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LGBTQ+ teens in homophobic high schools
I am a psychiatrist now but had another life teaching English in public high school for 17 years. My teaching life, in which I was an openly gay teacher, spanned 2001-2018 and was divided between two urban California schools – in Berkeley and San Leandro. I came out by responding honestly to student questions about whether I had a girlfriend, and what I did over the weekend. At Berkeley High my openness wasn’t an issue at all. The school had a vibrant Gay Straight Alliance/GSA for years, there were many openly gay staff and many openly gay students. No students felt the need to come out to me in search of a gay mentor.
Two years later, I began teaching in San Leandro, 20 miles away, and it was a lesson in how even the San Francisco Bay Area, an LGBTQ+ bastion, could harbor homophobia. When I was hired in 2003, San Leandro High had one openly gay teacher, Q. I quickly realized how much braver his coming out was compared with mine in Berkeley.
In San Leandro, gay slurs were heard nonstop in the hallways, no students were out, and by the end of my first year Q had quit, confiding in me that he couldn’t handle the homophobic harassment from students anymore. There was no GSA. A few years ago, two lesbians had held hands during lunch and inspired the wrath of a group of parents who advocated for their expulsion. In response, a teacher tried to introduce gay sensitivity training into his class and the same group of parents tried to get him fired. He was reprimanded by the principal, he countersued in a case that went all the way to the California Supreme Court, and won. Comparing these two local high schools reinforced to me how visibility really matters in creating a childhood experience that is nurturing versus traumatizing.1
Two Chinese girls in love
N and T were two Chinese girls who grew up in San Leandro. They went to the same elementary school and had crushes on each other since then. In their junior year, they joined our first student GSA, becoming president and vice-president. They were out. And, of course, they must’ve known that their families, who would not have been supportive, would become aware. I remember sitting at an outdoor concert when I got a text from N warning me her father had found out and blamed me for having corrupted her. He planned on coming to school to demand I be fired. And such was the unrelenting pressure that N and T faced every time they went home from school and sat at their dinner tables. Eventually, they broke up. They didn’t do so tearfully, but more wearily.
This story illustrates how difficult it is for love between two LGBTQ+ teens to be nurtured. Love in youth can already be volatile because of the lack of emotional regulation and experience. The questioning of identity and the threat of family disintegration at a time when these teens do not have the economic means to protect themselves makes love dangerous. It is no wonder that gay teens are at increased risk for homelessness.2
The family incident that led to the girls’ breakup reveals how culture affects homophobic pressure. N resisted her parents’ disapproval for months, but she capitulated when her father had a heart attack and blamed it on her. “And it’s true,” N confided. “After my parents found out, they were continually stressed. I could see it affect their health. And it breaks my heart to see my dad in the hospital.”
For N, she had not capitulated from fear, but perhaps because of filial piety, or one’s obligation to protect one’s parent. It was a choice between two heartbreaks. Double minorities, like N and T, face a double threat and often can find no safe place. One of my patients who is gay and Black put it best: “It’s like being beaten up at school only to come home to another beating.” This double threat is evidenced by the higher suicide risk of ethnicities who are LGBTQ+ relative to their white counterparts.3
The confusion of a gay athlete
R was a star point guard, a senior who had secured an athletic scholarship, and was recognized as the best athlete in our county. A popular boy, he flaunted his physique and flirted with all the girls. And then when he was enrolled in my class, he began flirting with all the boys, too. There was gossip that R was bisexual. Then one day, not unexpectedly, he came out to me as gay. He admitted he only flirted with girls for his reputation.
By this time many students had come out to me but he flirted with me with his revelation. I corrected him and warned him unequivocally that it was inappropriate but I was worried because I knew he had placed his trust in me. I also knew he came from a homophobic family that was violent – his father had attacked him physically at a school game and our coaches had to pull him off.
Instinctively, I felt I had to have a witness so I confided in another teacher and documented the situation meticulously. Then, one day, just as I feared, he went too far. He stayed after class and said he wanted to show me something on his phone. And that something turned out to be a picture of himself naked. I immediately confiscated the phone and reported it to the administration. This was not how I wanted him to come out: His family notified by the police that he had sexually harassed his teacher, expulsion pending, and scholarship inevitably revoked. Fortunately, we did find a resolution that restored R’s future.
Let’s examine the circumstances that could’ve informed his transgressive behavior. If we consider sexual harassment a form of bullying, R’s history of having a father who publicly bullied him – and may have bullied others in front of him – is a known risk factor.4 It is also common knowledge that organized team sports were and still are a bastion of homophobia and that gay athletes had to accept a culture of explicit homophobia.5
So, it is not hard to understand the constant public pressures that R faced in addition to those from his family. Let’s also consider that appropriate sexual behaviors are not something we are born with, but something that is learned. Of course, inappropriate sexual behavior also happens in the heterosexual world. But heterosexual sexual behavior often has more accepted paths of trial and error. Children experiment with these behaviors and are corrected by adults and older peers as they mature.
However, for homosexual behaviors, there is not usually the fine-tuning about what is appropriate.
Summary
An educational environment where LGBTQ+ persons are highly visible and accepted is a more nurturing environment for LGBTQ teens than one that is not. Specific subcultures within the LGBTQ population involving race, culture, gender, and athletics modulate the experience of coming out and the nature of homophobic oppression.
Dr. Nguyen is a first-year psychiatry resident at the University of San Francisco School of Medicine at Fresno.
References
1. Kosciw JG et al. The effect of negative school climate on academic outcomes for LGBT youth and the role of in-school supports. J Sch Violence. 2013;12(1):45-63.
2. Center for American Progress. Gay and Transgender Youth Homelessness by the Numbers. June 21, 2010).
3. O’Donnell S et al. Increased risk of suicide attempts among Black and Latino lesbians, gay men, and bisexuals. Am J Public Health. 2011;101(6):1055-9.
4. Farrington D and Baldry A. Individual risk factors for school bullying. J Aggress Confl Peace Res. 2010 Jan;2(1):4-16.
5. Anderson E. Openly gay athletes: Contesting hegemonic masculinity in a homophobic environment Gend Soc. 2002 Dec:16(6):860-77.
I am a psychiatrist now but had another life teaching English in public high school for 17 years. My teaching life, in which I was an openly gay teacher, spanned 2001-2018 and was divided between two urban California schools – in Berkeley and San Leandro. I came out by responding honestly to student questions about whether I had a girlfriend, and what I did over the weekend. At Berkeley High my openness wasn’t an issue at all. The school had a vibrant Gay Straight Alliance/GSA for years, there were many openly gay staff and many openly gay students. No students felt the need to come out to me in search of a gay mentor.
Two years later, I began teaching in San Leandro, 20 miles away, and it was a lesson in how even the San Francisco Bay Area, an LGBTQ+ bastion, could harbor homophobia. When I was hired in 2003, San Leandro High had one openly gay teacher, Q. I quickly realized how much braver his coming out was compared with mine in Berkeley.
In San Leandro, gay slurs were heard nonstop in the hallways, no students were out, and by the end of my first year Q had quit, confiding in me that he couldn’t handle the homophobic harassment from students anymore. There was no GSA. A few years ago, two lesbians had held hands during lunch and inspired the wrath of a group of parents who advocated for their expulsion. In response, a teacher tried to introduce gay sensitivity training into his class and the same group of parents tried to get him fired. He was reprimanded by the principal, he countersued in a case that went all the way to the California Supreme Court, and won. Comparing these two local high schools reinforced to me how visibility really matters in creating a childhood experience that is nurturing versus traumatizing.1
Two Chinese girls in love
N and T were two Chinese girls who grew up in San Leandro. They went to the same elementary school and had crushes on each other since then. In their junior year, they joined our first student GSA, becoming president and vice-president. They were out. And, of course, they must’ve known that their families, who would not have been supportive, would become aware. I remember sitting at an outdoor concert when I got a text from N warning me her father had found out and blamed me for having corrupted her. He planned on coming to school to demand I be fired. And such was the unrelenting pressure that N and T faced every time they went home from school and sat at their dinner tables. Eventually, they broke up. They didn’t do so tearfully, but more wearily.
This story illustrates how difficult it is for love between two LGBTQ+ teens to be nurtured. Love in youth can already be volatile because of the lack of emotional regulation and experience. The questioning of identity and the threat of family disintegration at a time when these teens do not have the economic means to protect themselves makes love dangerous. It is no wonder that gay teens are at increased risk for homelessness.2
The family incident that led to the girls’ breakup reveals how culture affects homophobic pressure. N resisted her parents’ disapproval for months, but she capitulated when her father had a heart attack and blamed it on her. “And it’s true,” N confided. “After my parents found out, they were continually stressed. I could see it affect their health. And it breaks my heart to see my dad in the hospital.”
For N, she had not capitulated from fear, but perhaps because of filial piety, or one’s obligation to protect one’s parent. It was a choice between two heartbreaks. Double minorities, like N and T, face a double threat and often can find no safe place. One of my patients who is gay and Black put it best: “It’s like being beaten up at school only to come home to another beating.” This double threat is evidenced by the higher suicide risk of ethnicities who are LGBTQ+ relative to their white counterparts.3
The confusion of a gay athlete
R was a star point guard, a senior who had secured an athletic scholarship, and was recognized as the best athlete in our county. A popular boy, he flaunted his physique and flirted with all the girls. And then when he was enrolled in my class, he began flirting with all the boys, too. There was gossip that R was bisexual. Then one day, not unexpectedly, he came out to me as gay. He admitted he only flirted with girls for his reputation.
By this time many students had come out to me but he flirted with me with his revelation. I corrected him and warned him unequivocally that it was inappropriate but I was worried because I knew he had placed his trust in me. I also knew he came from a homophobic family that was violent – his father had attacked him physically at a school game and our coaches had to pull him off.
Instinctively, I felt I had to have a witness so I confided in another teacher and documented the situation meticulously. Then, one day, just as I feared, he went too far. He stayed after class and said he wanted to show me something on his phone. And that something turned out to be a picture of himself naked. I immediately confiscated the phone and reported it to the administration. This was not how I wanted him to come out: His family notified by the police that he had sexually harassed his teacher, expulsion pending, and scholarship inevitably revoked. Fortunately, we did find a resolution that restored R’s future.
Let’s examine the circumstances that could’ve informed his transgressive behavior. If we consider sexual harassment a form of bullying, R’s history of having a father who publicly bullied him – and may have bullied others in front of him – is a known risk factor.4 It is also common knowledge that organized team sports were and still are a bastion of homophobia and that gay athletes had to accept a culture of explicit homophobia.5
So, it is not hard to understand the constant public pressures that R faced in addition to those from his family. Let’s also consider that appropriate sexual behaviors are not something we are born with, but something that is learned. Of course, inappropriate sexual behavior also happens in the heterosexual world. But heterosexual sexual behavior often has more accepted paths of trial and error. Children experiment with these behaviors and are corrected by adults and older peers as they mature.
However, for homosexual behaviors, there is not usually the fine-tuning about what is appropriate.
Summary
An educational environment where LGBTQ+ persons are highly visible and accepted is a more nurturing environment for LGBTQ teens than one that is not. Specific subcultures within the LGBTQ population involving race, culture, gender, and athletics modulate the experience of coming out and the nature of homophobic oppression.
Dr. Nguyen is a first-year psychiatry resident at the University of San Francisco School of Medicine at Fresno.
References
1. Kosciw JG et al. The effect of negative school climate on academic outcomes for LGBT youth and the role of in-school supports. J Sch Violence. 2013;12(1):45-63.
2. Center for American Progress. Gay and Transgender Youth Homelessness by the Numbers. June 21, 2010).
3. O’Donnell S et al. Increased risk of suicide attempts among Black and Latino lesbians, gay men, and bisexuals. Am J Public Health. 2011;101(6):1055-9.
4. Farrington D and Baldry A. Individual risk factors for school bullying. J Aggress Confl Peace Res. 2010 Jan;2(1):4-16.
5. Anderson E. Openly gay athletes: Contesting hegemonic masculinity in a homophobic environment Gend Soc. 2002 Dec:16(6):860-77.
I am a psychiatrist now but had another life teaching English in public high school for 17 years. My teaching life, in which I was an openly gay teacher, spanned 2001-2018 and was divided between two urban California schools – in Berkeley and San Leandro. I came out by responding honestly to student questions about whether I had a girlfriend, and what I did over the weekend. At Berkeley High my openness wasn’t an issue at all. The school had a vibrant Gay Straight Alliance/GSA for years, there were many openly gay staff and many openly gay students. No students felt the need to come out to me in search of a gay mentor.
Two years later, I began teaching in San Leandro, 20 miles away, and it was a lesson in how even the San Francisco Bay Area, an LGBTQ+ bastion, could harbor homophobia. When I was hired in 2003, San Leandro High had one openly gay teacher, Q. I quickly realized how much braver his coming out was compared with mine in Berkeley.
In San Leandro, gay slurs were heard nonstop in the hallways, no students were out, and by the end of my first year Q had quit, confiding in me that he couldn’t handle the homophobic harassment from students anymore. There was no GSA. A few years ago, two lesbians had held hands during lunch and inspired the wrath of a group of parents who advocated for their expulsion. In response, a teacher tried to introduce gay sensitivity training into his class and the same group of parents tried to get him fired. He was reprimanded by the principal, he countersued in a case that went all the way to the California Supreme Court, and won. Comparing these two local high schools reinforced to me how visibility really matters in creating a childhood experience that is nurturing versus traumatizing.1
Two Chinese girls in love
N and T were two Chinese girls who grew up in San Leandro. They went to the same elementary school and had crushes on each other since then. In their junior year, they joined our first student GSA, becoming president and vice-president. They were out. And, of course, they must’ve known that their families, who would not have been supportive, would become aware. I remember sitting at an outdoor concert when I got a text from N warning me her father had found out and blamed me for having corrupted her. He planned on coming to school to demand I be fired. And such was the unrelenting pressure that N and T faced every time they went home from school and sat at their dinner tables. Eventually, they broke up. They didn’t do so tearfully, but more wearily.
This story illustrates how difficult it is for love between two LGBTQ+ teens to be nurtured. Love in youth can already be volatile because of the lack of emotional regulation and experience. The questioning of identity and the threat of family disintegration at a time when these teens do not have the economic means to protect themselves makes love dangerous. It is no wonder that gay teens are at increased risk for homelessness.2
The family incident that led to the girls’ breakup reveals how culture affects homophobic pressure. N resisted her parents’ disapproval for months, but she capitulated when her father had a heart attack and blamed it on her. “And it’s true,” N confided. “After my parents found out, they were continually stressed. I could see it affect their health. And it breaks my heart to see my dad in the hospital.”
For N, she had not capitulated from fear, but perhaps because of filial piety, or one’s obligation to protect one’s parent. It was a choice between two heartbreaks. Double minorities, like N and T, face a double threat and often can find no safe place. One of my patients who is gay and Black put it best: “It’s like being beaten up at school only to come home to another beating.” This double threat is evidenced by the higher suicide risk of ethnicities who are LGBTQ+ relative to their white counterparts.3
The confusion of a gay athlete
R was a star point guard, a senior who had secured an athletic scholarship, and was recognized as the best athlete in our county. A popular boy, he flaunted his physique and flirted with all the girls. And then when he was enrolled in my class, he began flirting with all the boys, too. There was gossip that R was bisexual. Then one day, not unexpectedly, he came out to me as gay. He admitted he only flirted with girls for his reputation.
By this time many students had come out to me but he flirted with me with his revelation. I corrected him and warned him unequivocally that it was inappropriate but I was worried because I knew he had placed his trust in me. I also knew he came from a homophobic family that was violent – his father had attacked him physically at a school game and our coaches had to pull him off.
Instinctively, I felt I had to have a witness so I confided in another teacher and documented the situation meticulously. Then, one day, just as I feared, he went too far. He stayed after class and said he wanted to show me something on his phone. And that something turned out to be a picture of himself naked. I immediately confiscated the phone and reported it to the administration. This was not how I wanted him to come out: His family notified by the police that he had sexually harassed his teacher, expulsion pending, and scholarship inevitably revoked. Fortunately, we did find a resolution that restored R’s future.
Let’s examine the circumstances that could’ve informed his transgressive behavior. If we consider sexual harassment a form of bullying, R’s history of having a father who publicly bullied him – and may have bullied others in front of him – is a known risk factor.4 It is also common knowledge that organized team sports were and still are a bastion of homophobia and that gay athletes had to accept a culture of explicit homophobia.5
So, it is not hard to understand the constant public pressures that R faced in addition to those from his family. Let’s also consider that appropriate sexual behaviors are not something we are born with, but something that is learned. Of course, inappropriate sexual behavior also happens in the heterosexual world. But heterosexual sexual behavior often has more accepted paths of trial and error. Children experiment with these behaviors and are corrected by adults and older peers as they mature.
However, for homosexual behaviors, there is not usually the fine-tuning about what is appropriate.
Summary
An educational environment where LGBTQ+ persons are highly visible and accepted is a more nurturing environment for LGBTQ teens than one that is not. Specific subcultures within the LGBTQ population involving race, culture, gender, and athletics modulate the experience of coming out and the nature of homophobic oppression.
Dr. Nguyen is a first-year psychiatry resident at the University of San Francisco School of Medicine at Fresno.
References
1. Kosciw JG et al. The effect of negative school climate on academic outcomes for LGBT youth and the role of in-school supports. J Sch Violence. 2013;12(1):45-63.
2. Center for American Progress. Gay and Transgender Youth Homelessness by the Numbers. June 21, 2010).
3. O’Donnell S et al. Increased risk of suicide attempts among Black and Latino lesbians, gay men, and bisexuals. Am J Public Health. 2011;101(6):1055-9.
4. Farrington D and Baldry A. Individual risk factors for school bullying. J Aggress Confl Peace Res. 2010 Jan;2(1):4-16.
5. Anderson E. Openly gay athletes: Contesting hegemonic masculinity in a homophobic environment Gend Soc. 2002 Dec:16(6):860-77.
Cultivating strength: Psychological well-being after nonfatal suicide attempts
A study of three separate nationally representative samples of nearly 9,000 U.S. military veterans found psychological well-being – defined in terms of having a high sense of purpose, social connectedness, and happiness – to be significantly diminished among veteran suicide attempt survivors relative to nonattempters, even decades after their last attempt.1
Despite the trend toward diminished well-being, many veterans who survived a suicide attempt reported average to optimal levels of well-being. Specifically, 52%-60% of veterans reporting a prior suicide attempt also reported experiencing as much purpose, social connection, and happiness as veterans without a suicide attempt history. Remarkably, a small subset (2-7%) of veteran attempt survivors even reported higher levels of well-being than veterans without a suicide attempt history.
Thus,
These data are notable because, in 2021, approximately 1.4 million U.S. adults made a nonfatal suicide attempt. Historically, suicide research has understandably emphasized the study of risk factors that increase the likelihood that someone dies by suicide. Given that a prior suicide attempt is among the top risk factors for suicide, virtually all research on suicide attempt survivors has focused on their elevated risk for future suicidality. Yet, 9 out of 10 people who have made a nonfatal suicide attempt do not go on to die by suicide. It is thus critical to investigate the quality of life of the millions of suicide attempt survivors.
To date, we know little about a question keenly important to suicide attempt survivors and their loved ones: What is the possibility of rebuilding a meaningful, high-quality life after a suicide attempt?
In addition to reporting on the prevalence of high levels of psychological well-being after a nonfatal suicide attempt, it is pivotal to investigate factors that may help facilitate this outcome. To that end, we identified personal characteristics associated with high levels of well-being. Notably, it was malleable psychological strengths such as optimism and a curious mindset, more than the mere absence of symptoms, that were linked to higher levels of well-being among veteran suicide attempt survivors.
Current suicide prevention interventions and treatments, which often focus on mitigating immediate suicide risk by treating symptoms, may be overlooking the importance of cultivating and building psychological strengths that may help promote greater well-being and enriched lives. Moreover, treatments that emphasize such strengths might be particularly fruitful in mitigating suicide risk in veterans, as veterans may be more receptive to prevention and treatment initiatives that embrace the cultivation and bolstering of strengths that are inherent in military culture and values, such as resilience and perseverance in the face of life challenges.2
One notable caveat to this study is that the data were cross-sectional, meaning they were collected at a single time point. As such, the authors cannot conclude that factors such as curiosity necessarily caused higher levels of well-being in veterans, as opposed to well-being causing higher levels of curiosity.
Similarly, while one can infer that psychological well-being was near-absent at the time of a suicide attempt, well-being of attempt survivors was not assessed before their attempt. Longitudinal studies that follow attempt survivors over time are needed to understand how well-being changes over time for suicide attempt survivors and the causal chain in what predicts that change.
Nevertheless, the results of this large, multicohort study serve as an important first step toward a more comprehensive view of prognosis after a suicide attempt. Just as the process that leads to a suicide attempt is complex, so too is the process of recovery after an attempt. While this study provides sound estimates of well-being outcomes and some possible candidates that might facilitate these outcomes, a critical next step for future research is to replicate and extend these findings. To do so, it is pivotal to extend the assessment scope beyond symptom-based measures and include measures of well-being.
Additionally, the investment in resources into longer-term examinations following suicide attempts is essential to understand different pathways toward achieving greater well-being. Providing hope is vital and potentially lifesaving, as one of the most common experiences reported before a suicide attempt is an unremitting sense of hopelessness. Continued research on well-being has the potential to impart a more balanced, nuanced prognosis after a suicide attempt that challenges perceptions of an invariably bleak prospect of recovery after suicidality.
Collectively, these results highlight the importance of broadening the scope of how the mental health field views and treats psychiatric difficulties to include a greater focus on recovery-based outcomes and personal strengths that help facilitate recovery from adverse life experiences such as suicide attempts.
People desire lives that they enjoy and find meaningful, and having a history of suicide attempts does not preclude the prospect of such a life. It is time that suicide research reflects the vast landscape of potential outcomes after a suicide attempt that goes beyond the prediction of future suicide risk.
Mr. Brown is a doctoral student of clinical psychology at the University of South Florida, Tampa. Dr. Rottenberg is director of the Mood and Emotion Lab and area director of the department of clinical psychology, University of South Florida.
References
1. Brown BA et al. Psychological well-being in US veterans with non-fatal suicide attempts: A multi-cohort population-based study. J Affect Disord. 2022 Oct 1;314:34-43. doi: 10.1016/j.jad.2022.07.003.
2. Bryan CJ et al. Understanding and preventing military suicide. Arch Suicide Res. 2012;16(2):95-110. doi: 10.1080/13811118.2012.667321.
A study of three separate nationally representative samples of nearly 9,000 U.S. military veterans found psychological well-being – defined in terms of having a high sense of purpose, social connectedness, and happiness – to be significantly diminished among veteran suicide attempt survivors relative to nonattempters, even decades after their last attempt.1
Despite the trend toward diminished well-being, many veterans who survived a suicide attempt reported average to optimal levels of well-being. Specifically, 52%-60% of veterans reporting a prior suicide attempt also reported experiencing as much purpose, social connection, and happiness as veterans without a suicide attempt history. Remarkably, a small subset (2-7%) of veteran attempt survivors even reported higher levels of well-being than veterans without a suicide attempt history.
Thus,
These data are notable because, in 2021, approximately 1.4 million U.S. adults made a nonfatal suicide attempt. Historically, suicide research has understandably emphasized the study of risk factors that increase the likelihood that someone dies by suicide. Given that a prior suicide attempt is among the top risk factors for suicide, virtually all research on suicide attempt survivors has focused on their elevated risk for future suicidality. Yet, 9 out of 10 people who have made a nonfatal suicide attempt do not go on to die by suicide. It is thus critical to investigate the quality of life of the millions of suicide attempt survivors.
To date, we know little about a question keenly important to suicide attempt survivors and their loved ones: What is the possibility of rebuilding a meaningful, high-quality life after a suicide attempt?
In addition to reporting on the prevalence of high levels of psychological well-being after a nonfatal suicide attempt, it is pivotal to investigate factors that may help facilitate this outcome. To that end, we identified personal characteristics associated with high levels of well-being. Notably, it was malleable psychological strengths such as optimism and a curious mindset, more than the mere absence of symptoms, that were linked to higher levels of well-being among veteran suicide attempt survivors.
Current suicide prevention interventions and treatments, which often focus on mitigating immediate suicide risk by treating symptoms, may be overlooking the importance of cultivating and building psychological strengths that may help promote greater well-being and enriched lives. Moreover, treatments that emphasize such strengths might be particularly fruitful in mitigating suicide risk in veterans, as veterans may be more receptive to prevention and treatment initiatives that embrace the cultivation and bolstering of strengths that are inherent in military culture and values, such as resilience and perseverance in the face of life challenges.2
One notable caveat to this study is that the data were cross-sectional, meaning they were collected at a single time point. As such, the authors cannot conclude that factors such as curiosity necessarily caused higher levels of well-being in veterans, as opposed to well-being causing higher levels of curiosity.
Similarly, while one can infer that psychological well-being was near-absent at the time of a suicide attempt, well-being of attempt survivors was not assessed before their attempt. Longitudinal studies that follow attempt survivors over time are needed to understand how well-being changes over time for suicide attempt survivors and the causal chain in what predicts that change.
Nevertheless, the results of this large, multicohort study serve as an important first step toward a more comprehensive view of prognosis after a suicide attempt. Just as the process that leads to a suicide attempt is complex, so too is the process of recovery after an attempt. While this study provides sound estimates of well-being outcomes and some possible candidates that might facilitate these outcomes, a critical next step for future research is to replicate and extend these findings. To do so, it is pivotal to extend the assessment scope beyond symptom-based measures and include measures of well-being.
Additionally, the investment in resources into longer-term examinations following suicide attempts is essential to understand different pathways toward achieving greater well-being. Providing hope is vital and potentially lifesaving, as one of the most common experiences reported before a suicide attempt is an unremitting sense of hopelessness. Continued research on well-being has the potential to impart a more balanced, nuanced prognosis after a suicide attempt that challenges perceptions of an invariably bleak prospect of recovery after suicidality.
Collectively, these results highlight the importance of broadening the scope of how the mental health field views and treats psychiatric difficulties to include a greater focus on recovery-based outcomes and personal strengths that help facilitate recovery from adverse life experiences such as suicide attempts.
People desire lives that they enjoy and find meaningful, and having a history of suicide attempts does not preclude the prospect of such a life. It is time that suicide research reflects the vast landscape of potential outcomes after a suicide attempt that goes beyond the prediction of future suicide risk.
Mr. Brown is a doctoral student of clinical psychology at the University of South Florida, Tampa. Dr. Rottenberg is director of the Mood and Emotion Lab and area director of the department of clinical psychology, University of South Florida.
References
1. Brown BA et al. Psychological well-being in US veterans with non-fatal suicide attempts: A multi-cohort population-based study. J Affect Disord. 2022 Oct 1;314:34-43. doi: 10.1016/j.jad.2022.07.003.
2. Bryan CJ et al. Understanding and preventing military suicide. Arch Suicide Res. 2012;16(2):95-110. doi: 10.1080/13811118.2012.667321.
A study of three separate nationally representative samples of nearly 9,000 U.S. military veterans found psychological well-being – defined in terms of having a high sense of purpose, social connectedness, and happiness – to be significantly diminished among veteran suicide attempt survivors relative to nonattempters, even decades after their last attempt.1
Despite the trend toward diminished well-being, many veterans who survived a suicide attempt reported average to optimal levels of well-being. Specifically, 52%-60% of veterans reporting a prior suicide attempt also reported experiencing as much purpose, social connection, and happiness as veterans without a suicide attempt history. Remarkably, a small subset (2-7%) of veteran attempt survivors even reported higher levels of well-being than veterans without a suicide attempt history.
Thus,
These data are notable because, in 2021, approximately 1.4 million U.S. adults made a nonfatal suicide attempt. Historically, suicide research has understandably emphasized the study of risk factors that increase the likelihood that someone dies by suicide. Given that a prior suicide attempt is among the top risk factors for suicide, virtually all research on suicide attempt survivors has focused on their elevated risk for future suicidality. Yet, 9 out of 10 people who have made a nonfatal suicide attempt do not go on to die by suicide. It is thus critical to investigate the quality of life of the millions of suicide attempt survivors.
To date, we know little about a question keenly important to suicide attempt survivors and their loved ones: What is the possibility of rebuilding a meaningful, high-quality life after a suicide attempt?
In addition to reporting on the prevalence of high levels of psychological well-being after a nonfatal suicide attempt, it is pivotal to investigate factors that may help facilitate this outcome. To that end, we identified personal characteristics associated with high levels of well-being. Notably, it was malleable psychological strengths such as optimism and a curious mindset, more than the mere absence of symptoms, that were linked to higher levels of well-being among veteran suicide attempt survivors.
Current suicide prevention interventions and treatments, which often focus on mitigating immediate suicide risk by treating symptoms, may be overlooking the importance of cultivating and building psychological strengths that may help promote greater well-being and enriched lives. Moreover, treatments that emphasize such strengths might be particularly fruitful in mitigating suicide risk in veterans, as veterans may be more receptive to prevention and treatment initiatives that embrace the cultivation and bolstering of strengths that are inherent in military culture and values, such as resilience and perseverance in the face of life challenges.2
One notable caveat to this study is that the data were cross-sectional, meaning they were collected at a single time point. As such, the authors cannot conclude that factors such as curiosity necessarily caused higher levels of well-being in veterans, as opposed to well-being causing higher levels of curiosity.
Similarly, while one can infer that psychological well-being was near-absent at the time of a suicide attempt, well-being of attempt survivors was not assessed before their attempt. Longitudinal studies that follow attempt survivors over time are needed to understand how well-being changes over time for suicide attempt survivors and the causal chain in what predicts that change.
Nevertheless, the results of this large, multicohort study serve as an important first step toward a more comprehensive view of prognosis after a suicide attempt. Just as the process that leads to a suicide attempt is complex, so too is the process of recovery after an attempt. While this study provides sound estimates of well-being outcomes and some possible candidates that might facilitate these outcomes, a critical next step for future research is to replicate and extend these findings. To do so, it is pivotal to extend the assessment scope beyond symptom-based measures and include measures of well-being.
Additionally, the investment in resources into longer-term examinations following suicide attempts is essential to understand different pathways toward achieving greater well-being. Providing hope is vital and potentially lifesaving, as one of the most common experiences reported before a suicide attempt is an unremitting sense of hopelessness. Continued research on well-being has the potential to impart a more balanced, nuanced prognosis after a suicide attempt that challenges perceptions of an invariably bleak prospect of recovery after suicidality.
Collectively, these results highlight the importance of broadening the scope of how the mental health field views and treats psychiatric difficulties to include a greater focus on recovery-based outcomes and personal strengths that help facilitate recovery from adverse life experiences such as suicide attempts.
People desire lives that they enjoy and find meaningful, and having a history of suicide attempts does not preclude the prospect of such a life. It is time that suicide research reflects the vast landscape of potential outcomes after a suicide attempt that goes beyond the prediction of future suicide risk.
Mr. Brown is a doctoral student of clinical psychology at the University of South Florida, Tampa. Dr. Rottenberg is director of the Mood and Emotion Lab and area director of the department of clinical psychology, University of South Florida.
References
1. Brown BA et al. Psychological well-being in US veterans with non-fatal suicide attempts: A multi-cohort population-based study. J Affect Disord. 2022 Oct 1;314:34-43. doi: 10.1016/j.jad.2022.07.003.
2. Bryan CJ et al. Understanding and preventing military suicide. Arch Suicide Res. 2012;16(2):95-110. doi: 10.1080/13811118.2012.667321.
Notes on direct admission of pediatric patients
Scenario: Yesterday you saw a 6-month-old infant with what appeared to be viral gastroenteritis and mild dehydration. When you called his parents today to check on his condition he was not improving despite your recommendations about his diet and oral rehydration. Should you have him brought to your office for a reevaluation, have his parents take him to the local emergency department for evaluation and probable hospital admission, or ask his parents to take him to the hospital telling them that you will call and arrange for a direct admission.
Obviously, I haven’t given you enough background information to allow you to give me an answer you are comfortable with. What time of day is it? Is it a holiday weekend? What’s the weather like? How far is it from the patient’s home to your office? To the emergency department? How is the local ED staffed? Are there hospitalists? What is their training?
Whether or not you choose to see the patient first in the office, is direct admission to the hospital an option that you are likely to choose? What steps do you take to see that it happens smoothly?
At least one-quarter of the unscheduled pediatric hospitalizations begin with a direct admission, meaning that the patients are not first evaluated in that hospital’s ED. In a recent policy statement, the American Academy of Pediatrics Committee on Hospital Care explored the pluses and minuses of direct admission and issued a list of seven recommendations. Among the concerns raised by the authors are “potential delays in initial evaluation and treatment, inconsistent admission processes, and difficulties in determining the appropriateness of patients for direct admission.” The committee makes it clear that they understand each community has it own strengths and challenges and the unique needs of each patient make it difficult to define a set of recommendations that fits all.
However, as I read through the committee’s seven recommendations, one leapt off the screen as a unifying concept that should apply in every situation. Recommendation No. 2 reads, “[There should be] clear systems of communication between members of the health care team and with families of children requiring admission.”
First, who is on this “health care team”? Are you a team member with the hospital folks – the ED nurses and doctors, the hospitalists, the floor nurses? Do you share an employer? Are you in the same town? Have your ever met them face to face? Do you do so regularly?
I assume you call the ED or the pediatric floor to arrange a direct admit? Maybe you don’t. I can recall working in situations where several infamous “local docs” would just send the patients in with a scribbled note (or not) and no phone call. Will you be speaking to folks who are even vaguely familiar with you or even your name? Do you get to speak with people who will be hands on with the patient?
Obviously, where I’m going with this is that, if you and the hospital staff are truly on the same health care team, communication should flow freely among the members and having some familiarity allows this to happen more smoothly. It can start on our end as the referring physician by making the call personally. Likewise, the receiving hospital must make frontline people available so you can speak with staff who will be working with the patient. Do you have enough information to tell the family what to expect?
Of course legible and complete records are a must. But nothing beats personal contact and a name. If you can tell a parent “I spoke to Martha, the nurse who will meet you on the floor,” that can be a giant first step forward in the healing process.
Most of us trained at hospitals that accepted direct admit patients and can remember the challenges. And most of us recall EDs that weren’t pediatric friendly. Whether our local situation favors direct admission or ED preadmission evaluation, it is our job to make the communication flow with the patient’s safety and the family’s comfort in mind.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Scenario: Yesterday you saw a 6-month-old infant with what appeared to be viral gastroenteritis and mild dehydration. When you called his parents today to check on his condition he was not improving despite your recommendations about his diet and oral rehydration. Should you have him brought to your office for a reevaluation, have his parents take him to the local emergency department for evaluation and probable hospital admission, or ask his parents to take him to the hospital telling them that you will call and arrange for a direct admission.
Obviously, I haven’t given you enough background information to allow you to give me an answer you are comfortable with. What time of day is it? Is it a holiday weekend? What’s the weather like? How far is it from the patient’s home to your office? To the emergency department? How is the local ED staffed? Are there hospitalists? What is their training?
Whether or not you choose to see the patient first in the office, is direct admission to the hospital an option that you are likely to choose? What steps do you take to see that it happens smoothly?
At least one-quarter of the unscheduled pediatric hospitalizations begin with a direct admission, meaning that the patients are not first evaluated in that hospital’s ED. In a recent policy statement, the American Academy of Pediatrics Committee on Hospital Care explored the pluses and minuses of direct admission and issued a list of seven recommendations. Among the concerns raised by the authors are “potential delays in initial evaluation and treatment, inconsistent admission processes, and difficulties in determining the appropriateness of patients for direct admission.” The committee makes it clear that they understand each community has it own strengths and challenges and the unique needs of each patient make it difficult to define a set of recommendations that fits all.
However, as I read through the committee’s seven recommendations, one leapt off the screen as a unifying concept that should apply in every situation. Recommendation No. 2 reads, “[There should be] clear systems of communication between members of the health care team and with families of children requiring admission.”
First, who is on this “health care team”? Are you a team member with the hospital folks – the ED nurses and doctors, the hospitalists, the floor nurses? Do you share an employer? Are you in the same town? Have your ever met them face to face? Do you do so regularly?
I assume you call the ED or the pediatric floor to arrange a direct admit? Maybe you don’t. I can recall working in situations where several infamous “local docs” would just send the patients in with a scribbled note (or not) and no phone call. Will you be speaking to folks who are even vaguely familiar with you or even your name? Do you get to speak with people who will be hands on with the patient?
Obviously, where I’m going with this is that, if you and the hospital staff are truly on the same health care team, communication should flow freely among the members and having some familiarity allows this to happen more smoothly. It can start on our end as the referring physician by making the call personally. Likewise, the receiving hospital must make frontline people available so you can speak with staff who will be working with the patient. Do you have enough information to tell the family what to expect?
Of course legible and complete records are a must. But nothing beats personal contact and a name. If you can tell a parent “I spoke to Martha, the nurse who will meet you on the floor,” that can be a giant first step forward in the healing process.
Most of us trained at hospitals that accepted direct admit patients and can remember the challenges. And most of us recall EDs that weren’t pediatric friendly. Whether our local situation favors direct admission or ED preadmission evaluation, it is our job to make the communication flow with the patient’s safety and the family’s comfort in mind.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Scenario: Yesterday you saw a 6-month-old infant with what appeared to be viral gastroenteritis and mild dehydration. When you called his parents today to check on his condition he was not improving despite your recommendations about his diet and oral rehydration. Should you have him brought to your office for a reevaluation, have his parents take him to the local emergency department for evaluation and probable hospital admission, or ask his parents to take him to the hospital telling them that you will call and arrange for a direct admission.
Obviously, I haven’t given you enough background information to allow you to give me an answer you are comfortable with. What time of day is it? Is it a holiday weekend? What’s the weather like? How far is it from the patient’s home to your office? To the emergency department? How is the local ED staffed? Are there hospitalists? What is their training?
Whether or not you choose to see the patient first in the office, is direct admission to the hospital an option that you are likely to choose? What steps do you take to see that it happens smoothly?
At least one-quarter of the unscheduled pediatric hospitalizations begin with a direct admission, meaning that the patients are not first evaluated in that hospital’s ED. In a recent policy statement, the American Academy of Pediatrics Committee on Hospital Care explored the pluses and minuses of direct admission and issued a list of seven recommendations. Among the concerns raised by the authors are “potential delays in initial evaluation and treatment, inconsistent admission processes, and difficulties in determining the appropriateness of patients for direct admission.” The committee makes it clear that they understand each community has it own strengths and challenges and the unique needs of each patient make it difficult to define a set of recommendations that fits all.
However, as I read through the committee’s seven recommendations, one leapt off the screen as a unifying concept that should apply in every situation. Recommendation No. 2 reads, “[There should be] clear systems of communication between members of the health care team and with families of children requiring admission.”
First, who is on this “health care team”? Are you a team member with the hospital folks – the ED nurses and doctors, the hospitalists, the floor nurses? Do you share an employer? Are you in the same town? Have your ever met them face to face? Do you do so regularly?
I assume you call the ED or the pediatric floor to arrange a direct admit? Maybe you don’t. I can recall working in situations where several infamous “local docs” would just send the patients in with a scribbled note (or not) and no phone call. Will you be speaking to folks who are even vaguely familiar with you or even your name? Do you get to speak with people who will be hands on with the patient?
Obviously, where I’m going with this is that, if you and the hospital staff are truly on the same health care team, communication should flow freely among the members and having some familiarity allows this to happen more smoothly. It can start on our end as the referring physician by making the call personally. Likewise, the receiving hospital must make frontline people available so you can speak with staff who will be working with the patient. Do you have enough information to tell the family what to expect?
Of course legible and complete records are a must. But nothing beats personal contact and a name. If you can tell a parent “I spoke to Martha, the nurse who will meet you on the floor,” that can be a giant first step forward in the healing process.
Most of us trained at hospitals that accepted direct admit patients and can remember the challenges. And most of us recall EDs that weren’t pediatric friendly. Whether our local situation favors direct admission or ED preadmission evaluation, it is our job to make the communication flow with the patient’s safety and the family’s comfort in mind.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Will new guidelines widen the gap in treating childhood obesity?
In the United States, the Centers for Disease Control and Prevention estimates that nearly one in five children have obesity. Since the 1980s, the number of children with obesity has been increasing, with each generation reaching higher rates and greater weights at earlier ages. Even with extensive efforts from parents, clinicians, educators, and policymakers to limit the excessive weight gain among children, the number of obesity and severe obesity diagnoses keeps rising.
In response to this critical public health challenge, the American Academy of Pediatrics (AAP) introduced new clinical practice guidelines for the evaluation and management of obesity in children and adolescents. Developed by an expert panel, the new AAP guidelines present a departure in the conceptualization of obesity, recognizing the role that social determinants of health play in contributing to excessive weight gain.
As a community health researcher who investigates disparities in childhood obesity, I applaud the paradigm shift from the AAP. I specifically endorse the recognition that obesity is a very serious metabolic disease that won’t go away unless we introduce systemic changes and effective treatments.
However, I, like so many of my colleagues and anyone aware of the access barriers to the recommended treatments, worry about the consequences that the new guidelines will have in the context of current and future health disparities.
A recent study, published in Pediatrics, showed that childhood obesity disparities are widening. Younger generations of children are reaching higher weights at younger ages. These alarming trends are greater among Black children and children growing up with the greatest socioeconomic disadvantages. The new AAP guidelines – even while driven by good intentions – can exacerbate these differences and set children who are able to live healthy lives further apart from those with disproportionate obesity risks, who lack access to the treatments recommended by the AAP.
Rather than “watchful waiting,” to see if children outgrow obesity, the new guidelines call for “aggressive treatment,” as reported by this news organization. At least 26 hours of in-person intensive health behavior and lifestyle counseling and treatment are recommended for children aged 2 years old or older who meet the obesity criteria. For children aged 12 years or older, the AAP recommends complementing lifestyle counseling with pharmacotherapy. This breakthrough welcomes the use of promising antiobesity medications (for example, orlistat, Wegovy [semaglutide], Saxenda [liraglutide], Qsymia (phentermine and topiramate]) approved by the Food and Drug Administration for long-term use in children aged 12 and up. For children 13 years or older with severe obesity, bariatric surgery should be considered.
Will cost barriers continue to increase disparity?
The very promising semaglutide (Wegovy) is a GLP-1–based medication currently offered for about $1,000 per month. As with other chronic diseases, children should be prepared to take obesity medications for prolonged periods of time. A study conducted in adults found that when the medication is suspended, any weight loss can be regained. The costs of bariatric surgery total over $20,000.
In the U.S. health care system, at current prices, very few of the children in need of the medications or surgical treatments have access to them. Most private health insurance companies and Medicaid reject coverage for childhood obesity treatments. Barriers to treatment access are greater for Black and Hispanic children, children growing up in poverty, and children living in the U.S. South region, all of whom are more likely to develop obesity earlier in life than their White and wealthier counterparts.
The AAP recognized that a substantial time and financial commitment is required to follow the new treatment recommendations. Members of the AAP Expert Committee that developed the guidelines stated that they are “aware of the multitude of barriers to treatment that patients and their families face.”
Nevertheless, the recognition of the role of social determinants of health in the development of childhood obesity didn’t motivate the introduction of treatment options that aren’t unattainable for most U.S. families.
It’s important to step away from the conclusion that because of the price tag, at the population level, the new AAP guidelines will be inconsequential. This conclusion fails to recognize the potential harm that the guidelines may introduce. In the context of childhood obesity disparities, the new treatment recommendations probably will widen the childhood obesity prevalence gap between the haves – who will benefit from the options available to reduce childhood obesity – and the have-nots, whose obesity rates will continue with their growth.
We live in a world of the haves and have-nots. This applies to financial resources as well as obesity rates. In the long term, the optimists hope that the GLP-1 medications will become ubiquitous, generics will be developed, and insurance companies will expand coverage and grant access to most children in need of effective obesity treatment options. Until this happens, unless intentional policies are promptly introduced, childhood obesity disparities will continue to widen.
To avoid the increasing disparities, brave and intentional actions are required. A lack of attention dealt to this known problem will result in a lost opportunity for the AAP, legislators, and others in a position to help U.S. children.
Liliana Aguayo, PhD, MPH, is assistant professor, Clinical Research Track, Hubert Department of Global Health, Emory University, Atlanta. A version of this article first appeared on Medscape.com.
In the United States, the Centers for Disease Control and Prevention estimates that nearly one in five children have obesity. Since the 1980s, the number of children with obesity has been increasing, with each generation reaching higher rates and greater weights at earlier ages. Even with extensive efforts from parents, clinicians, educators, and policymakers to limit the excessive weight gain among children, the number of obesity and severe obesity diagnoses keeps rising.
In response to this critical public health challenge, the American Academy of Pediatrics (AAP) introduced new clinical practice guidelines for the evaluation and management of obesity in children and adolescents. Developed by an expert panel, the new AAP guidelines present a departure in the conceptualization of obesity, recognizing the role that social determinants of health play in contributing to excessive weight gain.
As a community health researcher who investigates disparities in childhood obesity, I applaud the paradigm shift from the AAP. I specifically endorse the recognition that obesity is a very serious metabolic disease that won’t go away unless we introduce systemic changes and effective treatments.
However, I, like so many of my colleagues and anyone aware of the access barriers to the recommended treatments, worry about the consequences that the new guidelines will have in the context of current and future health disparities.
A recent study, published in Pediatrics, showed that childhood obesity disparities are widening. Younger generations of children are reaching higher weights at younger ages. These alarming trends are greater among Black children and children growing up with the greatest socioeconomic disadvantages. The new AAP guidelines – even while driven by good intentions – can exacerbate these differences and set children who are able to live healthy lives further apart from those with disproportionate obesity risks, who lack access to the treatments recommended by the AAP.
Rather than “watchful waiting,” to see if children outgrow obesity, the new guidelines call for “aggressive treatment,” as reported by this news organization. At least 26 hours of in-person intensive health behavior and lifestyle counseling and treatment are recommended for children aged 2 years old or older who meet the obesity criteria. For children aged 12 years or older, the AAP recommends complementing lifestyle counseling with pharmacotherapy. This breakthrough welcomes the use of promising antiobesity medications (for example, orlistat, Wegovy [semaglutide], Saxenda [liraglutide], Qsymia (phentermine and topiramate]) approved by the Food and Drug Administration for long-term use in children aged 12 and up. For children 13 years or older with severe obesity, bariatric surgery should be considered.
Will cost barriers continue to increase disparity?
The very promising semaglutide (Wegovy) is a GLP-1–based medication currently offered for about $1,000 per month. As with other chronic diseases, children should be prepared to take obesity medications for prolonged periods of time. A study conducted in adults found that when the medication is suspended, any weight loss can be regained. The costs of bariatric surgery total over $20,000.
In the U.S. health care system, at current prices, very few of the children in need of the medications or surgical treatments have access to them. Most private health insurance companies and Medicaid reject coverage for childhood obesity treatments. Barriers to treatment access are greater for Black and Hispanic children, children growing up in poverty, and children living in the U.S. South region, all of whom are more likely to develop obesity earlier in life than their White and wealthier counterparts.
The AAP recognized that a substantial time and financial commitment is required to follow the new treatment recommendations. Members of the AAP Expert Committee that developed the guidelines stated that they are “aware of the multitude of barriers to treatment that patients and their families face.”
Nevertheless, the recognition of the role of social determinants of health in the development of childhood obesity didn’t motivate the introduction of treatment options that aren’t unattainable for most U.S. families.
It’s important to step away from the conclusion that because of the price tag, at the population level, the new AAP guidelines will be inconsequential. This conclusion fails to recognize the potential harm that the guidelines may introduce. In the context of childhood obesity disparities, the new treatment recommendations probably will widen the childhood obesity prevalence gap between the haves – who will benefit from the options available to reduce childhood obesity – and the have-nots, whose obesity rates will continue with their growth.
We live in a world of the haves and have-nots. This applies to financial resources as well as obesity rates. In the long term, the optimists hope that the GLP-1 medications will become ubiquitous, generics will be developed, and insurance companies will expand coverage and grant access to most children in need of effective obesity treatment options. Until this happens, unless intentional policies are promptly introduced, childhood obesity disparities will continue to widen.
To avoid the increasing disparities, brave and intentional actions are required. A lack of attention dealt to this known problem will result in a lost opportunity for the AAP, legislators, and others in a position to help U.S. children.
Liliana Aguayo, PhD, MPH, is assistant professor, Clinical Research Track, Hubert Department of Global Health, Emory University, Atlanta. A version of this article first appeared on Medscape.com.
In the United States, the Centers for Disease Control and Prevention estimates that nearly one in five children have obesity. Since the 1980s, the number of children with obesity has been increasing, with each generation reaching higher rates and greater weights at earlier ages. Even with extensive efforts from parents, clinicians, educators, and policymakers to limit the excessive weight gain among children, the number of obesity and severe obesity diagnoses keeps rising.
In response to this critical public health challenge, the American Academy of Pediatrics (AAP) introduced new clinical practice guidelines for the evaluation and management of obesity in children and adolescents. Developed by an expert panel, the new AAP guidelines present a departure in the conceptualization of obesity, recognizing the role that social determinants of health play in contributing to excessive weight gain.
As a community health researcher who investigates disparities in childhood obesity, I applaud the paradigm shift from the AAP. I specifically endorse the recognition that obesity is a very serious metabolic disease that won’t go away unless we introduce systemic changes and effective treatments.
However, I, like so many of my colleagues and anyone aware of the access barriers to the recommended treatments, worry about the consequences that the new guidelines will have in the context of current and future health disparities.
A recent study, published in Pediatrics, showed that childhood obesity disparities are widening. Younger generations of children are reaching higher weights at younger ages. These alarming trends are greater among Black children and children growing up with the greatest socioeconomic disadvantages. The new AAP guidelines – even while driven by good intentions – can exacerbate these differences and set children who are able to live healthy lives further apart from those with disproportionate obesity risks, who lack access to the treatments recommended by the AAP.
Rather than “watchful waiting,” to see if children outgrow obesity, the new guidelines call for “aggressive treatment,” as reported by this news organization. At least 26 hours of in-person intensive health behavior and lifestyle counseling and treatment are recommended for children aged 2 years old or older who meet the obesity criteria. For children aged 12 years or older, the AAP recommends complementing lifestyle counseling with pharmacotherapy. This breakthrough welcomes the use of promising antiobesity medications (for example, orlistat, Wegovy [semaglutide], Saxenda [liraglutide], Qsymia (phentermine and topiramate]) approved by the Food and Drug Administration for long-term use in children aged 12 and up. For children 13 years or older with severe obesity, bariatric surgery should be considered.
Will cost barriers continue to increase disparity?
The very promising semaglutide (Wegovy) is a GLP-1–based medication currently offered for about $1,000 per month. As with other chronic diseases, children should be prepared to take obesity medications for prolonged periods of time. A study conducted in adults found that when the medication is suspended, any weight loss can be regained. The costs of bariatric surgery total over $20,000.
In the U.S. health care system, at current prices, very few of the children in need of the medications or surgical treatments have access to them. Most private health insurance companies and Medicaid reject coverage for childhood obesity treatments. Barriers to treatment access are greater for Black and Hispanic children, children growing up in poverty, and children living in the U.S. South region, all of whom are more likely to develop obesity earlier in life than their White and wealthier counterparts.
The AAP recognized that a substantial time and financial commitment is required to follow the new treatment recommendations. Members of the AAP Expert Committee that developed the guidelines stated that they are “aware of the multitude of barriers to treatment that patients and their families face.”
Nevertheless, the recognition of the role of social determinants of health in the development of childhood obesity didn’t motivate the introduction of treatment options that aren’t unattainable for most U.S. families.
It’s important to step away from the conclusion that because of the price tag, at the population level, the new AAP guidelines will be inconsequential. This conclusion fails to recognize the potential harm that the guidelines may introduce. In the context of childhood obesity disparities, the new treatment recommendations probably will widen the childhood obesity prevalence gap between the haves – who will benefit from the options available to reduce childhood obesity – and the have-nots, whose obesity rates will continue with their growth.
We live in a world of the haves and have-nots. This applies to financial resources as well as obesity rates. In the long term, the optimists hope that the GLP-1 medications will become ubiquitous, generics will be developed, and insurance companies will expand coverage and grant access to most children in need of effective obesity treatment options. Until this happens, unless intentional policies are promptly introduced, childhood obesity disparities will continue to widen.
To avoid the increasing disparities, brave and intentional actions are required. A lack of attention dealt to this known problem will result in a lost opportunity for the AAP, legislators, and others in a position to help U.S. children.
Liliana Aguayo, PhD, MPH, is assistant professor, Clinical Research Track, Hubert Department of Global Health, Emory University, Atlanta. A version of this article first appeared on Medscape.com.
Can particles in dairy and beef cause cancer and MS?
In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?
However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.
In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.
Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
Acid radicals
However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.
According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
Viral progeny
In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.
The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
‘Breast milk is healthy’
Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.
The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
Colon cancer
To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.
The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
Institutional skepticism
When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?
The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.
BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.
Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
Association with MS?
Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”
However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.
Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?
However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.
In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.
Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
Acid radicals
However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.
According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
Viral progeny
In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.
The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
‘Breast milk is healthy’
Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.
The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
Colon cancer
To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.
The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
Institutional skepticism
When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?
The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.
BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.
Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
Association with MS?
Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”
However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.
Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?
However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.
In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.
Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
Acid radicals
However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.
According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
Viral progeny
In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.
The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
‘Breast milk is healthy’
Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.
The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
Colon cancer
To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.
The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
Institutional skepticism
When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?
The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.
BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.
Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
Association with MS?
Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”
However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.
Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
The 2023 ‘Meddy’ awards
Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...
Best depiction of emergency medicine’s rollercoaster
M*A*S*H (1970)
The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.
Best ‘is there a doctor in the house?’ moment
Field of Dreams (1989)
When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.
Most unethical doctor
Elvis (2022)
No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”
Best self-use of a defibrillator
Casino Royale (2006)
We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.
Best worst patient lying about an injury
Tár (2022)
Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.
Best therapy for a speech disorder
The King’s Speech (2010)
Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”
A version of this article first appeared on Medscape.com.
Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...
Best depiction of emergency medicine’s rollercoaster
M*A*S*H (1970)
The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.
Best ‘is there a doctor in the house?’ moment
Field of Dreams (1989)
When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.
Most unethical doctor
Elvis (2022)
No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”
Best self-use of a defibrillator
Casino Royale (2006)
We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.
Best worst patient lying about an injury
Tár (2022)
Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.
Best therapy for a speech disorder
The King’s Speech (2010)
Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”
A version of this article first appeared on Medscape.com.
Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...
Best depiction of emergency medicine’s rollercoaster
M*A*S*H (1970)
The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.
Best ‘is there a doctor in the house?’ moment
Field of Dreams (1989)
When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.
Most unethical doctor
Elvis (2022)
No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”
Best self-use of a defibrillator
Casino Royale (2006)
We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.
Best worst patient lying about an injury
Tár (2022)
Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.
Best therapy for a speech disorder
The King’s Speech (2010)
Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”
A version of this article first appeared on Medscape.com.
A surfing PA leads an intense beach rescue
There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.
In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.
I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.
I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.
Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.
The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.
At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.
The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”
The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.
Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.
By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.
We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.
The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.
For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!
While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”
A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.
The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.
Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered.
When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”
He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.
I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”
Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.
A version of this article first appeared on Medscape.com.
There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.
In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.
I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.
I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.
Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.
The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.
At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.
The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”
The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.
Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.
By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.
We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.
The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.
For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!
While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”
A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.
The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.
Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered.
When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”
He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.
I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”
Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.
A version of this article first appeared on Medscape.com.
There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.
In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.
I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.
I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.
Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.
The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.
At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.
The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”
The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.
Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.
By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.
We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.
The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.
For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!
While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”
A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.
The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.
Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered.
When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”
He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.
I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”
Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.
A version of this article first appeared on Medscape.com.
A 9-year-old male presents with multiple thick scaly plaques on scalp, ears, and trunk
Given the characteristic clinical presentation, the most likely diagnosis is psoriasis.
Psoriasis is a chronic immune-mediated disease that is characterized by well-demarcated thick scaly plaques on face, scalp, and intertriginous skin. Psoriasis is more common in adults than children, but the incidence of psoriasis in children has increased over time.1 Clinical presentation of psoriasis includes erythematous hyperkeratotic plaques, usually sharply demarcated. Pediatric patients may have multiple small papules and plaques less than 1 cm in size – “drop-size” – known as guttate lesions. Scalp and facial involvement are common in children. Chronic, inflamed plaques with coarse scale can involve ears, elbows, knees, and umbilicus, and nail changes can include pits, ridges, hyperkeratosis, and onycholysis or “oil spots.” While the diagnosis is clinical, biopsy can sometimes be useful to distinguish psoriasis from other papulosquamous conditions. Psoriasis in children is associated with obesity, higher rates of cardiovascular disease over a lifetime, as well as arthritis and mental health disorders.2
What’s the differential diagnosis?
The differential diagnosis for psoriasis can include papulosquamous diseases such as nummular eczema, pityriasis rosea, and pityriasis rubra pilaris. Tinea corporis may also be considered.
Nummular eczema, also known as “discoid eczema” is characterized by multiple pruritic, coin-shaped, eczematous lesions that may be actively oozing. The term “nummular” is derived from the Latin for “coin,” as lesions are distinct and annular. It is commonly associated with atopic dermatitis, and may be seen with contact dermatitis as well. Oozing, lichenification, hyperpigmentation and limited extent of skin coverage can help distinguish nummular dermatitis from psoriasis.
Pityriasis rosea is a common self-limited disease that is characterized by the appearance of acute, oval, papulosquamous patches on the trunk and proximal areas of the extremities. It usually begins with a characteristic “herald” patch, a single round or oval, sharply demarcated, pink lesion on the chest, neck, or back. Pityriasis rosea and guttate psoriasis may show similar clinical findings but the latter lacks a herald patch and is often preceded by streptococcal throat infection.
Pityriasis rubra pilaris is a rarer inflammatory disease characterized by follicular, hyperkeratotic papules, thick orange waxy palms (palmoplantar keratoderma), and erythroderma. It can also cause hair loss, nail changes, and itching. The rash shows areas with no involvement, “islands of sparing,” which is a signature characteristic of pityriasis rubra pilaris. Skin biopsies are an important diagnostic tool for pityriasis rubra pilaris. In the case of circumscribed pityriasis rubra pilaris, it may look similar to psoriasis, but it can be differentiated in that it is often accompanied by characteristic follicular papules and involvement of the palms, which are more waxy and orange in color.
When evaluating annular scaly patches, it is always important to consider tinea corporis. Tinea corporis will commonly have an annular border of scale with relative clearing in the center of lesions. In addition, when topical corticosteroids are used for prolonged periods, skin fungal infections can develop into “tinea incognito,” with paradoxical worsening since the immune response is suppressed and the fungal infection worsens.
Our patient had been previously treated with topical corticosteroids (medium to high strength) and topical calcineurin inhibitors without significant improvement. Other topical therapies for psoriasis include vitamin analogues, tazarotene, and newer therapies such as topical roflumilast (a phosphodiesterase-4 inhibitor approved for psoriasis in children over 12 years of age).3,4 In addition, as the indications for biological agents have been expanded, there are various options for treating psoriasis in children and adolescents when more active treatment is needed. Systemic therapies for more severe disease include traditional systemic immunosuppressives (for example, methotrexate, cyclosporine) and biologic agents. The four biologic agents currently approved for children are etanercept, ustekinumab, ixekizumab, and secukinumab. Our patient was treated with ustekinumab, which is an injectable biologic agent that blocks interleukin-12/23, with good response to date.
Dr. Al-Nabti is a clinical fellow in the division of pediatric and adolescent dermatology; Dr. Choi is a visiting research physician in the division of pediatric and adolescent dermatology; and Dr. Eichenfield is vice-chair of the department of dermatology and professor of dermatology and pediatrics, all at the University of California, San Diego, and Rady Children’s Hospital, San Diego. They have no relevant disclosures.
References
1. Tollefson MM et al. J Am Acad Dermatol. 2010;62(6):979-87.
2. Menter A et al. J Am Acad Dermatol. 2020;82(1):161-201.
3. Mark G et al. JAMA. 2022;328(11):1073-84.
4. Eichenfield LF et al. Pediatr Dermatol. 2018;35(2):170-81.
Given the characteristic clinical presentation, the most likely diagnosis is psoriasis.
Psoriasis is a chronic immune-mediated disease that is characterized by well-demarcated thick scaly plaques on face, scalp, and intertriginous skin. Psoriasis is more common in adults than children, but the incidence of psoriasis in children has increased over time.1 Clinical presentation of psoriasis includes erythematous hyperkeratotic plaques, usually sharply demarcated. Pediatric patients may have multiple small papules and plaques less than 1 cm in size – “drop-size” – known as guttate lesions. Scalp and facial involvement are common in children. Chronic, inflamed plaques with coarse scale can involve ears, elbows, knees, and umbilicus, and nail changes can include pits, ridges, hyperkeratosis, and onycholysis or “oil spots.” While the diagnosis is clinical, biopsy can sometimes be useful to distinguish psoriasis from other papulosquamous conditions. Psoriasis in children is associated with obesity, higher rates of cardiovascular disease over a lifetime, as well as arthritis and mental health disorders.2
What’s the differential diagnosis?
The differential diagnosis for psoriasis can include papulosquamous diseases such as nummular eczema, pityriasis rosea, and pityriasis rubra pilaris. Tinea corporis may also be considered.
Nummular eczema, also known as “discoid eczema” is characterized by multiple pruritic, coin-shaped, eczematous lesions that may be actively oozing. The term “nummular” is derived from the Latin for “coin,” as lesions are distinct and annular. It is commonly associated with atopic dermatitis, and may be seen with contact dermatitis as well. Oozing, lichenification, hyperpigmentation and limited extent of skin coverage can help distinguish nummular dermatitis from psoriasis.
Pityriasis rosea is a common self-limited disease that is characterized by the appearance of acute, oval, papulosquamous patches on the trunk and proximal areas of the extremities. It usually begins with a characteristic “herald” patch, a single round or oval, sharply demarcated, pink lesion on the chest, neck, or back. Pityriasis rosea and guttate psoriasis may show similar clinical findings but the latter lacks a herald patch and is often preceded by streptococcal throat infection.
Pityriasis rubra pilaris is a rarer inflammatory disease characterized by follicular, hyperkeratotic papules, thick orange waxy palms (palmoplantar keratoderma), and erythroderma. It can also cause hair loss, nail changes, and itching. The rash shows areas with no involvement, “islands of sparing,” which is a signature characteristic of pityriasis rubra pilaris. Skin biopsies are an important diagnostic tool for pityriasis rubra pilaris. In the case of circumscribed pityriasis rubra pilaris, it may look similar to psoriasis, but it can be differentiated in that it is often accompanied by characteristic follicular papules and involvement of the palms, which are more waxy and orange in color.
When evaluating annular scaly patches, it is always important to consider tinea corporis. Tinea corporis will commonly have an annular border of scale with relative clearing in the center of lesions. In addition, when topical corticosteroids are used for prolonged periods, skin fungal infections can develop into “tinea incognito,” with paradoxical worsening since the immune response is suppressed and the fungal infection worsens.
Our patient had been previously treated with topical corticosteroids (medium to high strength) and topical calcineurin inhibitors without significant improvement. Other topical therapies for psoriasis include vitamin analogues, tazarotene, and newer therapies such as topical roflumilast (a phosphodiesterase-4 inhibitor approved for psoriasis in children over 12 years of age).3,4 In addition, as the indications for biological agents have been expanded, there are various options for treating psoriasis in children and adolescents when more active treatment is needed. Systemic therapies for more severe disease include traditional systemic immunosuppressives (for example, methotrexate, cyclosporine) and biologic agents. The four biologic agents currently approved for children are etanercept, ustekinumab, ixekizumab, and secukinumab. Our patient was treated with ustekinumab, which is an injectable biologic agent that blocks interleukin-12/23, with good response to date.
Dr. Al-Nabti is a clinical fellow in the division of pediatric and adolescent dermatology; Dr. Choi is a visiting research physician in the division of pediatric and adolescent dermatology; and Dr. Eichenfield is vice-chair of the department of dermatology and professor of dermatology and pediatrics, all at the University of California, San Diego, and Rady Children’s Hospital, San Diego. They have no relevant disclosures.
References
1. Tollefson MM et al. J Am Acad Dermatol. 2010;62(6):979-87.
2. Menter A et al. J Am Acad Dermatol. 2020;82(1):161-201.
3. Mark G et al. JAMA. 2022;328(11):1073-84.
4. Eichenfield LF et al. Pediatr Dermatol. 2018;35(2):170-81.
Given the characteristic clinical presentation, the most likely diagnosis is psoriasis.
Psoriasis is a chronic immune-mediated disease that is characterized by well-demarcated thick scaly plaques on face, scalp, and intertriginous skin. Psoriasis is more common in adults than children, but the incidence of psoriasis in children has increased over time.1 Clinical presentation of psoriasis includes erythematous hyperkeratotic plaques, usually sharply demarcated. Pediatric patients may have multiple small papules and plaques less than 1 cm in size – “drop-size” – known as guttate lesions. Scalp and facial involvement are common in children. Chronic, inflamed plaques with coarse scale can involve ears, elbows, knees, and umbilicus, and nail changes can include pits, ridges, hyperkeratosis, and onycholysis or “oil spots.” While the diagnosis is clinical, biopsy can sometimes be useful to distinguish psoriasis from other papulosquamous conditions. Psoriasis in children is associated with obesity, higher rates of cardiovascular disease over a lifetime, as well as arthritis and mental health disorders.2
What’s the differential diagnosis?
The differential diagnosis for psoriasis can include papulosquamous diseases such as nummular eczema, pityriasis rosea, and pityriasis rubra pilaris. Tinea corporis may also be considered.
Nummular eczema, also known as “discoid eczema” is characterized by multiple pruritic, coin-shaped, eczematous lesions that may be actively oozing. The term “nummular” is derived from the Latin for “coin,” as lesions are distinct and annular. It is commonly associated with atopic dermatitis, and may be seen with contact dermatitis as well. Oozing, lichenification, hyperpigmentation and limited extent of skin coverage can help distinguish nummular dermatitis from psoriasis.
Pityriasis rosea is a common self-limited disease that is characterized by the appearance of acute, oval, papulosquamous patches on the trunk and proximal areas of the extremities. It usually begins with a characteristic “herald” patch, a single round or oval, sharply demarcated, pink lesion on the chest, neck, or back. Pityriasis rosea and guttate psoriasis may show similar clinical findings but the latter lacks a herald patch and is often preceded by streptococcal throat infection.
Pityriasis rubra pilaris is a rarer inflammatory disease characterized by follicular, hyperkeratotic papules, thick orange waxy palms (palmoplantar keratoderma), and erythroderma. It can also cause hair loss, nail changes, and itching. The rash shows areas with no involvement, “islands of sparing,” which is a signature characteristic of pityriasis rubra pilaris. Skin biopsies are an important diagnostic tool for pityriasis rubra pilaris. In the case of circumscribed pityriasis rubra pilaris, it may look similar to psoriasis, but it can be differentiated in that it is often accompanied by characteristic follicular papules and involvement of the palms, which are more waxy and orange in color.
When evaluating annular scaly patches, it is always important to consider tinea corporis. Tinea corporis will commonly have an annular border of scale with relative clearing in the center of lesions. In addition, when topical corticosteroids are used for prolonged periods, skin fungal infections can develop into “tinea incognito,” with paradoxical worsening since the immune response is suppressed and the fungal infection worsens.
Our patient had been previously treated with topical corticosteroids (medium to high strength) and topical calcineurin inhibitors without significant improvement. Other topical therapies for psoriasis include vitamin analogues, tazarotene, and newer therapies such as topical roflumilast (a phosphodiesterase-4 inhibitor approved for psoriasis in children over 12 years of age).3,4 In addition, as the indications for biological agents have been expanded, there are various options for treating psoriasis in children and adolescents when more active treatment is needed. Systemic therapies for more severe disease include traditional systemic immunosuppressives (for example, methotrexate, cyclosporine) and biologic agents. The four biologic agents currently approved for children are etanercept, ustekinumab, ixekizumab, and secukinumab. Our patient was treated with ustekinumab, which is an injectable biologic agent that blocks interleukin-12/23, with good response to date.
Dr. Al-Nabti is a clinical fellow in the division of pediatric and adolescent dermatology; Dr. Choi is a visiting research physician in the division of pediatric and adolescent dermatology; and Dr. Eichenfield is vice-chair of the department of dermatology and professor of dermatology and pediatrics, all at the University of California, San Diego, and Rady Children’s Hospital, San Diego. They have no relevant disclosures.
References
1. Tollefson MM et al. J Am Acad Dermatol. 2010;62(6):979-87.
2. Menter A et al. J Am Acad Dermatol. 2020;82(1):161-201.
3. Mark G et al. JAMA. 2022;328(11):1073-84.
4. Eichenfield LF et al. Pediatr Dermatol. 2018;35(2):170-81.
A 9-year-old male is seen in the clinic with a 1-year history of multiple thick scaly plaques on scalp, ears, and trunk. He has been treated with hydrocortisone 1% ointment with no change in the lesions. He had upper respiratory tract symptoms 3 weeks prior to the visit.
Examination reveals erythematous, well-demarcated plaques of the anterior scalp with thick overlying micaceous scale with some extension onto the forehead and temples. Additionally, erythematous scaly patches on the ear, axilla, and umbilicus were noted. There was no palmar or plantar involvement. He denied joint swelling, stiffness, or pain in the morning.
Three surprising studies on exercise restriction and an exercise sweet spot
LIVE HCM: Surprising result No. 1
Rachel Lampert, MD, from Yale University, New Haven, Conn., presented results of the LIVE-HCM observational study of vigorous exercise in more than 1,600 patients with hypertrophic cardiomyopathy (40% female). The investigators aimed to determine whether engagement in vigorous exercise, including competitive sports, is associated with increased risk for life-threatening ventricular arrhythmia and/or mortality in patients with HCM.
Because of the myocardial disease, HCM comes with a risk for ventricular arrhythmia. Prevailing wisdom held that vigorous exercise in these patients would be hazardous. It was all expert opinion; there were no data. Now there are.
Dr. Lampert and colleagues recruited patients from 42 international HCM centers. Patients self-enrolled and the researchers created three groups based on self-reported levels of exercise – vigorous, moderate, and sedentary. The main comparison was between vigorous versus nonvigorous exercisers (including moderate and sedentary). The two groups were mostly matched on baseline characteristics and typical of patients with HCM.
The primary endpoint was a composite of death, resuscitated cardiac arrest, syncope likely caused by an arrhythmia, or an appropriate shock from an ICD.
The event rates were low in all groups and almost identical in vigorous versus nonvigorous exercisers. Sub-group analyses found no increased risk in HCM patients who identified as competitive athletes.
Dr. Lampert said these data “do not support universal restriction of vigorous exercise in patients with HCM.”
Return to play: Surprising result No. 2
Undergraduate student Katherine Martinez from Loyola University, Chicago, presented an observational analysis of 76 elite athletes with genetic heart disease who gained a return-to-play approval from four expert centers in the United States.
The three-step, return-to-play protocol from these specialized centers deserves emphasis. First was the initial evaluation, including two ECGs, 24-hour ECG monitor, echocardiography, and treadmill exercise testing. Second was a discussion between clinicians and patients regarding the athlete’s situation. The third step was to inform coaches and staff of the team and instruct athletes to obtain a personal AED, stay replenished with electrolytes, avoid QT-prolonging drugs, and continue with annual follow-up.
Slightly more than half of these patients had HCM and almost a third had long QT syndrome. Nearly one-third had an ICD implant and 22 were women.
Of the 76 athletes, 73 chose to return to play; however, 4 of these remained disqualified because of their team’s decision. Of the remaining 69, only 3 had one or more breakthrough cardiac events during 200 patient-years of follow-up.
These comprised one male Division I basketball player with HCM who had an ICD shock while moving furniture; another male Division 1 hockey player with long QT syndrome who was taking beta-blockers experienced syncope while coming off the bench and while cooking; and a third male professional hockey player with HCM, on beta-blockers, had syncope without exertion.
The authors concluded that when there was careful evaluation by experts and shared decision-making, a specific plan to return to sport can be put into place for the highest-level athletes.
Masters@Heart: Surprising result No. 3
Ruben De Bosscher MD, PhD, from KU Leuven (Belgium), presented the Masters@Heart study on behalf of a Belgian team of researchers. The question they asked was whether lifelong endurance exercise is associated with more coronary atherosclerosis than standard “normal” exercise levels.
That question brings up the paradox of exercise, which is that numerous observational studies find that exercise strongly associates with lower rates of cardiovascular events, but imaging studies also report high rates of coronary artery calcium in endurance athletes, especially in those who have run multiple marathons.
Masters@Heart investigators sought to explore this paradox by performing detailed coronary imaging in three groups – lifelong athletes, late-onset athletes (after age 30 years), and super-healthy controls. Through advertisements they obtained about 1,100 middle-aged male volunteers (mean age, 55 years). Of these, 605 men were selected at random to participate to reduce the chance of enrolling people who responded to the ads because of health concerns.
Investigators assigned those selected based on self-report of exercise. The control group was notable for their good health: they were free of any risk factors, took (almost) no meds, exercised regularly but not excessively (about 3 hours per week) and had a VO2 max of 122% of predicted.
The groups were well matched on baseline characteristics. Cycling predominated as the exercise of choice (this is a Belgian study after all). All patients had an extensive evaluation including coronary CT imaging.
European Heart Journal published the provocative results.
- Lifelong exercisers had a significantly higher CAC burden than controls, which confirms previous work.
- Lifelong exercisers had a higher percentage of multiple coronary plaques, plaques of at least 50%, and proximal plaques.
- There were no significant differences in the mixture of plaque types in the three groups. About two thirds of the plaques in each group were calcified and the remainder were deemed noncalcified or mixed.
- When looking only at noncalcified plaques, lifelong exercisers tended to have a higher prevalence of multiple plaques, plaques of at least 50%, and proximal plaques.
- So named “vulnerable” plaques were extremely infrequent in all three groups.
The authors concluded that lifelong endurance sport relative to a generic healthy lifestyle was not associated with more favorable coronary plaque composition.
Comments
Each of these three studies provided data where there was none. That is always a good thing.
The major theme from the first two studies is that expert opinion was too cautious. Doctors have long held the idea that patients with genetic heart disease, especially hypertrophic cardiomyopathy, are vulnerable, fragile even, when it comes to vigorous sport.
This new evidence upends this belief, as long as return to sport occurs in the setting of robust patient education and expert evaluation and surveillance.
Paternalism in prohibiting participation in sport because of genetic heart disease has joined the long list of medical reversals.
Masters@Heart provides a slightly different message. It finds that lifelong high-level exercise does not prevent coronary atherosclerosis in men. And, more provocatively, if replicated, might even show that long-term exposure to the biochemical, inflammatory, or hormonal effects of endurance training may actually be atherogenic. Like all good science, these findings raise more questions to explore in the realm of atherogenesis.
Two of the main limitations of the Belgian study was that the control arm was quite healthy; had the comparison arm been typical of sedentary controls in say, the Southeastern United States, the coronary lesions found in longtime exercisers may have looked more favorable. The more significant limitation is the lack of outcomes. Images of coronary arteries remain a surrogate marker. It’s possible that, like statins, higher levels of exercise may stabilize plaque and actually lower the risk for events.
The Belgian authors suggest – as many have – a J-curve of exercise benefits, wherein too little exercise is clearly bad, but too much exercise may also increase risk. In other words, for maximizing health, there may be a Goldilocks amount of exercise.
The problem with this idea comes in its pragmatic translation. The number of lifelong high-level, middle-aged endurance athletes that cite heart health reasons for their affliction is ... almost zero. Nearly everyone I have met in the endurance sport fraternity harbors no notion that racing a bike or running multiple marathons per year is a healthy endeavor.
Paternalism, therefore, would also fall in the realm of limiting lifelong exercise in addicted middle-aged athletes.
Via email, sports cardiologist Michael Emery, MD, reiterated the main immediate message from Masters@Heart: “Exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear honestly).”
I for one cannot give up on endurance exercise. I won’t likely race anymore but I am like the lab rat who needs to run on the wheel. Whether this affects my coronary plaque burden matters not to me.
Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
LIVE HCM: Surprising result No. 1
Rachel Lampert, MD, from Yale University, New Haven, Conn., presented results of the LIVE-HCM observational study of vigorous exercise in more than 1,600 patients with hypertrophic cardiomyopathy (40% female). The investigators aimed to determine whether engagement in vigorous exercise, including competitive sports, is associated with increased risk for life-threatening ventricular arrhythmia and/or mortality in patients with HCM.
Because of the myocardial disease, HCM comes with a risk for ventricular arrhythmia. Prevailing wisdom held that vigorous exercise in these patients would be hazardous. It was all expert opinion; there were no data. Now there are.
Dr. Lampert and colleagues recruited patients from 42 international HCM centers. Patients self-enrolled and the researchers created three groups based on self-reported levels of exercise – vigorous, moderate, and sedentary. The main comparison was between vigorous versus nonvigorous exercisers (including moderate and sedentary). The two groups were mostly matched on baseline characteristics and typical of patients with HCM.
The primary endpoint was a composite of death, resuscitated cardiac arrest, syncope likely caused by an arrhythmia, or an appropriate shock from an ICD.
The event rates were low in all groups and almost identical in vigorous versus nonvigorous exercisers. Sub-group analyses found no increased risk in HCM patients who identified as competitive athletes.
Dr. Lampert said these data “do not support universal restriction of vigorous exercise in patients with HCM.”
Return to play: Surprising result No. 2
Undergraduate student Katherine Martinez from Loyola University, Chicago, presented an observational analysis of 76 elite athletes with genetic heart disease who gained a return-to-play approval from four expert centers in the United States.
The three-step, return-to-play protocol from these specialized centers deserves emphasis. First was the initial evaluation, including two ECGs, 24-hour ECG monitor, echocardiography, and treadmill exercise testing. Second was a discussion between clinicians and patients regarding the athlete’s situation. The third step was to inform coaches and staff of the team and instruct athletes to obtain a personal AED, stay replenished with electrolytes, avoid QT-prolonging drugs, and continue with annual follow-up.
Slightly more than half of these patients had HCM and almost a third had long QT syndrome. Nearly one-third had an ICD implant and 22 were women.
Of the 76 athletes, 73 chose to return to play; however, 4 of these remained disqualified because of their team’s decision. Of the remaining 69, only 3 had one or more breakthrough cardiac events during 200 patient-years of follow-up.
These comprised one male Division I basketball player with HCM who had an ICD shock while moving furniture; another male Division 1 hockey player with long QT syndrome who was taking beta-blockers experienced syncope while coming off the bench and while cooking; and a third male professional hockey player with HCM, on beta-blockers, had syncope without exertion.
The authors concluded that when there was careful evaluation by experts and shared decision-making, a specific plan to return to sport can be put into place for the highest-level athletes.
Masters@Heart: Surprising result No. 3
Ruben De Bosscher MD, PhD, from KU Leuven (Belgium), presented the Masters@Heart study on behalf of a Belgian team of researchers. The question they asked was whether lifelong endurance exercise is associated with more coronary atherosclerosis than standard “normal” exercise levels.
That question brings up the paradox of exercise, which is that numerous observational studies find that exercise strongly associates with lower rates of cardiovascular events, but imaging studies also report high rates of coronary artery calcium in endurance athletes, especially in those who have run multiple marathons.
Masters@Heart investigators sought to explore this paradox by performing detailed coronary imaging in three groups – lifelong athletes, late-onset athletes (after age 30 years), and super-healthy controls. Through advertisements they obtained about 1,100 middle-aged male volunteers (mean age, 55 years). Of these, 605 men were selected at random to participate to reduce the chance of enrolling people who responded to the ads because of health concerns.
Investigators assigned those selected based on self-report of exercise. The control group was notable for their good health: they were free of any risk factors, took (almost) no meds, exercised regularly but not excessively (about 3 hours per week) and had a VO2 max of 122% of predicted.
The groups were well matched on baseline characteristics. Cycling predominated as the exercise of choice (this is a Belgian study after all). All patients had an extensive evaluation including coronary CT imaging.
European Heart Journal published the provocative results.
- Lifelong exercisers had a significantly higher CAC burden than controls, which confirms previous work.
- Lifelong exercisers had a higher percentage of multiple coronary plaques, plaques of at least 50%, and proximal plaques.
- There were no significant differences in the mixture of plaque types in the three groups. About two thirds of the plaques in each group were calcified and the remainder were deemed noncalcified or mixed.
- When looking only at noncalcified plaques, lifelong exercisers tended to have a higher prevalence of multiple plaques, plaques of at least 50%, and proximal plaques.
- So named “vulnerable” plaques were extremely infrequent in all three groups.
The authors concluded that lifelong endurance sport relative to a generic healthy lifestyle was not associated with more favorable coronary plaque composition.
Comments
Each of these three studies provided data where there was none. That is always a good thing.
The major theme from the first two studies is that expert opinion was too cautious. Doctors have long held the idea that patients with genetic heart disease, especially hypertrophic cardiomyopathy, are vulnerable, fragile even, when it comes to vigorous sport.
This new evidence upends this belief, as long as return to sport occurs in the setting of robust patient education and expert evaluation and surveillance.
Paternalism in prohibiting participation in sport because of genetic heart disease has joined the long list of medical reversals.
Masters@Heart provides a slightly different message. It finds that lifelong high-level exercise does not prevent coronary atherosclerosis in men. And, more provocatively, if replicated, might even show that long-term exposure to the biochemical, inflammatory, or hormonal effects of endurance training may actually be atherogenic. Like all good science, these findings raise more questions to explore in the realm of atherogenesis.
Two of the main limitations of the Belgian study was that the control arm was quite healthy; had the comparison arm been typical of sedentary controls in say, the Southeastern United States, the coronary lesions found in longtime exercisers may have looked more favorable. The more significant limitation is the lack of outcomes. Images of coronary arteries remain a surrogate marker. It’s possible that, like statins, higher levels of exercise may stabilize plaque and actually lower the risk for events.
The Belgian authors suggest – as many have – a J-curve of exercise benefits, wherein too little exercise is clearly bad, but too much exercise may also increase risk. In other words, for maximizing health, there may be a Goldilocks amount of exercise.
The problem with this idea comes in its pragmatic translation. The number of lifelong high-level, middle-aged endurance athletes that cite heart health reasons for their affliction is ... almost zero. Nearly everyone I have met in the endurance sport fraternity harbors no notion that racing a bike or running multiple marathons per year is a healthy endeavor.
Paternalism, therefore, would also fall in the realm of limiting lifelong exercise in addicted middle-aged athletes.
Via email, sports cardiologist Michael Emery, MD, reiterated the main immediate message from Masters@Heart: “Exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear honestly).”
I for one cannot give up on endurance exercise. I won’t likely race anymore but I am like the lab rat who needs to run on the wheel. Whether this affects my coronary plaque burden matters not to me.
Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
LIVE HCM: Surprising result No. 1
Rachel Lampert, MD, from Yale University, New Haven, Conn., presented results of the LIVE-HCM observational study of vigorous exercise in more than 1,600 patients with hypertrophic cardiomyopathy (40% female). The investigators aimed to determine whether engagement in vigorous exercise, including competitive sports, is associated with increased risk for life-threatening ventricular arrhythmia and/or mortality in patients with HCM.
Because of the myocardial disease, HCM comes with a risk for ventricular arrhythmia. Prevailing wisdom held that vigorous exercise in these patients would be hazardous. It was all expert opinion; there were no data. Now there are.
Dr. Lampert and colleagues recruited patients from 42 international HCM centers. Patients self-enrolled and the researchers created three groups based on self-reported levels of exercise – vigorous, moderate, and sedentary. The main comparison was between vigorous versus nonvigorous exercisers (including moderate and sedentary). The two groups were mostly matched on baseline characteristics and typical of patients with HCM.
The primary endpoint was a composite of death, resuscitated cardiac arrest, syncope likely caused by an arrhythmia, or an appropriate shock from an ICD.
The event rates were low in all groups and almost identical in vigorous versus nonvigorous exercisers. Sub-group analyses found no increased risk in HCM patients who identified as competitive athletes.
Dr. Lampert said these data “do not support universal restriction of vigorous exercise in patients with HCM.”
Return to play: Surprising result No. 2
Undergraduate student Katherine Martinez from Loyola University, Chicago, presented an observational analysis of 76 elite athletes with genetic heart disease who gained a return-to-play approval from four expert centers in the United States.
The three-step, return-to-play protocol from these specialized centers deserves emphasis. First was the initial evaluation, including two ECGs, 24-hour ECG monitor, echocardiography, and treadmill exercise testing. Second was a discussion between clinicians and patients regarding the athlete’s situation. The third step was to inform coaches and staff of the team and instruct athletes to obtain a personal AED, stay replenished with electrolytes, avoid QT-prolonging drugs, and continue with annual follow-up.
Slightly more than half of these patients had HCM and almost a third had long QT syndrome. Nearly one-third had an ICD implant and 22 were women.
Of the 76 athletes, 73 chose to return to play; however, 4 of these remained disqualified because of their team’s decision. Of the remaining 69, only 3 had one or more breakthrough cardiac events during 200 patient-years of follow-up.
These comprised one male Division I basketball player with HCM who had an ICD shock while moving furniture; another male Division 1 hockey player with long QT syndrome who was taking beta-blockers experienced syncope while coming off the bench and while cooking; and a third male professional hockey player with HCM, on beta-blockers, had syncope without exertion.
The authors concluded that when there was careful evaluation by experts and shared decision-making, a specific plan to return to sport can be put into place for the highest-level athletes.
Masters@Heart: Surprising result No. 3
Ruben De Bosscher MD, PhD, from KU Leuven (Belgium), presented the Masters@Heart study on behalf of a Belgian team of researchers. The question they asked was whether lifelong endurance exercise is associated with more coronary atherosclerosis than standard “normal” exercise levels.
That question brings up the paradox of exercise, which is that numerous observational studies find that exercise strongly associates with lower rates of cardiovascular events, but imaging studies also report high rates of coronary artery calcium in endurance athletes, especially in those who have run multiple marathons.
Masters@Heart investigators sought to explore this paradox by performing detailed coronary imaging in three groups – lifelong athletes, late-onset athletes (after age 30 years), and super-healthy controls. Through advertisements they obtained about 1,100 middle-aged male volunteers (mean age, 55 years). Of these, 605 men were selected at random to participate to reduce the chance of enrolling people who responded to the ads because of health concerns.
Investigators assigned those selected based on self-report of exercise. The control group was notable for their good health: they were free of any risk factors, took (almost) no meds, exercised regularly but not excessively (about 3 hours per week) and had a VO2 max of 122% of predicted.
The groups were well matched on baseline characteristics. Cycling predominated as the exercise of choice (this is a Belgian study after all). All patients had an extensive evaluation including coronary CT imaging.
European Heart Journal published the provocative results.
- Lifelong exercisers had a significantly higher CAC burden than controls, which confirms previous work.
- Lifelong exercisers had a higher percentage of multiple coronary plaques, plaques of at least 50%, and proximal plaques.
- There were no significant differences in the mixture of plaque types in the three groups. About two thirds of the plaques in each group were calcified and the remainder were deemed noncalcified or mixed.
- When looking only at noncalcified plaques, lifelong exercisers tended to have a higher prevalence of multiple plaques, plaques of at least 50%, and proximal plaques.
- So named “vulnerable” plaques were extremely infrequent in all three groups.
The authors concluded that lifelong endurance sport relative to a generic healthy lifestyle was not associated with more favorable coronary plaque composition.
Comments
Each of these three studies provided data where there was none. That is always a good thing.
The major theme from the first two studies is that expert opinion was too cautious. Doctors have long held the idea that patients with genetic heart disease, especially hypertrophic cardiomyopathy, are vulnerable, fragile even, when it comes to vigorous sport.
This new evidence upends this belief, as long as return to sport occurs in the setting of robust patient education and expert evaluation and surveillance.
Paternalism in prohibiting participation in sport because of genetic heart disease has joined the long list of medical reversals.
Masters@Heart provides a slightly different message. It finds that lifelong high-level exercise does not prevent coronary atherosclerosis in men. And, more provocatively, if replicated, might even show that long-term exposure to the biochemical, inflammatory, or hormonal effects of endurance training may actually be atherogenic. Like all good science, these findings raise more questions to explore in the realm of atherogenesis.
Two of the main limitations of the Belgian study was that the control arm was quite healthy; had the comparison arm been typical of sedentary controls in say, the Southeastern United States, the coronary lesions found in longtime exercisers may have looked more favorable. The more significant limitation is the lack of outcomes. Images of coronary arteries remain a surrogate marker. It’s possible that, like statins, higher levels of exercise may stabilize plaque and actually lower the risk for events.
The Belgian authors suggest – as many have – a J-curve of exercise benefits, wherein too little exercise is clearly bad, but too much exercise may also increase risk. In other words, for maximizing health, there may be a Goldilocks amount of exercise.
The problem with this idea comes in its pragmatic translation. The number of lifelong high-level, middle-aged endurance athletes that cite heart health reasons for their affliction is ... almost zero. Nearly everyone I have met in the endurance sport fraternity harbors no notion that racing a bike or running multiple marathons per year is a healthy endeavor.
Paternalism, therefore, would also fall in the realm of limiting lifelong exercise in addicted middle-aged athletes.
Via email, sports cardiologist Michael Emery, MD, reiterated the main immediate message from Masters@Heart: “Exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear honestly).”
I for one cannot give up on endurance exercise. I won’t likely race anymore but I am like the lab rat who needs to run on the wheel. Whether this affects my coronary plaque burden matters not to me.
Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
What’s it like to take Ozempic? A doctor’s own story
With the rising popularity of weight-loss drug injections, I’ve received many questions from patients about the pros, cons, and costs. While Ozempic (semaglutide) is perhaps the best known, it’s technically an agent approved only for type 2 diabetes that has been used off label for obesity. The same substance, semaglutide, is approved for use in obesity, but at a higher dose, under the brand name Wegovy. Alternatives are available, and results will vary depending on the specific agent used and the individual.
Ultimately, I decided to try these new injections for myself. I am not a paid representative for, nor an advocate of, any of these medications; I’m here only to share my personal experience.
In my discussions with patients about weight, I sometimes felt like an imposter. While I was overweight by medical standards, I fortunately had none of the underlying health problems. I wasn’t on medications for blood pressure nor did I have diabetes, but I was counseling people to lose weight and eat better while not always following my own advice.
Since having children and turning 40, my metabolism, like many other women’s, seems to have plummeted. I tried a number of older weight-loss medications, like phentermine and phendimetrazine, under the supervision of medical professionals.
Each time, the efforts worked for a short while, particularly when I followed good portion control and practiced moderate exercise. Once the side effects (that is, tachycardia, palpitations, mood changes, constipation) became intolerable, or I became tired or fearful of being on the medications too long, I’d stop and I would regain some of the weight.
When the newer subcutaneous injectable medications arrived on the scene and I started to talk to my patients about them, I was intrigued by their novel mode of action and seeming benefits.
These medications, glucagonlike peptide–1 (GLP-1) receptor agonists, were first approved for type 2 diabetes, and it soon became apparent that patients were losing significant amounts of weight taking them, so manufacturers conducted further trials in obesity patients without type 2 diabetes.
The first of these, liraglutide, is injected daily and was first approved as Victoza for type 2 diabetes; it later received an additional approval for obesity, in December 2014, as Saxenda.
Semaglutide, another of the new GLP-1 agonists, was first approved for type 2 diabetes as Ozempic but again was found to lead to substantial weight loss, so a subsequent approval of the drug for obesity, as Wegovy, came in June 2021. Semaglutide is injected once a week.
Semaglutide was branded a “game changer” when it was licensed for obesity because the mean weight loss seen in trials was around 15%, more than for any other drug and approaching what could be achieved with bariatric surgery, some doctors said.
These medications work in a different way from the older weight loss drugs, which had focused on the use of amphetamines. The newer medications became very popular because treating obesity helps lower blood glucose, blood pressure, cholesterol, kidney disease risk, and other comorbidities that occur with diabetes. Plus, for most people, there were fewer side effects.
I first tried Saxenda when it arrived on the market, via some samples that our pharmaceutical representative brought, both out of curiosity and to see if it would help me lose the stubborn baby weight. I ended up stopping the daily injections after my second or third week because of nausea and vomiting. I took a break, got a prescription for antinausea medicine, and tried again because it did indeed decrease my appetite. However, when I took my prescription to the pharmacy, my insurance wouldn’t cover it. It happens to doctors, too.
Fast-forward to 2017-2018. The baby weight was still holding on despite lifestyle changes, diet, and exercising. The newer drug classes hit the market, and again we had samples from our reps.
When Ozempic was on backorder, I switched to a low dose of Mounjaro (tirzepatide), a new dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, approved for type 2 diabetes in May 2022, again using it off label as a weekly injection, as it isn’t currently approved for weight loss. However, it does produce significant weight loss and is awaiting approval for obesity.
With these new medications, I noticed that both my patients and I didn’t complain as much about nausea and vomiting, but I did experience stomach upset, constipation, and acid reflux.
The appetite suppression is effective. It slows down the emptying of the gut so I feel full longer. I’ve lost 30 lb with these weekly injections and would like to lose another 20 lb. I follow a routine of reasonable, portion-controlled eating and moderate exercise (30 minutes of cardiovascular activity at least two to three times a week).
Discontinuing the medications may cause rebound weight gain, especially if I’m no longer following a routine of healthy eating and/or moderate exercise. I deal with minimal constipation by taking stool softeners, and I take antacids for acid reflux.
Here’s what I recommend applying when working with patients who have obesity: First, explain how these medications work. Then conduct a health history to make sure these injections are right for them. Patients with a family history of pancreatic cancer can’t take these medications. You also want to monitor use in patients with a history of hypoglycemia so their blood sugar doesn’t drop too low. It’s also important to make sure your patients are able to afford the medication. My husband takes Ozempic for diabetes, and recently we were told that a refill would cost about $1,500 a month, even with insurance. “Covered” doesn’t necessarily mean affordable.
Take a baseline hemoglobin A1c and repeat it after the patient has been on the medication for 2-3 weeks. Also remind them that they can’t rely solely on the medication but need to practice portion control and healthier eating and to exercise more.
For myself, I want to lose those remaining 20 lb or so by eating healthy and being physically active without having to rely on medication for the rest of my life. Research on these medications is still early so we don’t know the long-term effects yet.
As clinicians, I feel it’s okay to be honest with our patients about our own personal struggles to help them understand that they are not alone and that losing weight is a challenge for everyone.
Dr. Swiner is a family physician in Durham, N.C. She reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
With the rising popularity of weight-loss drug injections, I’ve received many questions from patients about the pros, cons, and costs. While Ozempic (semaglutide) is perhaps the best known, it’s technically an agent approved only for type 2 diabetes that has been used off label for obesity. The same substance, semaglutide, is approved for use in obesity, but at a higher dose, under the brand name Wegovy. Alternatives are available, and results will vary depending on the specific agent used and the individual.
Ultimately, I decided to try these new injections for myself. I am not a paid representative for, nor an advocate of, any of these medications; I’m here only to share my personal experience.
In my discussions with patients about weight, I sometimes felt like an imposter. While I was overweight by medical standards, I fortunately had none of the underlying health problems. I wasn’t on medications for blood pressure nor did I have diabetes, but I was counseling people to lose weight and eat better while not always following my own advice.
Since having children and turning 40, my metabolism, like many other women’s, seems to have plummeted. I tried a number of older weight-loss medications, like phentermine and phendimetrazine, under the supervision of medical professionals.
Each time, the efforts worked for a short while, particularly when I followed good portion control and practiced moderate exercise. Once the side effects (that is, tachycardia, palpitations, mood changes, constipation) became intolerable, or I became tired or fearful of being on the medications too long, I’d stop and I would regain some of the weight.
When the newer subcutaneous injectable medications arrived on the scene and I started to talk to my patients about them, I was intrigued by their novel mode of action and seeming benefits.
These medications, glucagonlike peptide–1 (GLP-1) receptor agonists, were first approved for type 2 diabetes, and it soon became apparent that patients were losing significant amounts of weight taking them, so manufacturers conducted further trials in obesity patients without type 2 diabetes.
The first of these, liraglutide, is injected daily and was first approved as Victoza for type 2 diabetes; it later received an additional approval for obesity, in December 2014, as Saxenda.
Semaglutide, another of the new GLP-1 agonists, was first approved for type 2 diabetes as Ozempic but again was found to lead to substantial weight loss, so a subsequent approval of the drug for obesity, as Wegovy, came in June 2021. Semaglutide is injected once a week.
Semaglutide was branded a “game changer” when it was licensed for obesity because the mean weight loss seen in trials was around 15%, more than for any other drug and approaching what could be achieved with bariatric surgery, some doctors said.
These medications work in a different way from the older weight loss drugs, which had focused on the use of amphetamines. The newer medications became very popular because treating obesity helps lower blood glucose, blood pressure, cholesterol, kidney disease risk, and other comorbidities that occur with diabetes. Plus, for most people, there were fewer side effects.
I first tried Saxenda when it arrived on the market, via some samples that our pharmaceutical representative brought, both out of curiosity and to see if it would help me lose the stubborn baby weight. I ended up stopping the daily injections after my second or third week because of nausea and vomiting. I took a break, got a prescription for antinausea medicine, and tried again because it did indeed decrease my appetite. However, when I took my prescription to the pharmacy, my insurance wouldn’t cover it. It happens to doctors, too.
Fast-forward to 2017-2018. The baby weight was still holding on despite lifestyle changes, diet, and exercising. The newer drug classes hit the market, and again we had samples from our reps.
When Ozempic was on backorder, I switched to a low dose of Mounjaro (tirzepatide), a new dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, approved for type 2 diabetes in May 2022, again using it off label as a weekly injection, as it isn’t currently approved for weight loss. However, it does produce significant weight loss and is awaiting approval for obesity.
With these new medications, I noticed that both my patients and I didn’t complain as much about nausea and vomiting, but I did experience stomach upset, constipation, and acid reflux.
The appetite suppression is effective. It slows down the emptying of the gut so I feel full longer. I’ve lost 30 lb with these weekly injections and would like to lose another 20 lb. I follow a routine of reasonable, portion-controlled eating and moderate exercise (30 minutes of cardiovascular activity at least two to three times a week).
Discontinuing the medications may cause rebound weight gain, especially if I’m no longer following a routine of healthy eating and/or moderate exercise. I deal with minimal constipation by taking stool softeners, and I take antacids for acid reflux.
Here’s what I recommend applying when working with patients who have obesity: First, explain how these medications work. Then conduct a health history to make sure these injections are right for them. Patients with a family history of pancreatic cancer can’t take these medications. You also want to monitor use in patients with a history of hypoglycemia so their blood sugar doesn’t drop too low. It’s also important to make sure your patients are able to afford the medication. My husband takes Ozempic for diabetes, and recently we were told that a refill would cost about $1,500 a month, even with insurance. “Covered” doesn’t necessarily mean affordable.
Take a baseline hemoglobin A1c and repeat it after the patient has been on the medication for 2-3 weeks. Also remind them that they can’t rely solely on the medication but need to practice portion control and healthier eating and to exercise more.
For myself, I want to lose those remaining 20 lb or so by eating healthy and being physically active without having to rely on medication for the rest of my life. Research on these medications is still early so we don’t know the long-term effects yet.
As clinicians, I feel it’s okay to be honest with our patients about our own personal struggles to help them understand that they are not alone and that losing weight is a challenge for everyone.
Dr. Swiner is a family physician in Durham, N.C. She reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
With the rising popularity of weight-loss drug injections, I’ve received many questions from patients about the pros, cons, and costs. While Ozempic (semaglutide) is perhaps the best known, it’s technically an agent approved only for type 2 diabetes that has been used off label for obesity. The same substance, semaglutide, is approved for use in obesity, but at a higher dose, under the brand name Wegovy. Alternatives are available, and results will vary depending on the specific agent used and the individual.
Ultimately, I decided to try these new injections for myself. I am not a paid representative for, nor an advocate of, any of these medications; I’m here only to share my personal experience.
In my discussions with patients about weight, I sometimes felt like an imposter. While I was overweight by medical standards, I fortunately had none of the underlying health problems. I wasn’t on medications for blood pressure nor did I have diabetes, but I was counseling people to lose weight and eat better while not always following my own advice.
Since having children and turning 40, my metabolism, like many other women’s, seems to have plummeted. I tried a number of older weight-loss medications, like phentermine and phendimetrazine, under the supervision of medical professionals.
Each time, the efforts worked for a short while, particularly when I followed good portion control and practiced moderate exercise. Once the side effects (that is, tachycardia, palpitations, mood changes, constipation) became intolerable, or I became tired or fearful of being on the medications too long, I’d stop and I would regain some of the weight.
When the newer subcutaneous injectable medications arrived on the scene and I started to talk to my patients about them, I was intrigued by their novel mode of action and seeming benefits.
These medications, glucagonlike peptide–1 (GLP-1) receptor agonists, were first approved for type 2 diabetes, and it soon became apparent that patients were losing significant amounts of weight taking them, so manufacturers conducted further trials in obesity patients without type 2 diabetes.
The first of these, liraglutide, is injected daily and was first approved as Victoza for type 2 diabetes; it later received an additional approval for obesity, in December 2014, as Saxenda.
Semaglutide, another of the new GLP-1 agonists, was first approved for type 2 diabetes as Ozempic but again was found to lead to substantial weight loss, so a subsequent approval of the drug for obesity, as Wegovy, came in June 2021. Semaglutide is injected once a week.
Semaglutide was branded a “game changer” when it was licensed for obesity because the mean weight loss seen in trials was around 15%, more than for any other drug and approaching what could be achieved with bariatric surgery, some doctors said.
These medications work in a different way from the older weight loss drugs, which had focused on the use of amphetamines. The newer medications became very popular because treating obesity helps lower blood glucose, blood pressure, cholesterol, kidney disease risk, and other comorbidities that occur with diabetes. Plus, for most people, there were fewer side effects.
I first tried Saxenda when it arrived on the market, via some samples that our pharmaceutical representative brought, both out of curiosity and to see if it would help me lose the stubborn baby weight. I ended up stopping the daily injections after my second or third week because of nausea and vomiting. I took a break, got a prescription for antinausea medicine, and tried again because it did indeed decrease my appetite. However, when I took my prescription to the pharmacy, my insurance wouldn’t cover it. It happens to doctors, too.
Fast-forward to 2017-2018. The baby weight was still holding on despite lifestyle changes, diet, and exercising. The newer drug classes hit the market, and again we had samples from our reps.
When Ozempic was on backorder, I switched to a low dose of Mounjaro (tirzepatide), a new dual GLP-1 and glucose-dependent insulinotropic polypeptide agonist, approved for type 2 diabetes in May 2022, again using it off label as a weekly injection, as it isn’t currently approved for weight loss. However, it does produce significant weight loss and is awaiting approval for obesity.
With these new medications, I noticed that both my patients and I didn’t complain as much about nausea and vomiting, but I did experience stomach upset, constipation, and acid reflux.
The appetite suppression is effective. It slows down the emptying of the gut so I feel full longer. I’ve lost 30 lb with these weekly injections and would like to lose another 20 lb. I follow a routine of reasonable, portion-controlled eating and moderate exercise (30 minutes of cardiovascular activity at least two to three times a week).
Discontinuing the medications may cause rebound weight gain, especially if I’m no longer following a routine of healthy eating and/or moderate exercise. I deal with minimal constipation by taking stool softeners, and I take antacids for acid reflux.
Here’s what I recommend applying when working with patients who have obesity: First, explain how these medications work. Then conduct a health history to make sure these injections are right for them. Patients with a family history of pancreatic cancer can’t take these medications. You also want to monitor use in patients with a history of hypoglycemia so their blood sugar doesn’t drop too low. It’s also important to make sure your patients are able to afford the medication. My husband takes Ozempic for diabetes, and recently we were told that a refill would cost about $1,500 a month, even with insurance. “Covered” doesn’t necessarily mean affordable.
Take a baseline hemoglobin A1c and repeat it after the patient has been on the medication for 2-3 weeks. Also remind them that they can’t rely solely on the medication but need to practice portion control and healthier eating and to exercise more.
For myself, I want to lose those remaining 20 lb or so by eating healthy and being physically active without having to rely on medication for the rest of my life. Research on these medications is still early so we don’t know the long-term effects yet.
As clinicians, I feel it’s okay to be honest with our patients about our own personal struggles to help them understand that they are not alone and that losing weight is a challenge for everyone.
Dr. Swiner is a family physician in Durham, N.C. She reported no conflicts of interest.
A version of this article first appeared on Medscape.com.