidem • Ambien

Patients with chronic insomnia that does not improve with nonpharmacologic techniques often develop tolerance to sedative medications (benzodiazepines) prescribed for nightly use. When nonbenzodiazepine medications are used, tachyphylaxis can develop and these medications no longer initiate or maintain sleep. Strategies that alternate between these 2 types of agents are simple to follow and may allow patients to maintain sensitivity to both types of medications. In this article, I review the types, causes, evaluation, and treatment of insomnia; describe an alternating medication strategy to help patients avoid developing tolerance/tachyphylaxis; and present 3 fictional case vignettes to illustrate this approach.

A common, troubling condition

Insomnia is a common problem among psychiatric patients. Approximately 30% to 50% of adults experience occasional, short-term (<3 months) insomnia, and 5% to 10% experience chronic (≥3 months) insomnia,¹ with associated negative impacts on health and quality of life. Insomnia is sometimes primary and may have a hereditary component, but more often is associated with medical, neurologic, or psychiatric disorders.

Patterns of insomnia include difficulty falling asleep (initial or sleep-onset insomnia), remaining asleep (middle or sleep-maintenance insomnia), or falling back asleep after early awakening (late or sleep-offset insomnia). Sleep-onset insomnia correlates with high levels of anxiety and worrying, but once asleep, patients usually stay asleep. Sleep-maintenance problems involve multiple awakenings after falling asleep and taking hours to fall back to sleep. These patients experience inadequate sleep when they must wake up early for school or work. Early-awakening patients report feeling wide awake by 4 to 5 am and being unable to get back to sleep.

Caffeine is an important consideration for patients with sleep difficulties. Its use is widespread in much of the world, whether ingested as coffee, tea, in soft drinks, or in “energy” drinks that may contain as much as 200 mg of caffeine (twice the amount in a typical cup of brewed coffee). Caffeine may also be ingested as an ingredient of medications for headache or migraine. While some individuals maintain that they can fall asleep easily after drinking caffeinated coffee, many may not recognize the amount of caffeine they consume and its negative impact on sleep.² Author Michael Pollan stopped use of all caffeine and reported on the surprising positive effect on his sleep.³

Patients with mood, anxiety, or psychotic disorders are likely to experience insomnia intermittently or chronically, and insomnia predisposes some individuals to develop mood and anxiety symptoms.⁴ Patients with insomnia often experience anxiety focused on a fear of not getting adequate sleep, which creates a vicious cycle in which hyperarousal associated with fear of not sleeping complicates other causes of insomnia. A patient’s chronotype (preference for the time of day in which they carry out activities vs sleeping) also may play a role in sleep difficulties (Box⁵).

Box

Certain medications may contribute to insomnia, particularly stimulants. It is important to understand and explain to patients the time frame during which immediate-release or extended-release (ER) stimulants are active, which varies in individuals depending on liver enzyme activity. Other commonly used psychotropic medications—including bupropion, modafinil, armodafinil, atomoxetine, amphetamine salts, and methylphenidate—may interfere with sleep if used later in the day.⁶

Patients typically do not mention their use of alcohol and/or marijuana unless asked. Those who are binge drinkers or alcohol-dependent may expect alcohol to help them fall asleep, but usually find their sleep is disrupted and difficult to maintain. Patients may use marijuana to help them sleep, particularly marijuana high in tetrahydrocannabinol (THC). While it may help with sleep initiation, THC can disrupt sleep maintenance. Cannabidiol does not have intrinsic sedating effects and may even interfere with sleep.^7,8

Continue to: Women may be more likely...

Women may be more likely than men to experience insomnia.⁹ The onset of menopause can bring hot flashes that interfere with sleep.

Women with a history of mood disorders are more likely to have a history of premenstrual dysphoric disorder, postpartum depression, and unusual responses to oral contraceptives.¹⁰ These women are more likely to report problems with mood, energy, and sleep at perimenopause. Treatment with estrogen replacement may be an option for women without risk factors, such as clotting disorders, smoking history, or a personal or family history of breast or uterine cancer. For many who are not candidates for or who refuse estrogen replacement, use of a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor at low doses may help with vasomotor symptoms but not with insomnia.

Insomnia symptoms typically increase with age.¹¹ When sleep is adequate early in life but becomes a problem in midlife, an individual’s eating habits, obesity, and lack of exercise may be contributing factors. The typical American diet includes highly refined carbohydrates with excess salt; such foods are often readily available to the exclusion of healthy options. Overweight and obese patients may insist they eat a healthy diet with 3 meals per day, but a careful history often uncovers nighttime binge eating. Nighttime binge eating is rarely reported. This not only maintains obesity, but also interferes with sleep, since patients stay up late to avoid discovery by family members.¹² This lack of sleep can lead to an endless loop because insufficient sleep is a risk factor for obesity.¹³

Evaluating sleep difficulties

New patient evaluations should include a careful history beginning with childhood, including personal early childhood history and family psychiatric history. Patients often report the onset of sleep difficulty and anxiety during childhood, which should raise further questions about aspects of mood regulation from early life such as concentration, energy, motivation, appetite, and academic performance. While many children and adolescents are diagnosed with attention-deficit/hyperactivity disorder due to concentration problems that cause difficulties at school, be aware this might be part of a syndrome related to mood regulation.¹⁴ Unexpected responses to an SSRI—such as agitation, euphoria, or an immediate response with the first dose—should also raise suspicion of a mood disorder. Once the underlying mood disorder is stabilized, many patients report improved sleep.¹⁵

If a patient reports having difficulty falling and remaining asleep but is not sure if there is a pattern, keeping a sleep diary can help. Further questioning may uncover the cause. Does the patient have spontaneous jerks of lower extremities (restless leg syndrome) that interfere with falling asleep or wake them up? Have they noticed problems with dreams/nightmares that wake them, which could be associated with posttraumatic stress, anxiety, or depression? Have they been told by a partner that they act out dreams or are seemingly awake but not responsive, which could point to REM sleep behavior disorder or early Parkinson’s disease? Referral to a sleep laboratory and a neurologist can help establish the correct diagnosis and point to appropriate treatment.^16-18

Treatment options

Several cognitive-behavioral techniques, including cognitive-behavioral therapy for insomnia (CBT-I), yogic breathing, progressive relaxation, mindfulness meditation, and sleep hygiene techniques may help considerably,^19,20 but insomnia often remains difficult to treat. Pharmacotherapy is not necessarily more effective than nonpharmacologic approaches. Both options require the patient to take initiative to either find nonpharmacologic approaches or discuss the problem with a physician and agree to take medication.²¹ A trial comparing CBT-I to sedatives or the combination of CBT-I plus sedatives found higher rates of sleep with CBT-I for 3 months, after which improvement fluctuated; the combination showed sustained improvement for the entire 6-month trial.²² CBT-I has also been shown to be as effective with patients who do not have psychiatric illness as for those who are depressed, anxious, or stressed.²³ However, behavioral techniques that require regular practice may be difficult for individuals to maintain, particularly when they are depressed or anxious.

Continue to: Clinicians should understand...

Clinicians should understand the distinctions among the various types of pharmacotherapy for insomnia. Sedative-hypnotics include medications with varying half-lives and metabolic pathways. Short-acting benzodiazepines such as triazolam or alprazolam and the “z-drugs” zolpidem or zaleplon may help initiate sleep in patients with sleep-onset insomnia. Longer-acting benzodiazepines such as diazepam, clonazepam, or temazepam and the z-drug eszopiclone may also help with sleep maintenance.²³ Based on my clinical experience, individual patients may respond better to 1 type of medication over another, or even to different agents within the same class of sedative-hypnotics.

Some clinicians prescribe nonbenzodiazepine medications for sleep, such as doxepin (which is FDA-approved for treating insomnia) or off-label trazodone, mirtazapine, or quetiapine. Their antihistaminic properties confer sedating effects. Virtually all over-the-counter (OTC) medications for insomnia are antihistaminic. These OTC medications are not designed to treat insomnia, and the optimal dosage to maintain sleep without daytime sedation must be determined by trial and error. Sedating nonbenzodiazepine medications may be slowly absorbed if taken at bedtime (depending on whether they are taken with or without food) and cause daytime sedation and cognitive slowness in patients with sleep-onset and maintenance insomnia who must wake up early. Starting trazodone at 50 to 75 mg may cause slow metabolizers to wake up with considerable sedation, while fast metabolizers might never feel soundly asleep.²⁴

Patients with mood and anxiety disorders that complicate insomnia are often prescribed second-generation antipsychotics such as quetiapine, lurasidone, or olanzapine, which are sedating as well as mood-stabilizing. These approaches require careful attention to titrating doses and timing their use.

Problems with pharmacotherapy

When either benzodiazepines or nonbenzodiazepine medications are used on a long-standing, nightly basis, they often stop working well. It is not unusual that after days to weeks of taking a benzodiazepine, patients find they no longer stay asleep but can’t fall asleep if they don’t take them. Once tolerance develops, the individual experiences pharmacologic withdrawal with an inability to fall asleep or stay asleep. The medication becomes necessary but ineffective, and many patients increase their use to higher doses to fall asleep, and sometimes in early morning to maintain sleep. This leads to negative effects on cognition, coordination/balance, and mood during the day, especially in older patients.

Nonbenzodiazepine sedating medications do not lead to pharmacologic tolerance but do lead to tachyphylaxis as the CNS attempts to downregulate sedation to keep the organism safe. For some patients, this happens quickly, within a matter of days.²⁵ Others increase doses to stay asleep. For example, a patient with a starting dose of trazodone 75 mg/d might increase the dosage to 300 mg/d. While trazodone is approved in doses of 300 to 600 mg as an antidepressant, it is preferable to keep doses lower when used only for sedation.

Continue to: An alternating medication strategy

Alternating between medications from different classes can help patients avoid developing tolerance with benzodiazepines or tachyphylaxis as occurs with antihistaminic medications. It can be effective for patients with primary insomnia as well as for those whose sleep problems are associated with mood or anxiety disorders. Patients typically maintain sensitivity to any form of pharmacologic sedation for several nights without loss of effect but need to take a break to maintain the sedation effect. For example, in 1 case study, a 30-year-old female who rapidly developed tachyphylaxis to the sedative action of mirtazapine experienced a return of the medication’s sedative effects after taking a 3-day break.²⁵

To initiate an alternating strategy, the clinician must first help the patient establish a sedating dose of 2 medications from different classes, such as trazodone and zolpidem, and then instruct the patient to use each for 2 to 3 consecutive nights on an alternating basis. Patients can use calendars or pillboxes to avoid confusion about which medication to take on a given night. In many cases, this approach can work indefinitely.

The following 3 case vignettes illustrate how this alternating medication strategy can work.

CASE 1

Mr. B, age 58, is a married salesman whose territory includes 3 states. He drives from client to client from Monday through Thursday each week, staying overnight in hotels. He is comfortable talking to clients, has a close and supportive relationship with his wife, and enjoys socializing with friends. Mr. B has a high level of trait anxiety and perfectionism and is proud of his sales record throughout his career, but this leads to insomnia during his nights on the road, and often on Sunday night as he starts anticipating the week ahead. Mr. B denies having a depressed mood or cognitive problems. When on vacation with his wife he has no trouble sleeping. He has no psychiatric family history or any substantial medical problems. He simply wishes that he could sleep on work nights.

We set up an alternating medication approach. Mr. B takes trazodone 100 mg on the first night and 150 mg on the second and third nights. He then takes triazolam 0.25 mg for 2 nights; previously, he had found that zolpidem did not work as well for maintaining sleep. He can sleep adequately for the 2 weekend nights, then restarts the alternating pattern. Mr. B has done well with this regimen for >10 years.

Continue to: CASE 2

Ms. C, age 60, is widowed and has a successful career as a corporate attorney. She has been anxious since early childhood and has had trouble falling asleep for much of her life. Once she falls asleep on her sofa—often between 1 and 2 am—Ms. C can sleep soundly for 7 to 8 hours, but early morning work meetings require her to set an alarm for 6 am daily. Ms. C feels irritable and anxious on awakening but arrives at her office by 7:30 am, where she maintains a full schedule, with frequent 12-hour workdays. Ms. C did not experience significant insomnia or hot flashes with menopause at age 52 and does not use hormone replacement therapy.

Ms. C denies having depression, but experienced appropriate grief related to her husband’s illness and death from metastatic cancer 3 years ago. At the time, her internist prescribed escitalopram and zolpidem; escitalopram caused greater agitation and distress, so she stopped it after 10 days. Zolpidem 10 mg/d allowed her to sleep but she worried about taking it because her mother had long-standing sedative dependence. Ms. C lives alone, but her adult children live nearby, and she has a strong support system that includes colleagues at her firm, friends at her book club, and a support group for partners of cancer patients.

Ms. C tries trazodone, starting with 50 mg, but reports feeling agitated rather than sleepy and has cognitive fogginess in the morning. She is switched to quetiapine 50 mg, which she tolerates well and allows her to sleep soundly. To avoid developing tachyphylaxis with quetiapine, she takes eszopiclone 3 mg for 2 nights, alternating with quetiapine for 3 nights. This strategy allows her to reliably fall asleep by 11 pm, wake up at 6 am, and feel rested throughout the day.

CASE 3

Ms. D, age 55, is married with a long-standing diagnosis of generalized anxiety disorder (GAD), panic disorder, and depression so severe she is unable to work as a preschool teacher. She notes that past clinicians have prescribed a wide array of antidepressants and benzodiazepines but she remains anxious, agitated, and unable to sleep. She worries constantly about running out of benzodiazepines, which are “the only medication that helps me.” At the time of evaluation, her medications are venlafaxine ER 150 mg/d, lorazepam 1 mg 3 times daily and 2 mg at bedtime, and buspirone 15 mg 3 times daily, which she admits to not taking. She is overweight and does not exercise. She spends her days snacking and watching television. She can’t settle down enough to read and feels overwhelmed most of the time. Her adult children won’t allow her to babysit their young children because she dozes during the day.

Ms. D has a strong family history of psychiatric illness, including a father with bipolar I disorder and alcohol use disorder and a sister with schizoaffective disorder. Ms. D has never felt overtly manic, but has spent most of her life feeling depressed, anxious, and hopeless, and at times she has wished she was dead. She has had poor responses to many antidepressants, with transient euphoria followed by more anxiety.

Continue to: Rather than major depressive disorder...

Rather than major depressive disorder or GAD, Ms. D’s symptoms better meet the criteria for bipolar II disorder. She agrees to a slow taper of venlafaxine and a slow increase of divalproex, starting with 125 mg each evening. While taking venlafaxine 75 mg/d and divalproex 375 mg/d, she experiences distinct improvement in anxiety and agitation, which further improve after venlafaxine is stopped and divalproex is increased to 750 mg in the evening. She finds that she forgets daytime doses of lorazepam but depends on it to fall asleep. While taking quetiapine 50 mg and lorazepam 1 mg at bedtime, Ms. D reports sleeping soundly and feeling alert in the morning. Over several weeks, she tapers lorazepam slowly by 0.5 mg every 2 weeks. She finds she needs a higher dose of quetiapine to stay asleep, eventually requiring 400 mg each night. Ms. D says overall she feels better but is distressed because she has gained 25 lbs since starting divalproex and quetiapine.

To avoid further increases in quetiapine and maintain its sedating effect, Ms. D is switched to an alternating schedule of clonazepam 1.5 mg for 2 nights and quetiapine 300 mg for 3 nights. She agrees to begin exercising by walking in her neighborhood daily, and gradually increases this to 1 hour per day. After starting to exercise regularly, she finds she is oversedated by quetiapine at night, so she is gradually decreased to a dose of 150 mg, while still alternating with clonazepam 1.5 mg. Ms. D loses most of the weight she had gained and begins volunteering as a reading coach in the elementary school in her neighborhood.

Bottom Line

Patients with chronic insomnia can often maintain adequate sedation without developing tolerance to benzodiazepines or tachyphylaxis with nonsedating agents by using 2 sleep medications that have different mechanisms of action on an alternating schedule.

Related Resources

• Sateia MJ, Buysse DJ, Krystal AD, et al. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(2): 307-349. doi:10.5664/jcsm.6470
• Muppavarapu K, Muthukanagaraj M, Saeed SA. Cognitive-behavioral therapy for insomnia: a review of 8 studies. Current Psychiatry. 2020;19(9):40-46. doi:10.12788/cp.0040

Drug Brand Names

Alprazolam • Xanax
Armodafinil • Nuvigil
Atomoxetine • Strattera
Bupropion • Wellbutrin
Clonazepam • Klonopin
Diazepam • Valium
Divalproex • Depakote
Doxepin • Sinequan
Escitalopram • Lexapro
Eszopiclone • Lunesta
Lorazepam • Ativan
Lurasidone • Latuda
Methylphenidate • Concerta
Mirtazapine • Remeron
Modafinil • Provigil
Olanzapine • Zyprexa
Quetiapine • Seroquel
Temazepam • Restoril
Trazodone • Desyrel
Triazolam • Halcion
Venlafaxine • Effexor
Zaleplon • Sonata
Zolpidem • Ambien

Patients with chronic insomnia that does not improve with nonpharmacologic techniques often develop tolerance to sedative medications (benzodiazepines) prescribed for nightly use. When nonbenzodiazepine medications are used, tachyphylaxis can develop and these medications no longer initiate or maintain sleep. Strategies that alternate between these 2 types of agents are simple to follow and may allow patients to maintain sensitivity to both types of medications. In this article, I review the types, causes, evaluation, and treatment of insomnia; describe an alternating medication strategy to help patients avoid developing tolerance/tachyphylaxis; and present 3 fictional case vignettes to illustrate this approach.

A common, troubling condition

Insomnia is a common problem among psychiatric patients. Approximately 30% to 50% of adults experience occasional, short-term (<3 months) insomnia, and 5% to 10% experience chronic (≥3 months) insomnia,¹ with associated negative impacts on health and quality of life. Insomnia is sometimes primary and may have a hereditary component, but more often is associated with medical, neurologic, or psychiatric disorders.

Patterns of insomnia include difficulty falling asleep (initial or sleep-onset insomnia), remaining asleep (middle or sleep-maintenance insomnia), or falling back asleep after early awakening (late or sleep-offset insomnia). Sleep-onset insomnia correlates with high levels of anxiety and worrying, but once asleep, patients usually stay asleep. Sleep-maintenance problems involve multiple awakenings after falling asleep and taking hours to fall back to sleep. These patients experience inadequate sleep when they must wake up early for school or work. Early-awakening patients report feeling wide awake by 4 to 5 am and being unable to get back to sleep.

Caffeine is an important consideration for patients with sleep difficulties. Its use is widespread in much of the world, whether ingested as coffee, tea, in soft drinks, or in “energy” drinks that may contain as much as 200 mg of caffeine (twice the amount in a typical cup of brewed coffee). Caffeine may also be ingested as an ingredient of medications for headache or migraine. While some individuals maintain that they can fall asleep easily after drinking caffeinated coffee, many may not recognize the amount of caffeine they consume and its negative impact on sleep.² Author Michael Pollan stopped use of all caffeine and reported on the surprising positive effect on his sleep.³

Patients with mood, anxiety, or psychotic disorders are likely to experience insomnia intermittently or chronically, and insomnia predisposes some individuals to develop mood and anxiety symptoms.⁴ Patients with insomnia often experience anxiety focused on a fear of not getting adequate sleep, which creates a vicious cycle in which hyperarousal associated with fear of not sleeping complicates other causes of insomnia. A patient’s chronotype (preference for the time of day in which they carry out activities vs sleeping) also may play a role in sleep difficulties (Box⁵).

Box

Certain medications may contribute to insomnia, particularly stimulants. It is important to understand and explain to patients the time frame during which immediate-release or extended-release (ER) stimulants are active, which varies in individuals depending on liver enzyme activity. Other commonly used psychotropic medications—including bupropion, modafinil, armodafinil, atomoxetine, amphetamine salts, and methylphenidate—may interfere with sleep if used later in the day.⁶

Patients typically do not mention their use of alcohol and/or marijuana unless asked. Those who are binge drinkers or alcohol-dependent may expect alcohol to help them fall asleep, but usually find their sleep is disrupted and difficult to maintain. Patients may use marijuana to help them sleep, particularly marijuana high in tetrahydrocannabinol (THC). While it may help with sleep initiation, THC can disrupt sleep maintenance. Cannabidiol does not have intrinsic sedating effects and may even interfere with sleep.^7,8

Continue to: Women may be more likely...

Women may be more likely than men to experience insomnia.⁹ The onset of menopause can bring hot flashes that interfere with sleep.

Women with a history of mood disorders are more likely to have a history of premenstrual dysphoric disorder, postpartum depression, and unusual responses to oral contraceptives.¹⁰ These women are more likely to report problems with mood, energy, and sleep at perimenopause. Treatment with estrogen replacement may be an option for women without risk factors, such as clotting disorders, smoking history, or a personal or family history of breast or uterine cancer. For many who are not candidates for or who refuse estrogen replacement, use of a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor at low doses may help with vasomotor symptoms but not with insomnia.

Insomnia symptoms typically increase with age.¹¹ When sleep is adequate early in life but becomes a problem in midlife, an individual’s eating habits, obesity, and lack of exercise may be contributing factors. The typical American diet includes highly refined carbohydrates with excess salt; such foods are often readily available to the exclusion of healthy options. Overweight and obese patients may insist they eat a healthy diet with 3 meals per day, but a careful history often uncovers nighttime binge eating. Nighttime binge eating is rarely reported. This not only maintains obesity, but also interferes with sleep, since patients stay up late to avoid discovery by family members.¹² This lack of sleep can lead to an endless loop because insufficient sleep is a risk factor for obesity.¹³

Evaluating sleep difficulties

New patient evaluations should include a careful history beginning with childhood, including personal early childhood history and family psychiatric history. Patients often report the onset of sleep difficulty and anxiety during childhood, which should raise further questions about aspects of mood regulation from early life such as concentration, energy, motivation, appetite, and academic performance. While many children and adolescents are diagnosed with attention-deficit/hyperactivity disorder due to concentration problems that cause difficulties at school, be aware this might be part of a syndrome related to mood regulation.¹⁴ Unexpected responses to an SSRI—such as agitation, euphoria, or an immediate response with the first dose—should also raise suspicion of a mood disorder. Once the underlying mood disorder is stabilized, many patients report improved sleep.¹⁵

If a patient reports having difficulty falling and remaining asleep but is not sure if there is a pattern, keeping a sleep diary can help. Further questioning may uncover the cause. Does the patient have spontaneous jerks of lower extremities (restless leg syndrome) that interfere with falling asleep or wake them up? Have they noticed problems with dreams/nightmares that wake them, which could be associated with posttraumatic stress, anxiety, or depression? Have they been told by a partner that they act out dreams or are seemingly awake but not responsive, which could point to REM sleep behavior disorder or early Parkinson’s disease? Referral to a sleep laboratory and a neurologist can help establish the correct diagnosis and point to appropriate treatment.^16-18

Treatment options

Several cognitive-behavioral techniques, including cognitive-behavioral therapy for insomnia (CBT-I), yogic breathing, progressive relaxation, mindfulness meditation, and sleep hygiene techniques may help considerably,^19,20 but insomnia often remains difficult to treat. Pharmacotherapy is not necessarily more effective than nonpharmacologic approaches. Both options require the patient to take initiative to either find nonpharmacologic approaches or discuss the problem with a physician and agree to take medication.²¹ A trial comparing CBT-I to sedatives or the combination of CBT-I plus sedatives found higher rates of sleep with CBT-I for 3 months, after which improvement fluctuated; the combination showed sustained improvement for the entire 6-month trial.²² CBT-I has also been shown to be as effective with patients who do not have psychiatric illness as for those who are depressed, anxious, or stressed.²³ However, behavioral techniques that require regular practice may be difficult for individuals to maintain, particularly when they are depressed or anxious.

Continue to: Clinicians should understand...

Clinicians should understand the distinctions among the various types of pharmacotherapy for insomnia. Sedative-hypnotics include medications with varying half-lives and metabolic pathways. Short-acting benzodiazepines such as triazolam or alprazolam and the “z-drugs” zolpidem or zaleplon may help initiate sleep in patients with sleep-onset insomnia. Longer-acting benzodiazepines such as diazepam, clonazepam, or temazepam and the z-drug eszopiclone may also help with sleep maintenance.²³ Based on my clinical experience, individual patients may respond better to 1 type of medication over another, or even to different agents within the same class of sedative-hypnotics.

Some clinicians prescribe nonbenzodiazepine medications for sleep, such as doxepin (which is FDA-approved for treating insomnia) or off-label trazodone, mirtazapine, or quetiapine. Their antihistaminic properties confer sedating effects. Virtually all over-the-counter (OTC) medications for insomnia are antihistaminic. These OTC medications are not designed to treat insomnia, and the optimal dosage to maintain sleep without daytime sedation must be determined by trial and error. Sedating nonbenzodiazepine medications may be slowly absorbed if taken at bedtime (depending on whether they are taken with or without food) and cause daytime sedation and cognitive slowness in patients with sleep-onset and maintenance insomnia who must wake up early. Starting trazodone at 50 to 75 mg may cause slow metabolizers to wake up with considerable sedation, while fast metabolizers might never feel soundly asleep.²⁴

Patients with mood and anxiety disorders that complicate insomnia are often prescribed second-generation antipsychotics such as quetiapine, lurasidone, or olanzapine, which are sedating as well as mood-stabilizing. These approaches require careful attention to titrating doses and timing their use.

Problems with pharmacotherapy

When either benzodiazepines or nonbenzodiazepine medications are used on a long-standing, nightly basis, they often stop working well. It is not unusual that after days to weeks of taking a benzodiazepine, patients find they no longer stay asleep but can’t fall asleep if they don’t take them. Once tolerance develops, the individual experiences pharmacologic withdrawal with an inability to fall asleep or stay asleep. The medication becomes necessary but ineffective, and many patients increase their use to higher doses to fall asleep, and sometimes in early morning to maintain sleep. This leads to negative effects on cognition, coordination/balance, and mood during the day, especially in older patients.

Nonbenzodiazepine sedating medications do not lead to pharmacologic tolerance but do lead to tachyphylaxis as the CNS attempts to downregulate sedation to keep the organism safe. For some patients, this happens quickly, within a matter of days.²⁵ Others increase doses to stay asleep. For example, a patient with a starting dose of trazodone 75 mg/d might increase the dosage to 300 mg/d. While trazodone is approved in doses of 300 to 600 mg as an antidepressant, it is preferable to keep doses lower when used only for sedation.

Continue to: An alternating medication strategy

Alternating between medications from different classes can help patients avoid developing tolerance with benzodiazepines or tachyphylaxis as occurs with antihistaminic medications. It can be effective for patients with primary insomnia as well as for those whose sleep problems are associated with mood or anxiety disorders. Patients typically maintain sensitivity to any form of pharmacologic sedation for several nights without loss of effect but need to take a break to maintain the sedation effect. For example, in 1 case study, a 30-year-old female who rapidly developed tachyphylaxis to the sedative action of mirtazapine experienced a return of the medication’s sedative effects after taking a 3-day break.²⁵

To initiate an alternating strategy, the clinician must first help the patient establish a sedating dose of 2 medications from different classes, such as trazodone and zolpidem, and then instruct the patient to use each for 2 to 3 consecutive nights on an alternating basis. Patients can use calendars or pillboxes to avoid confusion about which medication to take on a given night. In many cases, this approach can work indefinitely.

The following 3 case vignettes illustrate how this alternating medication strategy can work.

CASE 1

Mr. B, age 58, is a married salesman whose territory includes 3 states. He drives from client to client from Monday through Thursday each week, staying overnight in hotels. He is comfortable talking to clients, has a close and supportive relationship with his wife, and enjoys socializing with friends. Mr. B has a high level of trait anxiety and perfectionism and is proud of his sales record throughout his career, but this leads to insomnia during his nights on the road, and often on Sunday night as he starts anticipating the week ahead. Mr. B denies having a depressed mood or cognitive problems. When on vacation with his wife he has no trouble sleeping. He has no psychiatric family history or any substantial medical problems. He simply wishes that he could sleep on work nights.

We set up an alternating medication approach. Mr. B takes trazodone 100 mg on the first night and 150 mg on the second and third nights. He then takes triazolam 0.25 mg for 2 nights; previously, he had found that zolpidem did not work as well for maintaining sleep. He can sleep adequately for the 2 weekend nights, then restarts the alternating pattern. Mr. B has done well with this regimen for >10 years.

Continue to: CASE 2

Ms. C, age 60, is widowed and has a successful career as a corporate attorney. She has been anxious since early childhood and has had trouble falling asleep for much of her life. Once she falls asleep on her sofa—often between 1 and 2 am—Ms. C can sleep soundly for 7 to 8 hours, but early morning work meetings require her to set an alarm for 6 am daily. Ms. C feels irritable and anxious on awakening but arrives at her office by 7:30 am, where she maintains a full schedule, with frequent 12-hour workdays. Ms. C did not experience significant insomnia or hot flashes with menopause at age 52 and does not use hormone replacement therapy.

Ms. C denies having depression, but experienced appropriate grief related to her husband’s illness and death from metastatic cancer 3 years ago. At the time, her internist prescribed escitalopram and zolpidem; escitalopram caused greater agitation and distress, so she stopped it after 10 days. Zolpidem 10 mg/d allowed her to sleep but she worried about taking it because her mother had long-standing sedative dependence. Ms. C lives alone, but her adult children live nearby, and she has a strong support system that includes colleagues at her firm, friends at her book club, and a support group for partners of cancer patients.

Ms. C tries trazodone, starting with 50 mg, but reports feeling agitated rather than sleepy and has cognitive fogginess in the morning. She is switched to quetiapine 50 mg, which she tolerates well and allows her to sleep soundly. To avoid developing tachyphylaxis with quetiapine, she takes eszopiclone 3 mg for 2 nights, alternating with quetiapine for 3 nights. This strategy allows her to reliably fall asleep by 11 pm, wake up at 6 am, and feel rested throughout the day.

CASE 3

Ms. D, age 55, is married with a long-standing diagnosis of generalized anxiety disorder (GAD), panic disorder, and depression so severe she is unable to work as a preschool teacher. She notes that past clinicians have prescribed a wide array of antidepressants and benzodiazepines but she remains anxious, agitated, and unable to sleep. She worries constantly about running out of benzodiazepines, which are “the only medication that helps me.” At the time of evaluation, her medications are venlafaxine ER 150 mg/d, lorazepam 1 mg 3 times daily and 2 mg at bedtime, and buspirone 15 mg 3 times daily, which she admits to not taking. She is overweight and does not exercise. She spends her days snacking and watching television. She can’t settle down enough to read and feels overwhelmed most of the time. Her adult children won’t allow her to babysit their young children because she dozes during the day.

Ms. D has a strong family history of psychiatric illness, including a father with bipolar I disorder and alcohol use disorder and a sister with schizoaffective disorder. Ms. D has never felt overtly manic, but has spent most of her life feeling depressed, anxious, and hopeless, and at times she has wished she was dead. She has had poor responses to many antidepressants, with transient euphoria followed by more anxiety.

Continue to: Rather than major depressive disorder...

Rather than major depressive disorder or GAD, Ms. D’s symptoms better meet the criteria for bipolar II disorder. She agrees to a slow taper of venlafaxine and a slow increase of divalproex, starting with 125 mg each evening. While taking venlafaxine 75 mg/d and divalproex 375 mg/d, she experiences distinct improvement in anxiety and agitation, which further improve after venlafaxine is stopped and divalproex is increased to 750 mg in the evening. She finds that she forgets daytime doses of lorazepam but depends on it to fall asleep. While taking quetiapine 50 mg and lorazepam 1 mg at bedtime, Ms. D reports sleeping soundly and feeling alert in the morning. Over several weeks, she tapers lorazepam slowly by 0.5 mg every 2 weeks. She finds she needs a higher dose of quetiapine to stay asleep, eventually requiring 400 mg each night. Ms. D says overall she feels better but is distressed because she has gained 25 lbs since starting divalproex and quetiapine.

To avoid further increases in quetiapine and maintain its sedating effect, Ms. D is switched to an alternating schedule of clonazepam 1.5 mg for 2 nights and quetiapine 300 mg for 3 nights. She agrees to begin exercising by walking in her neighborhood daily, and gradually increases this to 1 hour per day. After starting to exercise regularly, she finds she is oversedated by quetiapine at night, so she is gradually decreased to a dose of 150 mg, while still alternating with clonazepam 1.5 mg. Ms. D loses most of the weight she had gained and begins volunteering as a reading coach in the elementary school in her neighborhood.

Bottom Line

Patients with chronic insomnia can often maintain adequate sedation without developing tolerance to benzodiazepines or tachyphylaxis with nonsedating agents by using 2 sleep medications that have different mechanisms of action on an alternating schedule.

Related Resources

• Sateia MJ, Buysse DJ, Krystal AD, et al. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(2): 307-349. doi:10.5664/jcsm.6470
• Muppavarapu K, Muthukanagaraj M, Saeed SA. Cognitive-behavioral therapy for insomnia: a review of 8 studies. Current Psychiatry. 2020;19(9):40-46. doi:10.12788/cp.0040

Drug Brand Names

Alprazolam • Xanax
Armodafinil • Nuvigil
Atomoxetine • Strattera
Bupropion • Wellbutrin
Clonazepam • Klonopin
Diazepam • Valium
Divalproex • Depakote
Doxepin • Sinequan
Escitalopram • Lexapro
Eszopiclone • Lunesta
Lorazepam • Ativan
Lurasidone • Latuda
Methylphenidate • Concerta
Mirtazapine • Remeron
Modafinil • Provigil
Olanzapine • Zyprexa
Quetiapine • Seroquel
Temazepam • Restoril
Trazodone • Desyrel
Triazolam • Halcion
Venlafaxine • Effexor
Zaleplon • Sonata
Zolpidem • Ambien

Good riddance COVID-19 pandemic? Alas, that’s wishful thinking.

Many assume the pandemic is in our rearview mirror, but its biological, psychological, and social impacts continue to unfold. Its repercussions are etched into our brain, mind, emotions, behaviors, cognition, and outlook on life. Welcome to Pandemic 2.0.

Think of people who survive a heart attack. They experience multiple changes. Their initial ephemeral thrill of beating death is rapidly tempered with anxiety and worry about a future myocardial infarction and health issues in general. They become more risk-averse and more prone to dysphoria, irritability, and impatience. These individuals adopt a healthy lifestyle (diet and exercise), which they had neglected before. They develop more disciplined personality traits, feel a greater appreciation for being alive, and develop a closer affinity to family and friends. Simple things they had overlooked become more meaningful. They reevaluate their life goals, including career vs personal fulfilment. Some may overindulge in pleasurable activities in case their heart fails again. Some of those changes may be abrupt or transient, while others may become permanent features of their lives. And some may seek psychotherapy, which they may never have considered before.

The pandemic is the equivalent of a “societal cardiac arrest.” Its immediate impact was devastating. Bustling cities suddenly became ghost towns. Schools were closed, and children were locked at home with their parents, who were laid off. Businesses shut down; the economy tanked. Anxiety about being infected and dying skyrocketed, triggering a universal acute stress reaction that worsened the mental health of the population, but especially of the millions with preexisting psychiatric disorders. Routine medical and dental care stopped. Television and social media disseminated alarming updates about massive intensive care unit admissions and morgues overflowing with corpses of COVID-19 victims. Posttraumatic stress disorder (PTSD) was brewing across the nation as everyone faced this life-threatening pandemic.

The warp-speed development of vaccines for COVID-19 was equivalent to a defibrillator for the societal asystole, but the turmoil continued among the frazzled population. Some refused the vaccine due to conspiracy theories about their dangerous adverse effects. Employees in the private sector, state and federal government, and even the military who refused the mandatory vaccination lost their jobs. Controversy about shuttering schools and depriving children of face-to-face learning and socializing prompted some states to keep schools open, in contrast to most other states. Anger escalated about wearing masks, social distancing, and avoiding gatherings such as at restaurants or houses of worship. Cynicism and mistrust sprouted about the competence and reliability of health “experts” due to some conflicting signals, precluding wide adherence to medical advice.

The lingering effects of the COVID-19 pandemic

Those were the immediate repercussions of the pandemic. But what are its lingering effects? The sequelae extend across 1) the health care system; 2) the mental and emotional wellness of the population; 3) education; 4) work culture; 5) the economy; 6) societal operations; 7) technological and digital transformations; 8) mistrust in various societal institutions; 9) lack of confidence in medical information; and 10) preparedness for another pandemic due to a new strain.

As all psychiatrists know, the demand for mental health services continues to surge well after the pandemic has subsided, straining access to outpatient and inpatient care. Multiple lines of evidence confirm a deterioration in the long-term psychological well-being of children and adolescents because of lockdowns, social isolation, and anxiety about their own health and the health of their loved ones, leading to a serious rise in depression and suicidal behavior.^1-3

Contunue to: Adults who survived pandemic...

Adults who survived the pandemic experienced grief during 2 very stressful years, with no peace of mind or “normal living.” Many began to contemplate the meaning of life and reevaluate the future, waxing more philosophical and embarking on “personal archeology.” The fragility of life suddenly became a ubiquitous epiphany that changed people’s habits. Working from home, which was necessary during the pandemic, became a preferred option for many, and home became an emotional refuge, not just a physical, brick-and-mortar refuge. Millions decided to quit working altogether (the “great resignation”).

Sexual activity declined precipitously during the pandemic for singles (French kissing became “the kiss of death”) but intercourse increased among couples, eventuating in a significant rise in births after the pandemic (a baby boomlet). Sexual interest among college students declined after the pandemic, which may be either due to fear of getting infected or a sublimation of libido to invest the energy in other, less risky activities.

At the societal level, the pandemic’s sequelae included a major shift to virtual communications, not just in health care (telepsychiatry and telemedicine) but also in business. Technology saved the day during the nadir of the pandemic by enabling psychiatrists and psychotherapists to treat their patients remotely. This was not technologically feasible during the past century’s influenza pandemics (1918, 1957, and 1968).

The intellectual and social development of an entire generation of children was stunted due to the COVID-19 pandemic. Consequences will continue to emerge in the years to come and may have ripple effects on this generation’s functioning. This may have particularly affected children of lower socioeconomic status, whose families cannot afford private schools and who are in dire need of good education to put them on the path of upward mobility.

As for adults who did not get infected by COVID-19, they suffered in 2 ways. First, they experienced a certain degree of brain atrophy, which is known to occur in chronic stress. This is attributed to persistent hypercortisolemia, which is toxic to the hippocampus. PTSD is well known to be associated with hippocampal atrophy.⁴ Additionally, a significant proportion of adults who contracted the COVID-19 virus and “recovered” were subsequently diagnosed with “long COVID,” with multiple neuropsychiatric symptoms, including psychosis, mania, depression, and panic attacks, as well as memory impairment and loss of the senses of smell and taste. For these individuals, the pandemic has not subsided; they will carry its neuropsychiatric scars for a long time.

Continue to: Economically, the pandemic...

Economically, the pandemic caused a horrific economic setback in its acute phase, which prompted the government to spend trillions to support the unemployed as well as blighted businesses. The economic sequalae of deficit spending of unprecedented proportions due to the pandemic triggered painful inflation that is ongoing. Interestingly, the numerical terms “billion” and “trillion” lost their loftiness as very huge numbers. Few people realize that counting to a billion (at one number per second) would take 31.7 years, while counting to a trillion would take 31,700 years! The inflationary impact of spending $6 trillion (which would take almost 200,000 years to count) becomes mathematically jarring. And despite the heroic measures to support the economy, some business perished, although others were created, changing the human architecture of the economy.

The pandemic drastically suppressed the “hunting and gathering” instinct of humans and demolished the fabled concept of work ethic. The “great resignation,” coupled with a desire to work from home on a mass scale, led to a glut of vacant office space in many large cities, lowering the value of commercial real estate. Following the pandemic, there was an uptick in moving away from urban areas, reflecting a creative destruction and reversal of a decades-long trend to gravitate to cities to work or live.

There was also political fallout from the pandemic. Staying at home is conducive to overdosing on television and social media, leading to an intensification and ossification of political hyperpartisanship and the further displacement of religious beliefs by passionately entrenched political beliefs. This continues to have seismic effects on political stability and harmony in our country. The pandemic may have instigated new models of national voting, which triggered further political friction.

Other examples of the pandemic’s aftereffects include a shortage of lifeguards and truck drivers, replacing the traditional handshake with a first bump, and increased spending on pleasurable activities (reminiscent of the Roaring 20s following the 1918 influenza pandemic), which may reflect an instinct to “live it up” before another deadly pandemic occurs.

Ironically, as I was finishing writing this article in early September 2023, the government announced that COVID-19 cases were again rising and a new vaccine was available for the new viral “strain.”

Here we go again: as the French saying goes: plus ça change, plus c’est la même chose…

Good riddance COVID-19 pandemic? Alas, that’s wishful thinking.

Many assume the pandemic is in our rearview mirror, but its biological, psychological, and social impacts continue to unfold. Its repercussions are etched into our brain, mind, emotions, behaviors, cognition, and outlook on life. Welcome to Pandemic 2.0.

Think of people who survive a heart attack. They experience multiple changes. Their initial ephemeral thrill of beating death is rapidly tempered with anxiety and worry about a future myocardial infarction and health issues in general. They become more risk-averse and more prone to dysphoria, irritability, and impatience. These individuals adopt a healthy lifestyle (diet and exercise), which they had neglected before. They develop more disciplined personality traits, feel a greater appreciation for being alive, and develop a closer affinity to family and friends. Simple things they had overlooked become more meaningful. They reevaluate their life goals, including career vs personal fulfilment. Some may overindulge in pleasurable activities in case their heart fails again. Some of those changes may be abrupt or transient, while others may become permanent features of their lives. And some may seek psychotherapy, which they may never have considered before.

The pandemic is the equivalent of a “societal cardiac arrest.” Its immediate impact was devastating. Bustling cities suddenly became ghost towns. Schools were closed, and children were locked at home with their parents, who were laid off. Businesses shut down; the economy tanked. Anxiety about being infected and dying skyrocketed, triggering a universal acute stress reaction that worsened the mental health of the population, but especially of the millions with preexisting psychiatric disorders. Routine medical and dental care stopped. Television and social media disseminated alarming updates about massive intensive care unit admissions and morgues overflowing with corpses of COVID-19 victims. Posttraumatic stress disorder (PTSD) was brewing across the nation as everyone faced this life-threatening pandemic.

The warp-speed development of vaccines for COVID-19 was equivalent to a defibrillator for the societal asystole, but the turmoil continued among the frazzled population. Some refused the vaccine due to conspiracy theories about their dangerous adverse effects. Employees in the private sector, state and federal government, and even the military who refused the mandatory vaccination lost their jobs. Controversy about shuttering schools and depriving children of face-to-face learning and socializing prompted some states to keep schools open, in contrast to most other states. Anger escalated about wearing masks, social distancing, and avoiding gatherings such as at restaurants or houses of worship. Cynicism and mistrust sprouted about the competence and reliability of health “experts” due to some conflicting signals, precluding wide adherence to medical advice.

The lingering effects of the COVID-19 pandemic

Those were the immediate repercussions of the pandemic. But what are its lingering effects? The sequelae extend across 1) the health care system; 2) the mental and emotional wellness of the population; 3) education; 4) work culture; 5) the economy; 6) societal operations; 7) technological and digital transformations; 8) mistrust in various societal institutions; 9) lack of confidence in medical information; and 10) preparedness for another pandemic due to a new strain.

As all psychiatrists know, the demand for mental health services continues to surge well after the pandemic has subsided, straining access to outpatient and inpatient care. Multiple lines of evidence confirm a deterioration in the long-term psychological well-being of children and adolescents because of lockdowns, social isolation, and anxiety about their own health and the health of their loved ones, leading to a serious rise in depression and suicidal behavior.^1-3

Contunue to: Adults who survived pandemic...

Adults who survived the pandemic experienced grief during 2 very stressful years, with no peace of mind or “normal living.” Many began to contemplate the meaning of life and reevaluate the future, waxing more philosophical and embarking on “personal archeology.” The fragility of life suddenly became a ubiquitous epiphany that changed people’s habits. Working from home, which was necessary during the pandemic, became a preferred option for many, and home became an emotional refuge, not just a physical, brick-and-mortar refuge. Millions decided to quit working altogether (the “great resignation”).

Sexual activity declined precipitously during the pandemic for singles (French kissing became “the kiss of death”) but intercourse increased among couples, eventuating in a significant rise in births after the pandemic (a baby boomlet). Sexual interest among college students declined after the pandemic, which may be either due to fear of getting infected or a sublimation of libido to invest the energy in other, less risky activities.

At the societal level, the pandemic’s sequelae included a major shift to virtual communications, not just in health care (telepsychiatry and telemedicine) but also in business. Technology saved the day during the nadir of the pandemic by enabling psychiatrists and psychotherapists to treat their patients remotely. This was not technologically feasible during the past century’s influenza pandemics (1918, 1957, and 1968).

The intellectual and social development of an entire generation of children was stunted due to the COVID-19 pandemic. Consequences will continue to emerge in the years to come and may have ripple effects on this generation’s functioning. This may have particularly affected children of lower socioeconomic status, whose families cannot afford private schools and who are in dire need of good education to put them on the path of upward mobility.

As for adults who did not get infected by COVID-19, they suffered in 2 ways. First, they experienced a certain degree of brain atrophy, which is known to occur in chronic stress. This is attributed to persistent hypercortisolemia, which is toxic to the hippocampus. PTSD is well known to be associated with hippocampal atrophy.⁴ Additionally, a significant proportion of adults who contracted the COVID-19 virus and “recovered” were subsequently diagnosed with “long COVID,” with multiple neuropsychiatric symptoms, including psychosis, mania, depression, and panic attacks, as well as memory impairment and loss of the senses of smell and taste. For these individuals, the pandemic has not subsided; they will carry its neuropsychiatric scars for a long time.

Continue to: Economically, the pandemic...

Economically, the pandemic caused a horrific economic setback in its acute phase, which prompted the government to spend trillions to support the unemployed as well as blighted businesses. The economic sequalae of deficit spending of unprecedented proportions due to the pandemic triggered painful inflation that is ongoing. Interestingly, the numerical terms “billion” and “trillion” lost their loftiness as very huge numbers. Few people realize that counting to a billion (at one number per second) would take 31.7 years, while counting to a trillion would take 31,700 years! The inflationary impact of spending $6 trillion (which would take almost 200,000 years to count) becomes mathematically jarring. And despite the heroic measures to support the economy, some business perished, although others were created, changing the human architecture of the economy.

The pandemic drastically suppressed the “hunting and gathering” instinct of humans and demolished the fabled concept of work ethic. The “great resignation,” coupled with a desire to work from home on a mass scale, led to a glut of vacant office space in many large cities, lowering the value of commercial real estate. Following the pandemic, there was an uptick in moving away from urban areas, reflecting a creative destruction and reversal of a decades-long trend to gravitate to cities to work or live.

There was also political fallout from the pandemic. Staying at home is conducive to overdosing on television and social media, leading to an intensification and ossification of political hyperpartisanship and the further displacement of religious beliefs by passionately entrenched political beliefs. This continues to have seismic effects on political stability and harmony in our country. The pandemic may have instigated new models of national voting, which triggered further political friction.

Other examples of the pandemic’s aftereffects include a shortage of lifeguards and truck drivers, replacing the traditional handshake with a first bump, and increased spending on pleasurable activities (reminiscent of the Roaring 20s following the 1918 influenza pandemic), which may reflect an instinct to “live it up” before another deadly pandemic occurs.

Ironically, as I was finishing writing this article in early September 2023, the government announced that COVID-19 cases were again rising and a new vaccine was available for the new viral “strain.”

Here we go again: as the French saying goes: plus ça change, plus c’est la même chose…

Good riddance COVID-19 pandemic? Alas, that’s wishful thinking.

Many assume the pandemic is in our rearview mirror, but its biological, psychological, and social impacts continue to unfold. Its repercussions are etched into our brain, mind, emotions, behaviors, cognition, and outlook on life. Welcome to Pandemic 2.0.

Think of people who survive a heart attack. They experience multiple changes. Their initial ephemeral thrill of beating death is rapidly tempered with anxiety and worry about a future myocardial infarction and health issues in general. They become more risk-averse and more prone to dysphoria, irritability, and impatience. These individuals adopt a healthy lifestyle (diet and exercise), which they had neglected before. They develop more disciplined personality traits, feel a greater appreciation for being alive, and develop a closer affinity to family and friends. Simple things they had overlooked become more meaningful. They reevaluate their life goals, including career vs personal fulfilment. Some may overindulge in pleasurable activities in case their heart fails again. Some of those changes may be abrupt or transient, while others may become permanent features of their lives. And some may seek psychotherapy, which they may never have considered before.

The pandemic is the equivalent of a “societal cardiac arrest.” Its immediate impact was devastating. Bustling cities suddenly became ghost towns. Schools were closed, and children were locked at home with their parents, who were laid off. Businesses shut down; the economy tanked. Anxiety about being infected and dying skyrocketed, triggering a universal acute stress reaction that worsened the mental health of the population, but especially of the millions with preexisting psychiatric disorders. Routine medical and dental care stopped. Television and social media disseminated alarming updates about massive intensive care unit admissions and morgues overflowing with corpses of COVID-19 victims. Posttraumatic stress disorder (PTSD) was brewing across the nation as everyone faced this life-threatening pandemic.

The warp-speed development of vaccines for COVID-19 was equivalent to a defibrillator for the societal asystole, but the turmoil continued among the frazzled population. Some refused the vaccine due to conspiracy theories about their dangerous adverse effects. Employees in the private sector, state and federal government, and even the military who refused the mandatory vaccination lost their jobs. Controversy about shuttering schools and depriving children of face-to-face learning and socializing prompted some states to keep schools open, in contrast to most other states. Anger escalated about wearing masks, social distancing, and avoiding gatherings such as at restaurants or houses of worship. Cynicism and mistrust sprouted about the competence and reliability of health “experts” due to some conflicting signals, precluding wide adherence to medical advice.

The lingering effects of the COVID-19 pandemic

Those were the immediate repercussions of the pandemic. But what are its lingering effects? The sequelae extend across 1) the health care system; 2) the mental and emotional wellness of the population; 3) education; 4) work culture; 5) the economy; 6) societal operations; 7) technological and digital transformations; 8) mistrust in various societal institutions; 9) lack of confidence in medical information; and 10) preparedness for another pandemic due to a new strain.

As all psychiatrists know, the demand for mental health services continues to surge well after the pandemic has subsided, straining access to outpatient and inpatient care. Multiple lines of evidence confirm a deterioration in the long-term psychological well-being of children and adolescents because of lockdowns, social isolation, and anxiety about their own health and the health of their loved ones, leading to a serious rise in depression and suicidal behavior.^1-3

Contunue to: Adults who survived pandemic...

Adults who survived the pandemic experienced grief during 2 very stressful years, with no peace of mind or “normal living.” Many began to contemplate the meaning of life and reevaluate the future, waxing more philosophical and embarking on “personal archeology.” The fragility of life suddenly became a ubiquitous epiphany that changed people’s habits. Working from home, which was necessary during the pandemic, became a preferred option for many, and home became an emotional refuge, not just a physical, brick-and-mortar refuge. Millions decided to quit working altogether (the “great resignation”).

Sexual activity declined precipitously during the pandemic for singles (French kissing became “the kiss of death”) but intercourse increased among couples, eventuating in a significant rise in births after the pandemic (a baby boomlet). Sexual interest among college students declined after the pandemic, which may be either due to fear of getting infected or a sublimation of libido to invest the energy in other, less risky activities.

At the societal level, the pandemic’s sequelae included a major shift to virtual communications, not just in health care (telepsychiatry and telemedicine) but also in business. Technology saved the day during the nadir of the pandemic by enabling psychiatrists and psychotherapists to treat their patients remotely. This was not technologically feasible during the past century’s influenza pandemics (1918, 1957, and 1968).

The intellectual and social development of an entire generation of children was stunted due to the COVID-19 pandemic. Consequences will continue to emerge in the years to come and may have ripple effects on this generation’s functioning. This may have particularly affected children of lower socioeconomic status, whose families cannot afford private schools and who are in dire need of good education to put them on the path of upward mobility.

As for adults who did not get infected by COVID-19, they suffered in 2 ways. First, they experienced a certain degree of brain atrophy, which is known to occur in chronic stress. This is attributed to persistent hypercortisolemia, which is toxic to the hippocampus. PTSD is well known to be associated with hippocampal atrophy.⁴ Additionally, a significant proportion of adults who contracted the COVID-19 virus and “recovered” were subsequently diagnosed with “long COVID,” with multiple neuropsychiatric symptoms, including psychosis, mania, depression, and panic attacks, as well as memory impairment and loss of the senses of smell and taste. For these individuals, the pandemic has not subsided; they will carry its neuropsychiatric scars for a long time.

Continue to: Economically, the pandemic...

Economically, the pandemic caused a horrific economic setback in its acute phase, which prompted the government to spend trillions to support the unemployed as well as blighted businesses. The economic sequalae of deficit spending of unprecedented proportions due to the pandemic triggered painful inflation that is ongoing. Interestingly, the numerical terms “billion” and “trillion” lost their loftiness as very huge numbers. Few people realize that counting to a billion (at one number per second) would take 31.7 years, while counting to a trillion would take 31,700 years! The inflationary impact of spending $6 trillion (which would take almost 200,000 years to count) becomes mathematically jarring. And despite the heroic measures to support the economy, some business perished, although others were created, changing the human architecture of the economy.

The pandemic drastically suppressed the “hunting and gathering” instinct of humans and demolished the fabled concept of work ethic. The “great resignation,” coupled with a desire to work from home on a mass scale, led to a glut of vacant office space in many large cities, lowering the value of commercial real estate. Following the pandemic, there was an uptick in moving away from urban areas, reflecting a creative destruction and reversal of a decades-long trend to gravitate to cities to work or live.

There was also political fallout from the pandemic. Staying at home is conducive to overdosing on television and social media, leading to an intensification and ossification of political hyperpartisanship and the further displacement of religious beliefs by passionately entrenched political beliefs. This continues to have seismic effects on political stability and harmony in our country. The pandemic may have instigated new models of national voting, which triggered further political friction.

Other examples of the pandemic’s aftereffects include a shortage of lifeguards and truck drivers, replacing the traditional handshake with a first bump, and increased spending on pleasurable activities (reminiscent of the Roaring 20s following the 1918 influenza pandemic), which may reflect an instinct to “live it up” before another deadly pandemic occurs.

Ironically, as I was finishing writing this article in early September 2023, the government announced that COVID-19 cases were again rising and a new vaccine was available for the new viral “strain.”

Here we go again: as the French saying goes: plus ça change, plus c’est la même chose…