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Understanding the enduring power of caste
Isabel Wilkerson’s naming of the malady facilitates space for a shift in thinking.
America has been struggling to understand its racial dynamics since the arrival of enslaved Africans more than 400 years ago. Today, with much of the world more polarized than ever, and certainly in our United States, there is a need for something to shift us from our fear and survival paranoid schizoid (us-vs.-them) position to an integrated form if we are to come out of this unusual democratic and societal unrest whole.
Yet, we’ve never had the lexicon to adequately describe the sociopolitical dynamics rooted in race and racism and their power to shape the thinking of all who originate in this country and all who enter its self-made borders whether forcefully or voluntarily. Enter Isabel Wilkerson, a Pulitzer Prize–winning, former New York Times Chicago bureau chief, and author of “The Warmth of Other Suns: The Epic Story of America’s Great Migration” (New York: Random House, 2010) with her second book, “Caste: The Origins of Our Discontents” (New York: Random House, 2020).
Ms. Wilkerson quickly gets to work in an engaging storytelling style of weaving past to present with ideas she supports with letters from the past, historians’ impressions, research studies, and data. Her observations and research are bookended by the lead up to the 2016 presidential election and its aftermath on the one end, and the impending 2020 presidential election on the other. In her view, the reemergence of violence that has accelerated in the 21st century and the renewed commitment to promote white supremacy can be understood if we expand our view of race and racism to consider the enduring power of caste. For, in Ms. Wilkerson’s view, the fear of the 2042 U.S. census (which is predicted to reflect for the first time a non-White majority) is a driving force behind the dominant caste’s determination to maintain the status quo power dynamics in the United States.
In an effort to explain American’s racial hierarchy, Ms. Wilkerson explains the need for a new lexicon “that may sound like a foreign language,” but this is intentional on her part. She writes:
“To recalibrate how we see ourselves, I use language that may be more commonly associated with people in other cultures, to suggest a new way of understanding our hierarchy: Dominant caste, ruling majority, favored caste, or upper caste, instead of, or in addition to, white. Middle castes instead of, or in addition to, Asian or Latino. Subordinate caste, lowest caste, bottom caste, disfavored caste, historically stigmatized instead of African-American. Original, conquered, or indigenous peoples instead of, or in addition to, Native American. Marginalized people in addition to, or instead of, women of any race, or minorities of any kind.”
Early in the book Ms. Wilkerson anchors her argument in Rev. Dr. Martin Luther King Jr.’s sojourn to India. Rather than focus on the known history of Dr. King’s admiration of Mohandas Gandhi, Ms. Wilkerson directs our attention to Dr. King’s discovery of his connection to Dalits, those who had been considered “untouchables” until Bhimrao Ramji Ambedkar, the Indian economist, jurist, social reformer, and Dalit leader, fiercely and successfully advocated for a rebranding of his caste of origin; instead of “untouchables” they would be considered Dalits or “broken people.” Dr. King did not meet Mr. Ambedkar, who died 3 years before this journey, but Ms. Wilkerson writes that Dr. King acknowledged the kinship, “And he said unto himself, Yes, I am an untouchable, and every Negro in the United States is an untouchable.” The Dalits and Dr. King recognized in each other their shared positions as subordinates in a global caste system.
In answering the question about the difference between racism and casteism, Ms. Wilkerson writes:
“Because caste and race are interwoven in America, it can be hard to separate the two. ... Casteism is the investment in keeping the hierarchy as it is in order to maintain your own ranking, advantage, privilege, or to elevate yourself above others or to keep others beneath you.”
Reading “Caste: The Origins of Our Discontents” is akin to the experience of gaining relief after struggling for years with a chronic malady that has a fluctuating course: Under the surface is low-grade pain that is compartmentalized and often met with denial or gaslighting when symptoms and systems are reported to members of the dominant caste. Yet, when there are acute flare-ups and increasingly frequent deadly encounters, the defenses of denial are painfully revealed; structures are broken and sometimes burned down. This has been the clinical course of racism, particularly in the United States. In that vein, an early reaction while reading “Caste” might be comparable to hearing an interpretation that educates, clarifies, resonates, and lands perfectly on the right diagnosis at the right moment.
Approach proves clarifying
In conceptualizing the malady as one of caste, Ms. Wilkerson achieves several things simultaneously – she names the malady, thus providing a lexicon, describes its symptoms, and most importantly, in our opinion, shares some of the compelling data from her field studies. By focusing on India, Nazi Germany, and the United States, she describes how easily one system influences another in the global effort to maintain power among the privileged.
This is not a new way of conceptualizing racial hierarchy; however, what is truly persuasive is Ms. Wilkerson’s ability to weave her rigorous research, sociopolitical analysis, and cogent psychological insights and interpretations to explain the 400-year trajectory of racialized caste in the United States. She achieves this exigent task with beautiful prose that motivates the reader to return time and time again to learn gut-wrenching painful historical details. She summarizes truths that have been unearthed (again) about Germany, India, and, in particular, the United States during her research and travels around the world. In doing so, she provides vivid examples of racism layered on caste. Consider the following:
“The Nazis were impressed by the American custom of lynching its subordinate caste of African-Americans, having become aware of the ritual torture and mutilations that typically accompanied them. Hitler especially marveled at the American ‘knack for maintaining an air of robust innocence in the wake of mass death.’ ” Ms. Wilkerson informs us that Hitler sent emissaries to study America’s Jim Crow system and then imported some features to orchestrate the Holocaust in Nazi Germany.
and a corresponding sense of inadequacy in the presence of someone who is considered to be from a higher caste.
A painful account of interpersonal racism is captured as Ms. Wilkerson recounts her experience after a routine business flight from Chicago to Detroit. She details her difficulty leaving a rental car parking lot because she had become so disoriented after being profiled and accosted by Drug Enforcement Administration agents who had intercepted her in the airport terminal and followed her onto the airport shuttle bus as she attempted to reach her destination. She provides a description of “getting turned around in a parking lot that I had been to dozens of times, going in circles, not able to get out, not registering the signs to the exit, not seeing how to get to Interstate 94, when I knew full well how to get to I-94 after all the times I’d driven it. ... This was the thievery of caste, stealing the time and psychic resources of the marginalized, draining energy in an already uphill competition. They were not, like me, frozen and disoriented, trying to make sense of a public violation that seemed all the more menacing now that I could see it in full. The quiet mundanity of that terror has never left me, the scars outliving the cut.”
This account is consistent with the dissociative, disorienting dynamics of race-based trauma. Her experience is not uncommon and helps to explain the activism of those in the subordinate caste who have attained some measure of wealth, power, and influence, and are motivated to expend their resources (energy, time, fame, and/or wealth) to raise awareness about social and political injustices by calling out structural racism in medicine, protesting police use of force by taking a knee, boycotting sporting events, and even demanding that football stadiums be used as polling sites. At the end of the day, all of us who have “made it” know that when we leave our homes, our relegation to the subordinate caste determines how we are perceived and what landmines we must navigate to make it through the day and that determine whether we will make it home.
This tour de force work of art has the potential to be a game changer in the way that we think about racial polarization in the United States. It is hoped that this new language opens up a space that allows each of us to explore this hegemony while identifying our placement and actions we take to maintain it, for each of us undeniably has a position in this caste system.
Having this new lexicon summons to mind the reactions of patients who gain immediate relief from having their illnesses named. In the case of the U.S. malady that has gripped us all, Ms. Wilkerson reiterates the importance of naming the condition. She writes:
“Because, to truly understand America, we must open our eyes to the hidden work of a caste system that has gone unnamed but prevails among us to our collective detriment, to see that we have more in common with each other and with cultures that we might otherwise dismiss, and to summon the courage to consider that therein may lie the answers.”
The naming allows both doctor and patient to have greater insight, understanding its origins and course, as well as having hope that there is a remedy. Naming facilitates the space for a shift in thinking and implementation of treatment protocols, such as Nazi Germany’s “zero tolerance policy” of swastikas in comparison to the ongoing U.S. controversy about the display of Confederate symbols. At this point in history, we welcome a diagnosis that has the potential to shift us from these poles of dominant and subordinate, black and white, good and bad, toward integration and wholeness of the individual psyche and collective global community. This is similar to what Melanie Klein calls the depressive position. Ms. Wilkerson suggests, in relinquishing these polar splits, we increase our capacity to shift to a space where our psychic integration occurs and our inextricable interdependence and responsibility for one another are honored.
Dr. Dunlap is a psychiatrist and psychoanalyst, and clinical professor of psychiatry and behavioral sciences at George Washington University. She is interested in the management of “difference” – race, gender, ethnicity, and intersectionality – in dyadic relationships and group dynamics; and the impact of racism on interpersonal relationships in institutional structures. Dr. Dunlap practices in Washington and has no disclosures. Dr. Dennis is a clinical psychologist and psychoanalyst. Her interests are in gender and ethnic diversity, health equity, and supervision and training. Dr. Dennis practices in Washington and has no disclosures.
Isabel Wilkerson’s naming of the malady facilitates space for a shift in thinking.
Isabel Wilkerson’s naming of the malady facilitates space for a shift in thinking.
America has been struggling to understand its racial dynamics since the arrival of enslaved Africans more than 400 years ago. Today, with much of the world more polarized than ever, and certainly in our United States, there is a need for something to shift us from our fear and survival paranoid schizoid (us-vs.-them) position to an integrated form if we are to come out of this unusual democratic and societal unrest whole.
Yet, we’ve never had the lexicon to adequately describe the sociopolitical dynamics rooted in race and racism and their power to shape the thinking of all who originate in this country and all who enter its self-made borders whether forcefully or voluntarily. Enter Isabel Wilkerson, a Pulitzer Prize–winning, former New York Times Chicago bureau chief, and author of “The Warmth of Other Suns: The Epic Story of America’s Great Migration” (New York: Random House, 2010) with her second book, “Caste: The Origins of Our Discontents” (New York: Random House, 2020).
Ms. Wilkerson quickly gets to work in an engaging storytelling style of weaving past to present with ideas she supports with letters from the past, historians’ impressions, research studies, and data. Her observations and research are bookended by the lead up to the 2016 presidential election and its aftermath on the one end, and the impending 2020 presidential election on the other. In her view, the reemergence of violence that has accelerated in the 21st century and the renewed commitment to promote white supremacy can be understood if we expand our view of race and racism to consider the enduring power of caste. For, in Ms. Wilkerson’s view, the fear of the 2042 U.S. census (which is predicted to reflect for the first time a non-White majority) is a driving force behind the dominant caste’s determination to maintain the status quo power dynamics in the United States.
In an effort to explain American’s racial hierarchy, Ms. Wilkerson explains the need for a new lexicon “that may sound like a foreign language,” but this is intentional on her part. She writes:
“To recalibrate how we see ourselves, I use language that may be more commonly associated with people in other cultures, to suggest a new way of understanding our hierarchy: Dominant caste, ruling majority, favored caste, or upper caste, instead of, or in addition to, white. Middle castes instead of, or in addition to, Asian or Latino. Subordinate caste, lowest caste, bottom caste, disfavored caste, historically stigmatized instead of African-American. Original, conquered, or indigenous peoples instead of, or in addition to, Native American. Marginalized people in addition to, or instead of, women of any race, or minorities of any kind.”
Early in the book Ms. Wilkerson anchors her argument in Rev. Dr. Martin Luther King Jr.’s sojourn to India. Rather than focus on the known history of Dr. King’s admiration of Mohandas Gandhi, Ms. Wilkerson directs our attention to Dr. King’s discovery of his connection to Dalits, those who had been considered “untouchables” until Bhimrao Ramji Ambedkar, the Indian economist, jurist, social reformer, and Dalit leader, fiercely and successfully advocated for a rebranding of his caste of origin; instead of “untouchables” they would be considered Dalits or “broken people.” Dr. King did not meet Mr. Ambedkar, who died 3 years before this journey, but Ms. Wilkerson writes that Dr. King acknowledged the kinship, “And he said unto himself, Yes, I am an untouchable, and every Negro in the United States is an untouchable.” The Dalits and Dr. King recognized in each other their shared positions as subordinates in a global caste system.
In answering the question about the difference between racism and casteism, Ms. Wilkerson writes:
“Because caste and race are interwoven in America, it can be hard to separate the two. ... Casteism is the investment in keeping the hierarchy as it is in order to maintain your own ranking, advantage, privilege, or to elevate yourself above others or to keep others beneath you.”
Reading “Caste: The Origins of Our Discontents” is akin to the experience of gaining relief after struggling for years with a chronic malady that has a fluctuating course: Under the surface is low-grade pain that is compartmentalized and often met with denial or gaslighting when symptoms and systems are reported to members of the dominant caste. Yet, when there are acute flare-ups and increasingly frequent deadly encounters, the defenses of denial are painfully revealed; structures are broken and sometimes burned down. This has been the clinical course of racism, particularly in the United States. In that vein, an early reaction while reading “Caste” might be comparable to hearing an interpretation that educates, clarifies, resonates, and lands perfectly on the right diagnosis at the right moment.
Approach proves clarifying
In conceptualizing the malady as one of caste, Ms. Wilkerson achieves several things simultaneously – she names the malady, thus providing a lexicon, describes its symptoms, and most importantly, in our opinion, shares some of the compelling data from her field studies. By focusing on India, Nazi Germany, and the United States, she describes how easily one system influences another in the global effort to maintain power among the privileged.
This is not a new way of conceptualizing racial hierarchy; however, what is truly persuasive is Ms. Wilkerson’s ability to weave her rigorous research, sociopolitical analysis, and cogent psychological insights and interpretations to explain the 400-year trajectory of racialized caste in the United States. She achieves this exigent task with beautiful prose that motivates the reader to return time and time again to learn gut-wrenching painful historical details. She summarizes truths that have been unearthed (again) about Germany, India, and, in particular, the United States during her research and travels around the world. In doing so, she provides vivid examples of racism layered on caste. Consider the following:
“The Nazis were impressed by the American custom of lynching its subordinate caste of African-Americans, having become aware of the ritual torture and mutilations that typically accompanied them. Hitler especially marveled at the American ‘knack for maintaining an air of robust innocence in the wake of mass death.’ ” Ms. Wilkerson informs us that Hitler sent emissaries to study America’s Jim Crow system and then imported some features to orchestrate the Holocaust in Nazi Germany.
and a corresponding sense of inadequacy in the presence of someone who is considered to be from a higher caste.
A painful account of interpersonal racism is captured as Ms. Wilkerson recounts her experience after a routine business flight from Chicago to Detroit. She details her difficulty leaving a rental car parking lot because she had become so disoriented after being profiled and accosted by Drug Enforcement Administration agents who had intercepted her in the airport terminal and followed her onto the airport shuttle bus as she attempted to reach her destination. She provides a description of “getting turned around in a parking lot that I had been to dozens of times, going in circles, not able to get out, not registering the signs to the exit, not seeing how to get to Interstate 94, when I knew full well how to get to I-94 after all the times I’d driven it. ... This was the thievery of caste, stealing the time and psychic resources of the marginalized, draining energy in an already uphill competition. They were not, like me, frozen and disoriented, trying to make sense of a public violation that seemed all the more menacing now that I could see it in full. The quiet mundanity of that terror has never left me, the scars outliving the cut.”
This account is consistent with the dissociative, disorienting dynamics of race-based trauma. Her experience is not uncommon and helps to explain the activism of those in the subordinate caste who have attained some measure of wealth, power, and influence, and are motivated to expend their resources (energy, time, fame, and/or wealth) to raise awareness about social and political injustices by calling out structural racism in medicine, protesting police use of force by taking a knee, boycotting sporting events, and even demanding that football stadiums be used as polling sites. At the end of the day, all of us who have “made it” know that when we leave our homes, our relegation to the subordinate caste determines how we are perceived and what landmines we must navigate to make it through the day and that determine whether we will make it home.
This tour de force work of art has the potential to be a game changer in the way that we think about racial polarization in the United States. It is hoped that this new language opens up a space that allows each of us to explore this hegemony while identifying our placement and actions we take to maintain it, for each of us undeniably has a position in this caste system.
Having this new lexicon summons to mind the reactions of patients who gain immediate relief from having their illnesses named. In the case of the U.S. malady that has gripped us all, Ms. Wilkerson reiterates the importance of naming the condition. She writes:
“Because, to truly understand America, we must open our eyes to the hidden work of a caste system that has gone unnamed but prevails among us to our collective detriment, to see that we have more in common with each other and with cultures that we might otherwise dismiss, and to summon the courage to consider that therein may lie the answers.”
The naming allows both doctor and patient to have greater insight, understanding its origins and course, as well as having hope that there is a remedy. Naming facilitates the space for a shift in thinking and implementation of treatment protocols, such as Nazi Germany’s “zero tolerance policy” of swastikas in comparison to the ongoing U.S. controversy about the display of Confederate symbols. At this point in history, we welcome a diagnosis that has the potential to shift us from these poles of dominant and subordinate, black and white, good and bad, toward integration and wholeness of the individual psyche and collective global community. This is similar to what Melanie Klein calls the depressive position. Ms. Wilkerson suggests, in relinquishing these polar splits, we increase our capacity to shift to a space where our psychic integration occurs and our inextricable interdependence and responsibility for one another are honored.
Dr. Dunlap is a psychiatrist and psychoanalyst, and clinical professor of psychiatry and behavioral sciences at George Washington University. She is interested in the management of “difference” – race, gender, ethnicity, and intersectionality – in dyadic relationships and group dynamics; and the impact of racism on interpersonal relationships in institutional structures. Dr. Dunlap practices in Washington and has no disclosures. Dr. Dennis is a clinical psychologist and psychoanalyst. Her interests are in gender and ethnic diversity, health equity, and supervision and training. Dr. Dennis practices in Washington and has no disclosures.
America has been struggling to understand its racial dynamics since the arrival of enslaved Africans more than 400 years ago. Today, with much of the world more polarized than ever, and certainly in our United States, there is a need for something to shift us from our fear and survival paranoid schizoid (us-vs.-them) position to an integrated form if we are to come out of this unusual democratic and societal unrest whole.
Yet, we’ve never had the lexicon to adequately describe the sociopolitical dynamics rooted in race and racism and their power to shape the thinking of all who originate in this country and all who enter its self-made borders whether forcefully or voluntarily. Enter Isabel Wilkerson, a Pulitzer Prize–winning, former New York Times Chicago bureau chief, and author of “The Warmth of Other Suns: The Epic Story of America’s Great Migration” (New York: Random House, 2010) with her second book, “Caste: The Origins of Our Discontents” (New York: Random House, 2020).
Ms. Wilkerson quickly gets to work in an engaging storytelling style of weaving past to present with ideas she supports with letters from the past, historians’ impressions, research studies, and data. Her observations and research are bookended by the lead up to the 2016 presidential election and its aftermath on the one end, and the impending 2020 presidential election on the other. In her view, the reemergence of violence that has accelerated in the 21st century and the renewed commitment to promote white supremacy can be understood if we expand our view of race and racism to consider the enduring power of caste. For, in Ms. Wilkerson’s view, the fear of the 2042 U.S. census (which is predicted to reflect for the first time a non-White majority) is a driving force behind the dominant caste’s determination to maintain the status quo power dynamics in the United States.
In an effort to explain American’s racial hierarchy, Ms. Wilkerson explains the need for a new lexicon “that may sound like a foreign language,” but this is intentional on her part. She writes:
“To recalibrate how we see ourselves, I use language that may be more commonly associated with people in other cultures, to suggest a new way of understanding our hierarchy: Dominant caste, ruling majority, favored caste, or upper caste, instead of, or in addition to, white. Middle castes instead of, or in addition to, Asian or Latino. Subordinate caste, lowest caste, bottom caste, disfavored caste, historically stigmatized instead of African-American. Original, conquered, or indigenous peoples instead of, or in addition to, Native American. Marginalized people in addition to, or instead of, women of any race, or minorities of any kind.”
Early in the book Ms. Wilkerson anchors her argument in Rev. Dr. Martin Luther King Jr.’s sojourn to India. Rather than focus on the known history of Dr. King’s admiration of Mohandas Gandhi, Ms. Wilkerson directs our attention to Dr. King’s discovery of his connection to Dalits, those who had been considered “untouchables” until Bhimrao Ramji Ambedkar, the Indian economist, jurist, social reformer, and Dalit leader, fiercely and successfully advocated for a rebranding of his caste of origin; instead of “untouchables” they would be considered Dalits or “broken people.” Dr. King did not meet Mr. Ambedkar, who died 3 years before this journey, but Ms. Wilkerson writes that Dr. King acknowledged the kinship, “And he said unto himself, Yes, I am an untouchable, and every Negro in the United States is an untouchable.” The Dalits and Dr. King recognized in each other their shared positions as subordinates in a global caste system.
In answering the question about the difference between racism and casteism, Ms. Wilkerson writes:
“Because caste and race are interwoven in America, it can be hard to separate the two. ... Casteism is the investment in keeping the hierarchy as it is in order to maintain your own ranking, advantage, privilege, or to elevate yourself above others or to keep others beneath you.”
Reading “Caste: The Origins of Our Discontents” is akin to the experience of gaining relief after struggling for years with a chronic malady that has a fluctuating course: Under the surface is low-grade pain that is compartmentalized and often met with denial or gaslighting when symptoms and systems are reported to members of the dominant caste. Yet, when there are acute flare-ups and increasingly frequent deadly encounters, the defenses of denial are painfully revealed; structures are broken and sometimes burned down. This has been the clinical course of racism, particularly in the United States. In that vein, an early reaction while reading “Caste” might be comparable to hearing an interpretation that educates, clarifies, resonates, and lands perfectly on the right diagnosis at the right moment.
Approach proves clarifying
In conceptualizing the malady as one of caste, Ms. Wilkerson achieves several things simultaneously – she names the malady, thus providing a lexicon, describes its symptoms, and most importantly, in our opinion, shares some of the compelling data from her field studies. By focusing on India, Nazi Germany, and the United States, she describes how easily one system influences another in the global effort to maintain power among the privileged.
This is not a new way of conceptualizing racial hierarchy; however, what is truly persuasive is Ms. Wilkerson’s ability to weave her rigorous research, sociopolitical analysis, and cogent psychological insights and interpretations to explain the 400-year trajectory of racialized caste in the United States. She achieves this exigent task with beautiful prose that motivates the reader to return time and time again to learn gut-wrenching painful historical details. She summarizes truths that have been unearthed (again) about Germany, India, and, in particular, the United States during her research and travels around the world. In doing so, she provides vivid examples of racism layered on caste. Consider the following:
“The Nazis were impressed by the American custom of lynching its subordinate caste of African-Americans, having become aware of the ritual torture and mutilations that typically accompanied them. Hitler especially marveled at the American ‘knack for maintaining an air of robust innocence in the wake of mass death.’ ” Ms. Wilkerson informs us that Hitler sent emissaries to study America’s Jim Crow system and then imported some features to orchestrate the Holocaust in Nazi Germany.
and a corresponding sense of inadequacy in the presence of someone who is considered to be from a higher caste.
A painful account of interpersonal racism is captured as Ms. Wilkerson recounts her experience after a routine business flight from Chicago to Detroit. She details her difficulty leaving a rental car parking lot because she had become so disoriented after being profiled and accosted by Drug Enforcement Administration agents who had intercepted her in the airport terminal and followed her onto the airport shuttle bus as she attempted to reach her destination. She provides a description of “getting turned around in a parking lot that I had been to dozens of times, going in circles, not able to get out, not registering the signs to the exit, not seeing how to get to Interstate 94, when I knew full well how to get to I-94 after all the times I’d driven it. ... This was the thievery of caste, stealing the time and psychic resources of the marginalized, draining energy in an already uphill competition. They were not, like me, frozen and disoriented, trying to make sense of a public violation that seemed all the more menacing now that I could see it in full. The quiet mundanity of that terror has never left me, the scars outliving the cut.”
This account is consistent with the dissociative, disorienting dynamics of race-based trauma. Her experience is not uncommon and helps to explain the activism of those in the subordinate caste who have attained some measure of wealth, power, and influence, and are motivated to expend their resources (energy, time, fame, and/or wealth) to raise awareness about social and political injustices by calling out structural racism in medicine, protesting police use of force by taking a knee, boycotting sporting events, and even demanding that football stadiums be used as polling sites. At the end of the day, all of us who have “made it” know that when we leave our homes, our relegation to the subordinate caste determines how we are perceived and what landmines we must navigate to make it through the day and that determine whether we will make it home.
This tour de force work of art has the potential to be a game changer in the way that we think about racial polarization in the United States. It is hoped that this new language opens up a space that allows each of us to explore this hegemony while identifying our placement and actions we take to maintain it, for each of us undeniably has a position in this caste system.
Having this new lexicon summons to mind the reactions of patients who gain immediate relief from having their illnesses named. In the case of the U.S. malady that has gripped us all, Ms. Wilkerson reiterates the importance of naming the condition. She writes:
“Because, to truly understand America, we must open our eyes to the hidden work of a caste system that has gone unnamed but prevails among us to our collective detriment, to see that we have more in common with each other and with cultures that we might otherwise dismiss, and to summon the courage to consider that therein may lie the answers.”
The naming allows both doctor and patient to have greater insight, understanding its origins and course, as well as having hope that there is a remedy. Naming facilitates the space for a shift in thinking and implementation of treatment protocols, such as Nazi Germany’s “zero tolerance policy” of swastikas in comparison to the ongoing U.S. controversy about the display of Confederate symbols. At this point in history, we welcome a diagnosis that has the potential to shift us from these poles of dominant and subordinate, black and white, good and bad, toward integration and wholeness of the individual psyche and collective global community. This is similar to what Melanie Klein calls the depressive position. Ms. Wilkerson suggests, in relinquishing these polar splits, we increase our capacity to shift to a space where our psychic integration occurs and our inextricable interdependence and responsibility for one another are honored.
Dr. Dunlap is a psychiatrist and psychoanalyst, and clinical professor of psychiatry and behavioral sciences at George Washington University. She is interested in the management of “difference” – race, gender, ethnicity, and intersectionality – in dyadic relationships and group dynamics; and the impact of racism on interpersonal relationships in institutional structures. Dr. Dunlap practices in Washington and has no disclosures. Dr. Dennis is a clinical psychologist and psychoanalyst. Her interests are in gender and ethnic diversity, health equity, and supervision and training. Dr. Dennis practices in Washington and has no disclosures.
Suicide rates up significantly among adolescents, young adults
Suicide rates in young people aged 10-24 years increased significantly in 42 states from 2007-2009 to 2016-2018, according to a recent analysis from the National Center for Health Statistics.
Nationally, the suicide rate jumped 47%, based on the averages for the two 3-year periods, rising from 7.0 per 100,000 persons aged 10-24 years to 10.3 per 100,000. For all ages, the corresponding increase was 47%, Sally C. Curtin, MA, of the NCHS, said in a National Vital Statistics Report.
There was no state with a decrease in suicide rates for adolescents and young adults, as the other eight all had nonsignificant increases, the smallest being 14% in South Dakota. Three-year averages were used to increase statistical power for states with relatively small numbers of deaths but were still not enough to show significance for some large increases, such as the 48% rise in Delaware, Ms. Curtin noted.
In 2016-2018, Alaska’s suicide rate of 31.8 per 100,000 persons aged 10-24 years was the highest in the country, followed by South Dakota (23.6), Montana (23.2), and Wyoming (20.5). New Jersey had the lowest rate at 5.7 per 100,000, with New York and Rhode Island both slightly higher at 5.9 and Connecticut at 6.3, based on data from the National Vital Statistics System.
Even the low numbers, however, hide some large changes, as New Jersey (up by 39%) and New York (up by 44%) were among the 42 states with statistically significant increases, which ranged from 21.7% in Maryland to 110% in New Hampshire, Ms. Curtin said in the report. The increases seen in this analysis contrast with data from the preceding time period, as “the suicide rate among persons aged 10-24 was statistically stable from 2000 to 2007.”
SOURCE: Curtin SC. National Vital Statistics Reports. 2020;69(11)1-9.
Suicide rates in young people aged 10-24 years increased significantly in 42 states from 2007-2009 to 2016-2018, according to a recent analysis from the National Center for Health Statistics.
Nationally, the suicide rate jumped 47%, based on the averages for the two 3-year periods, rising from 7.0 per 100,000 persons aged 10-24 years to 10.3 per 100,000. For all ages, the corresponding increase was 47%, Sally C. Curtin, MA, of the NCHS, said in a National Vital Statistics Report.
There was no state with a decrease in suicide rates for adolescents and young adults, as the other eight all had nonsignificant increases, the smallest being 14% in South Dakota. Three-year averages were used to increase statistical power for states with relatively small numbers of deaths but were still not enough to show significance for some large increases, such as the 48% rise in Delaware, Ms. Curtin noted.
In 2016-2018, Alaska’s suicide rate of 31.8 per 100,000 persons aged 10-24 years was the highest in the country, followed by South Dakota (23.6), Montana (23.2), and Wyoming (20.5). New Jersey had the lowest rate at 5.7 per 100,000, with New York and Rhode Island both slightly higher at 5.9 and Connecticut at 6.3, based on data from the National Vital Statistics System.
Even the low numbers, however, hide some large changes, as New Jersey (up by 39%) and New York (up by 44%) were among the 42 states with statistically significant increases, which ranged from 21.7% in Maryland to 110% in New Hampshire, Ms. Curtin said in the report. The increases seen in this analysis contrast with data from the preceding time period, as “the suicide rate among persons aged 10-24 was statistically stable from 2000 to 2007.”
SOURCE: Curtin SC. National Vital Statistics Reports. 2020;69(11)1-9.
Suicide rates in young people aged 10-24 years increased significantly in 42 states from 2007-2009 to 2016-2018, according to a recent analysis from the National Center for Health Statistics.
Nationally, the suicide rate jumped 47%, based on the averages for the two 3-year periods, rising from 7.0 per 100,000 persons aged 10-24 years to 10.3 per 100,000. For all ages, the corresponding increase was 47%, Sally C. Curtin, MA, of the NCHS, said in a National Vital Statistics Report.
There was no state with a decrease in suicide rates for adolescents and young adults, as the other eight all had nonsignificant increases, the smallest being 14% in South Dakota. Three-year averages were used to increase statistical power for states with relatively small numbers of deaths but were still not enough to show significance for some large increases, such as the 48% rise in Delaware, Ms. Curtin noted.
In 2016-2018, Alaska’s suicide rate of 31.8 per 100,000 persons aged 10-24 years was the highest in the country, followed by South Dakota (23.6), Montana (23.2), and Wyoming (20.5). New Jersey had the lowest rate at 5.7 per 100,000, with New York and Rhode Island both slightly higher at 5.9 and Connecticut at 6.3, based on data from the National Vital Statistics System.
Even the low numbers, however, hide some large changes, as New Jersey (up by 39%) and New York (up by 44%) were among the 42 states with statistically significant increases, which ranged from 21.7% in Maryland to 110% in New Hampshire, Ms. Curtin said in the report. The increases seen in this analysis contrast with data from the preceding time period, as “the suicide rate among persons aged 10-24 was statistically stable from 2000 to 2007.”
SOURCE: Curtin SC. National Vital Statistics Reports. 2020;69(11)1-9.
Breathing enriched oxygen improves major depression
Maybe the hipsters patronizing trendy oxygen bars seeking elevation of mood back in the prepandemic era were actually onto something – because Israeli investigators have now shown in a pilot double-blind, placebo-controlled, randomized trial that breathing enriched oxygen on a nightly basis resulted in clinically meaningful symptomatic improvement in mild to moderate major depression.
“We saw a highly significant effect of normobaric hyperoxia therapy in lowering Hamilton Rating Scale for Depression scores,” R. Haim Belmaker, MD, reported at the virtual congress of the European College of Neuropsychopharmacology.
In addition, the patients on enriched oxygen also showed statistically significant and clinically meaningful improvements relative to sham-treated controls on the secondary endpoints of Clinical Global Impressions Scale, the World Health Organization–Five Well-Being Index, the Sheehan Disability Scale, and the Sense of Coherence Scale, added Dr. Belmaker, professor emeritus of psychiatry at the Ben Gurion University of the Negev in Beersheva, Israel.
Numerous PET imaging studies have documented diminished brain mitochondrial function in patients with depression or schizophrenia. And mitochondria need oxygen to do their work. Yet, the idea of administering enriched oxygen in an effort to boost mitochondrial energy metabolism has long been viewed with skepticism – even though it’s a simple and well-tolerated intervention – because of the fact that 90%-95% of the oxygen supply is carried bound to hemoglobin, and oxygen enrichment doesn’t further increase hemoglobin saturation in individuals with normal lung function. However, recently it has been shown that inspired enriched oxygen roughly doubles arterial oxygen tension, and while this doesn’t translate into anything close to a doubled oxygen supply to tissues, it may result in increased oxygen diffusion into brain tissue, the psychiatrist explained.
Normobaric hyperoxia therapy is not to be confused with hyperbaric oxygen therapy, which requires a special chamber to handle markedly increased atmospheric pressures and has some inherent dangers. Mobile bedside oxygen generator units for oxygen enrichment are commercially available over the counter. Those used in the Israeli study were about the size of a vacuum cleaner and weighed a little more than 40 lb. Much smaller, more convenient units are available as well, but are costlier.
Dr. Belmaker reported on 51 adults with mild or moderate symptoms of major depressive disorder and a mean 11-year disease history who were randomized double blind to breathe either 35% oxygen or normal air – that is, 21% oxygen – at 1 atm pressure delivered from an investigator-supplied oxygen generator through standard plastic nasal prongs at a flow rate of 5 L/min for 7 hours nightly for 1 month.
“Controls heard the same flow and felt the same feeling on the face but were receiving 21% oxygen,” he noted.
Oxygen generator units are capable of enriching air to more than 90% oxygen; however, the investigators wanted to be cautious in a pilot study of an untested therapy, and they found evidence from both animal and human studies that 40% oxygen is reassuringly safe. Study exclusion criteria included obesity, acute or chronic respiratory disease, psychosis, and suicidality.
The primary study endpoint was the change in Hamilton Rating Scale for Depression score at 1 month. From a mean baseline of 14.6, the score in the normobaric hyperoxia group dropped by more than 4 points while remaining unchanged in controls. In a subscale analysis, it was apparent that most of the improvement occurred in the anxiety and cognitive disturbance subscale domains, according to Dr. Belmaker.
Of note, all patients rated by blinded investigators as much improved or very much improved on the Clinical Global Impression scale came from the enriched oxygen group.
No treatment-related adverse events occurred in the study.
“We don’t know the mechanism of the benefit of oxygen on the brain. It’s complex. In stroke and acute MI we used to think oxygen was beneficial, but scientists now feel that it’s not,” the psychiatrist said. “This early data deserve replication with higher concentrations of oxygen, different time periods of application, and in different patient groups.”
He emphasized that, since individuals with physical illnesses – including sleep apnea and chronic obstructive pulmonary disease – were excluded from the study, it’s not possible to say whether normobaric hyperoxia therapy would have an antidepressant effect in such patients.
“I would be especially careful with the normobaric oxygen in any patients with any cardiovascular or hypertensive disease because the increased oxygen pressure can have the side effect of contracting cardiac capillaries as a reflex action. So I certainly cannot recommend applying this study in any patients with a physical disease at this point,” Dr. Belmaker emphasized.
He reported having no financial conflicts regarding the study, funded by a grant from the Brain and Behavior Research Foundation.
SOURCE: Belmaker RH. ECNP 2020, Session S.12.
Maybe the hipsters patronizing trendy oxygen bars seeking elevation of mood back in the prepandemic era were actually onto something – because Israeli investigators have now shown in a pilot double-blind, placebo-controlled, randomized trial that breathing enriched oxygen on a nightly basis resulted in clinically meaningful symptomatic improvement in mild to moderate major depression.
“We saw a highly significant effect of normobaric hyperoxia therapy in lowering Hamilton Rating Scale for Depression scores,” R. Haim Belmaker, MD, reported at the virtual congress of the European College of Neuropsychopharmacology.
In addition, the patients on enriched oxygen also showed statistically significant and clinically meaningful improvements relative to sham-treated controls on the secondary endpoints of Clinical Global Impressions Scale, the World Health Organization–Five Well-Being Index, the Sheehan Disability Scale, and the Sense of Coherence Scale, added Dr. Belmaker, professor emeritus of psychiatry at the Ben Gurion University of the Negev in Beersheva, Israel.
Numerous PET imaging studies have documented diminished brain mitochondrial function in patients with depression or schizophrenia. And mitochondria need oxygen to do their work. Yet, the idea of administering enriched oxygen in an effort to boost mitochondrial energy metabolism has long been viewed with skepticism – even though it’s a simple and well-tolerated intervention – because of the fact that 90%-95% of the oxygen supply is carried bound to hemoglobin, and oxygen enrichment doesn’t further increase hemoglobin saturation in individuals with normal lung function. However, recently it has been shown that inspired enriched oxygen roughly doubles arterial oxygen tension, and while this doesn’t translate into anything close to a doubled oxygen supply to tissues, it may result in increased oxygen diffusion into brain tissue, the psychiatrist explained.
Normobaric hyperoxia therapy is not to be confused with hyperbaric oxygen therapy, which requires a special chamber to handle markedly increased atmospheric pressures and has some inherent dangers. Mobile bedside oxygen generator units for oxygen enrichment are commercially available over the counter. Those used in the Israeli study were about the size of a vacuum cleaner and weighed a little more than 40 lb. Much smaller, more convenient units are available as well, but are costlier.
Dr. Belmaker reported on 51 adults with mild or moderate symptoms of major depressive disorder and a mean 11-year disease history who were randomized double blind to breathe either 35% oxygen or normal air – that is, 21% oxygen – at 1 atm pressure delivered from an investigator-supplied oxygen generator through standard plastic nasal prongs at a flow rate of 5 L/min for 7 hours nightly for 1 month.
“Controls heard the same flow and felt the same feeling on the face but were receiving 21% oxygen,” he noted.
Oxygen generator units are capable of enriching air to more than 90% oxygen; however, the investigators wanted to be cautious in a pilot study of an untested therapy, and they found evidence from both animal and human studies that 40% oxygen is reassuringly safe. Study exclusion criteria included obesity, acute or chronic respiratory disease, psychosis, and suicidality.
The primary study endpoint was the change in Hamilton Rating Scale for Depression score at 1 month. From a mean baseline of 14.6, the score in the normobaric hyperoxia group dropped by more than 4 points while remaining unchanged in controls. In a subscale analysis, it was apparent that most of the improvement occurred in the anxiety and cognitive disturbance subscale domains, according to Dr. Belmaker.
Of note, all patients rated by blinded investigators as much improved or very much improved on the Clinical Global Impression scale came from the enriched oxygen group.
No treatment-related adverse events occurred in the study.
“We don’t know the mechanism of the benefit of oxygen on the brain. It’s complex. In stroke and acute MI we used to think oxygen was beneficial, but scientists now feel that it’s not,” the psychiatrist said. “This early data deserve replication with higher concentrations of oxygen, different time periods of application, and in different patient groups.”
He emphasized that, since individuals with physical illnesses – including sleep apnea and chronic obstructive pulmonary disease – were excluded from the study, it’s not possible to say whether normobaric hyperoxia therapy would have an antidepressant effect in such patients.
“I would be especially careful with the normobaric oxygen in any patients with any cardiovascular or hypertensive disease because the increased oxygen pressure can have the side effect of contracting cardiac capillaries as a reflex action. So I certainly cannot recommend applying this study in any patients with a physical disease at this point,” Dr. Belmaker emphasized.
He reported having no financial conflicts regarding the study, funded by a grant from the Brain and Behavior Research Foundation.
SOURCE: Belmaker RH. ECNP 2020, Session S.12.
Maybe the hipsters patronizing trendy oxygen bars seeking elevation of mood back in the prepandemic era were actually onto something – because Israeli investigators have now shown in a pilot double-blind, placebo-controlled, randomized trial that breathing enriched oxygen on a nightly basis resulted in clinically meaningful symptomatic improvement in mild to moderate major depression.
“We saw a highly significant effect of normobaric hyperoxia therapy in lowering Hamilton Rating Scale for Depression scores,” R. Haim Belmaker, MD, reported at the virtual congress of the European College of Neuropsychopharmacology.
In addition, the patients on enriched oxygen also showed statistically significant and clinically meaningful improvements relative to sham-treated controls on the secondary endpoints of Clinical Global Impressions Scale, the World Health Organization–Five Well-Being Index, the Sheehan Disability Scale, and the Sense of Coherence Scale, added Dr. Belmaker, professor emeritus of psychiatry at the Ben Gurion University of the Negev in Beersheva, Israel.
Numerous PET imaging studies have documented diminished brain mitochondrial function in patients with depression or schizophrenia. And mitochondria need oxygen to do their work. Yet, the idea of administering enriched oxygen in an effort to boost mitochondrial energy metabolism has long been viewed with skepticism – even though it’s a simple and well-tolerated intervention – because of the fact that 90%-95% of the oxygen supply is carried bound to hemoglobin, and oxygen enrichment doesn’t further increase hemoglobin saturation in individuals with normal lung function. However, recently it has been shown that inspired enriched oxygen roughly doubles arterial oxygen tension, and while this doesn’t translate into anything close to a doubled oxygen supply to tissues, it may result in increased oxygen diffusion into brain tissue, the psychiatrist explained.
Normobaric hyperoxia therapy is not to be confused with hyperbaric oxygen therapy, which requires a special chamber to handle markedly increased atmospheric pressures and has some inherent dangers. Mobile bedside oxygen generator units for oxygen enrichment are commercially available over the counter. Those used in the Israeli study were about the size of a vacuum cleaner and weighed a little more than 40 lb. Much smaller, more convenient units are available as well, but are costlier.
Dr. Belmaker reported on 51 adults with mild or moderate symptoms of major depressive disorder and a mean 11-year disease history who were randomized double blind to breathe either 35% oxygen or normal air – that is, 21% oxygen – at 1 atm pressure delivered from an investigator-supplied oxygen generator through standard plastic nasal prongs at a flow rate of 5 L/min for 7 hours nightly for 1 month.
“Controls heard the same flow and felt the same feeling on the face but were receiving 21% oxygen,” he noted.
Oxygen generator units are capable of enriching air to more than 90% oxygen; however, the investigators wanted to be cautious in a pilot study of an untested therapy, and they found evidence from both animal and human studies that 40% oxygen is reassuringly safe. Study exclusion criteria included obesity, acute or chronic respiratory disease, psychosis, and suicidality.
The primary study endpoint was the change in Hamilton Rating Scale for Depression score at 1 month. From a mean baseline of 14.6, the score in the normobaric hyperoxia group dropped by more than 4 points while remaining unchanged in controls. In a subscale analysis, it was apparent that most of the improvement occurred in the anxiety and cognitive disturbance subscale domains, according to Dr. Belmaker.
Of note, all patients rated by blinded investigators as much improved or very much improved on the Clinical Global Impression scale came from the enriched oxygen group.
No treatment-related adverse events occurred in the study.
“We don’t know the mechanism of the benefit of oxygen on the brain. It’s complex. In stroke and acute MI we used to think oxygen was beneficial, but scientists now feel that it’s not,” the psychiatrist said. “This early data deserve replication with higher concentrations of oxygen, different time periods of application, and in different patient groups.”
He emphasized that, since individuals with physical illnesses – including sleep apnea and chronic obstructive pulmonary disease – were excluded from the study, it’s not possible to say whether normobaric hyperoxia therapy would have an antidepressant effect in such patients.
“I would be especially careful with the normobaric oxygen in any patients with any cardiovascular or hypertensive disease because the increased oxygen pressure can have the side effect of contracting cardiac capillaries as a reflex action. So I certainly cannot recommend applying this study in any patients with a physical disease at this point,” Dr. Belmaker emphasized.
He reported having no financial conflicts regarding the study, funded by a grant from the Brain and Behavior Research Foundation.
SOURCE: Belmaker RH. ECNP 2020, Session S.12.
FROM ECNP 2020
More female specialists, but gender gap persists in pay, survey finds
More female physicians are becoming specialists, a Medscape survey finds, and five specialties have seen particularly large increases during the last 5 years.
Obstetrician/gynecologists and pediatricians had the largest female representation at 58% and those percentages were both up from 50% in 2015, according to the Medscape Female Physician Compensation Report 2020.
Rheumatology saw a dramatic jump in numbers of women from 29% in 2015 to 54% now. Dermatology increased from 32% to 49%, and family medicine rose from 35% to 43% during that time.
Specialist pay gap narrows slightly
The gender gap was the same this year in primary care — women made 25% less ($212,000 vs. $264,000).
The gap in specialists narrowed slightly. Women made 31% less this year ($286,000 vs $375,000) instead of the 33% less reported in last year’s survey, a difference of $89,000 this year.
The gender pay gap was consistent across all race and age groups and was consistent in responses about net worth. Whereas 57% of male physicians had a net worth of $1 million or more, only 40% of female physicians did. Twice as many male physicians as female physicians had a net worth of more than $5 million (10% vs. 5%).
“Many physicians expect the gender pay gap to narrow in the coming years,” John Prescott, MD, chief academic officer of the Association of American Medical Colleges, said in an interview.
“Yet, it is a challenging task, requiring an institutional commitment to transparency, cross-campus collaboration, ongoing communication, dedicated resources, and enlightened leadership,” he said.
Female physicians working in office-based, solo practices made the most overall at $290,000; women in outpatient settings made the least at $223,000.
The survey included more than 4,500 responses. The responses were collected during the early part of the year and do not reflect changes in income expected from the COVID-19 pandemic.
An analysis in Health Affairs, for instance, predicted that primary care practices would lose $67,774 in gross revenue per full-time-equivalent physician in calendar year 2020 because of the pandemic.
Most physicians did not experience a significant financial loss in 2019, but COVID-19 may, at least temporarily, change those answers in next year’s report, physicians predicted.
Women more likely than men to live above their means
More women this year (39%) said they live below their means than answered that way last year (31%). Female physicians were more likely to say they lived above their means than were their male counterparts (8% vs. 6%).
Greenwald Wealth Management in St. Louis Park, Minn., says aiming for putting away 20% of total gross salary is a good financial goal.
Women in this year’s survey spent about 7% less time seeing patients than did their male counterparts (35.9 hours a week vs. 38.8). The average for all physicians was 37.8 hours a week. Add the 15.6 average hours per week physicians spend on paperwork, and they are putting in 53-hour workweeks on average overall.
Asked what parts of their job they found most rewarding, women were more likely than were men to say “gratitude/relationships with patients” (31% vs. 25%). They were less likely than were men to answer that the most rewarding part was “being very good at what I do/finding answers/diagnoses” (22% vs. 25%) or “making good money at a job I like” (9% vs. 13%).
Most female physicians — and physicians overall — said they would choose medicine again. But two specialties saw a substantial increase in that answer.
This year, 79% of those in physical medicine and rehabilitation said they would choose medicine again (compared with 66% last year) and 84% of gastroenterologists answered that way (compared with 76% in 2019).
Psychiatrists, however, were in the group least likely to say they would choose their specialty again along with those in internal medicine, family medicine, and diabetes and endocrinology.
Female physicians in orthopedics, radiology, and dermatology were most likely to choose their specialties again (91% - 92%).
Female physicians were less likely to use physician assistants in their practices than were their male colleagues (31% vs. 38%) but more likely to use NPs (52% vs. 50%). More than a third (38%) of male and female physicians reported they use neither.
A version of this article originally appeared on Medscape.com.
More female physicians are becoming specialists, a Medscape survey finds, and five specialties have seen particularly large increases during the last 5 years.
Obstetrician/gynecologists and pediatricians had the largest female representation at 58% and those percentages were both up from 50% in 2015, according to the Medscape Female Physician Compensation Report 2020.
Rheumatology saw a dramatic jump in numbers of women from 29% in 2015 to 54% now. Dermatology increased from 32% to 49%, and family medicine rose from 35% to 43% during that time.
Specialist pay gap narrows slightly
The gender gap was the same this year in primary care — women made 25% less ($212,000 vs. $264,000).
The gap in specialists narrowed slightly. Women made 31% less this year ($286,000 vs $375,000) instead of the 33% less reported in last year’s survey, a difference of $89,000 this year.
The gender pay gap was consistent across all race and age groups and was consistent in responses about net worth. Whereas 57% of male physicians had a net worth of $1 million or more, only 40% of female physicians did. Twice as many male physicians as female physicians had a net worth of more than $5 million (10% vs. 5%).
“Many physicians expect the gender pay gap to narrow in the coming years,” John Prescott, MD, chief academic officer of the Association of American Medical Colleges, said in an interview.
“Yet, it is a challenging task, requiring an institutional commitment to transparency, cross-campus collaboration, ongoing communication, dedicated resources, and enlightened leadership,” he said.
Female physicians working in office-based, solo practices made the most overall at $290,000; women in outpatient settings made the least at $223,000.
The survey included more than 4,500 responses. The responses were collected during the early part of the year and do not reflect changes in income expected from the COVID-19 pandemic.
An analysis in Health Affairs, for instance, predicted that primary care practices would lose $67,774 in gross revenue per full-time-equivalent physician in calendar year 2020 because of the pandemic.
Most physicians did not experience a significant financial loss in 2019, but COVID-19 may, at least temporarily, change those answers in next year’s report, physicians predicted.
Women more likely than men to live above their means
More women this year (39%) said they live below their means than answered that way last year (31%). Female physicians were more likely to say they lived above their means than were their male counterparts (8% vs. 6%).
Greenwald Wealth Management in St. Louis Park, Minn., says aiming for putting away 20% of total gross salary is a good financial goal.
Women in this year’s survey spent about 7% less time seeing patients than did their male counterparts (35.9 hours a week vs. 38.8). The average for all physicians was 37.8 hours a week. Add the 15.6 average hours per week physicians spend on paperwork, and they are putting in 53-hour workweeks on average overall.
Asked what parts of their job they found most rewarding, women were more likely than were men to say “gratitude/relationships with patients” (31% vs. 25%). They were less likely than were men to answer that the most rewarding part was “being very good at what I do/finding answers/diagnoses” (22% vs. 25%) or “making good money at a job I like” (9% vs. 13%).
Most female physicians — and physicians overall — said they would choose medicine again. But two specialties saw a substantial increase in that answer.
This year, 79% of those in physical medicine and rehabilitation said they would choose medicine again (compared with 66% last year) and 84% of gastroenterologists answered that way (compared with 76% in 2019).
Psychiatrists, however, were in the group least likely to say they would choose their specialty again along with those in internal medicine, family medicine, and diabetes and endocrinology.
Female physicians in orthopedics, radiology, and dermatology were most likely to choose their specialties again (91% - 92%).
Female physicians were less likely to use physician assistants in their practices than were their male colleagues (31% vs. 38%) but more likely to use NPs (52% vs. 50%). More than a third (38%) of male and female physicians reported they use neither.
A version of this article originally appeared on Medscape.com.
More female physicians are becoming specialists, a Medscape survey finds, and five specialties have seen particularly large increases during the last 5 years.
Obstetrician/gynecologists and pediatricians had the largest female representation at 58% and those percentages were both up from 50% in 2015, according to the Medscape Female Physician Compensation Report 2020.
Rheumatology saw a dramatic jump in numbers of women from 29% in 2015 to 54% now. Dermatology increased from 32% to 49%, and family medicine rose from 35% to 43% during that time.
Specialist pay gap narrows slightly
The gender gap was the same this year in primary care — women made 25% less ($212,000 vs. $264,000).
The gap in specialists narrowed slightly. Women made 31% less this year ($286,000 vs $375,000) instead of the 33% less reported in last year’s survey, a difference of $89,000 this year.
The gender pay gap was consistent across all race and age groups and was consistent in responses about net worth. Whereas 57% of male physicians had a net worth of $1 million or more, only 40% of female physicians did. Twice as many male physicians as female physicians had a net worth of more than $5 million (10% vs. 5%).
“Many physicians expect the gender pay gap to narrow in the coming years,” John Prescott, MD, chief academic officer of the Association of American Medical Colleges, said in an interview.
“Yet, it is a challenging task, requiring an institutional commitment to transparency, cross-campus collaboration, ongoing communication, dedicated resources, and enlightened leadership,” he said.
Female physicians working in office-based, solo practices made the most overall at $290,000; women in outpatient settings made the least at $223,000.
The survey included more than 4,500 responses. The responses were collected during the early part of the year and do not reflect changes in income expected from the COVID-19 pandemic.
An analysis in Health Affairs, for instance, predicted that primary care practices would lose $67,774 in gross revenue per full-time-equivalent physician in calendar year 2020 because of the pandemic.
Most physicians did not experience a significant financial loss in 2019, but COVID-19 may, at least temporarily, change those answers in next year’s report, physicians predicted.
Women more likely than men to live above their means
More women this year (39%) said they live below their means than answered that way last year (31%). Female physicians were more likely to say they lived above their means than were their male counterparts (8% vs. 6%).
Greenwald Wealth Management in St. Louis Park, Minn., says aiming for putting away 20% of total gross salary is a good financial goal.
Women in this year’s survey spent about 7% less time seeing patients than did their male counterparts (35.9 hours a week vs. 38.8). The average for all physicians was 37.8 hours a week. Add the 15.6 average hours per week physicians spend on paperwork, and they are putting in 53-hour workweeks on average overall.
Asked what parts of their job they found most rewarding, women were more likely than were men to say “gratitude/relationships with patients” (31% vs. 25%). They were less likely than were men to answer that the most rewarding part was “being very good at what I do/finding answers/diagnoses” (22% vs. 25%) or “making good money at a job I like” (9% vs. 13%).
Most female physicians — and physicians overall — said they would choose medicine again. But two specialties saw a substantial increase in that answer.
This year, 79% of those in physical medicine and rehabilitation said they would choose medicine again (compared with 66% last year) and 84% of gastroenterologists answered that way (compared with 76% in 2019).
Psychiatrists, however, were in the group least likely to say they would choose their specialty again along with those in internal medicine, family medicine, and diabetes and endocrinology.
Female physicians in orthopedics, radiology, and dermatology were most likely to choose their specialties again (91% - 92%).
Female physicians were less likely to use physician assistants in their practices than were their male colleagues (31% vs. 38%) but more likely to use NPs (52% vs. 50%). More than a third (38%) of male and female physicians reported they use neither.
A version of this article originally appeared on Medscape.com.
New acute pain guidelines from the ACP and AAFP have limitations
The American College of Physicians and the American Academy of Family Physicians recently authored a guideline regarding the treatment of acute, non–low back, musculoskeletal injuries in adults in the outpatient setting.
According to the authors, musculoskeletal injuries result in more than 65 million medical visits a year with an annual estimated cost of $176.1 billion in 2010.
In summary, the guideline, which was published in the Annals of Internal Medicine, is based on a review of the best available evidence. The research reviewed by the guideline authors showed favorable results with topical NSAIDs, oral NSAIDs, oral acetaminophen, acupressure, and transcutaneous electrical nerve stimulation in reducing pain and/or improving function. The guideline authors “recommend that clinicians treat patients with acute pain from non–low back, musculoskeletal injuries with topical [NSAIDs] with or without gel as first-line therapy to reduce or relieve symptoms, including pain; improve physical function; and improve the patient’s treatment satisfaction (Grade: strong recommendation; moderate-certainty evidence).” Additionally, the guideline recommends against treating acute pain from non–low back, musculoskeletal injuries with opioids, including tramadol (Grade: conditional recommendation; low-certainty evidence).
The guideline also mentions improving function in relation to decreasing pain, which can be multifactorial.
Treating pain requires a multipronged approach. Many patients require more than one therapy to treat their pain, such as NSAIDs plus physical therapy. The ACP and AAFP did not make any recommendations for combination therapies in this guideline.
When physical therapy is needed
Nonopioid pain medications can do a great job of reducing a patient’s physical discomfort, which the evidence for these guideline demonstrates. However, much of the dysfunction caused by musculoskeletal injuries will not improve by reducing the pain alone. Physical therapy, exercise, and mobilization did not show a significant benefit in reducing symptoms in the systematic review and meta-analysis of randomized trials that appeared alongside the guideline. The type of pain, however, was not evaluated in relation to the effectiveness of these treatments. A fractured bone, for example, may heal just fine with casting and pain management, without the need for additional therapies. However, the muscles surrounding that bone can atrophy and become weak from not being used. Physical therapy may be needed to restrengthen those muscles. Therefore, a multifaceted approach is often needed, even for uncomplicated conditions.
Mental pain often comes with physical pain, and this is an aspect of care that is often neglected. It can be quite devastating for patients to not be able to do the things they were previously able to do. While this is easily recognized in professional athletes when they can no longer play, it is not so readily apparent with a mother who is just trying to take care of her kids. As doctors, especially those of us in family medicine, we should be addressing more than just physical pain.
Patients can also do activities that exacerbate their pain. As doctors, we need to be asking questions that help us determine whether a patient’s pain is caused by a particular action. Maybe that increase in shoulder pain is due to nothing more than lifting something heavy rather than a failure in a prescribed medication. Pain diaries are helpful, and clinicians don’t use them often enough.
How pain affects mental health
Acute injuries can also lead to disability. Many patients become quite distressed about being unable to work. They often need Famiy & Medical Leave Act forms filled out, and this task usually falls to the primary care doctor. In addition to assessing the pain, we need to be evaluating, at each visit, a patient’s level of functioning and their ability to do their job.
Every patient responds to pain differently, and it is important to evaluate patients’ mindsets regarding theirs. A patient may be in severe pain and may try to ignore it for a variety of reasons. A patient may “catastrophize” their pain, believing only the worst outcome will happen to them. Helping patients set appropriate expectations and having a positive mindset can help.
Overall, the new recommendations are a great tool as a guideline, but they are not complete enough to be the only ones used in managing acute, non–low back, musculoskeletal pain in adults.
They are very important for clinicians who may be prescribing opioid medications for patients with this type of pain. Amid an opioid crisis, it is the responsibility of every doctor to prescribe these medications appropriately. The evidence clearly shows they provide little benefit and place patients at risk of addiction.
We should all be following these recommendations as the baseline of care for acute pain. However, we need to delve deeper and manage all the components involved. We would be ignoring very real suffering in our patients if we limited our focus to only the physical discomfort.
Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Rutgers RWJ Medical School.
SOURCE: Ann Intern Med. 2020 Aug 18. doi: 10.7326/M19-3602.
The American College of Physicians and the American Academy of Family Physicians recently authored a guideline regarding the treatment of acute, non–low back, musculoskeletal injuries in adults in the outpatient setting.
According to the authors, musculoskeletal injuries result in more than 65 million medical visits a year with an annual estimated cost of $176.1 billion in 2010.
In summary, the guideline, which was published in the Annals of Internal Medicine, is based on a review of the best available evidence. The research reviewed by the guideline authors showed favorable results with topical NSAIDs, oral NSAIDs, oral acetaminophen, acupressure, and transcutaneous electrical nerve stimulation in reducing pain and/or improving function. The guideline authors “recommend that clinicians treat patients with acute pain from non–low back, musculoskeletal injuries with topical [NSAIDs] with or without gel as first-line therapy to reduce or relieve symptoms, including pain; improve physical function; and improve the patient’s treatment satisfaction (Grade: strong recommendation; moderate-certainty evidence).” Additionally, the guideline recommends against treating acute pain from non–low back, musculoskeletal injuries with opioids, including tramadol (Grade: conditional recommendation; low-certainty evidence).
The guideline also mentions improving function in relation to decreasing pain, which can be multifactorial.
Treating pain requires a multipronged approach. Many patients require more than one therapy to treat their pain, such as NSAIDs plus physical therapy. The ACP and AAFP did not make any recommendations for combination therapies in this guideline.
When physical therapy is needed
Nonopioid pain medications can do a great job of reducing a patient’s physical discomfort, which the evidence for these guideline demonstrates. However, much of the dysfunction caused by musculoskeletal injuries will not improve by reducing the pain alone. Physical therapy, exercise, and mobilization did not show a significant benefit in reducing symptoms in the systematic review and meta-analysis of randomized trials that appeared alongside the guideline. The type of pain, however, was not evaluated in relation to the effectiveness of these treatments. A fractured bone, for example, may heal just fine with casting and pain management, without the need for additional therapies. However, the muscles surrounding that bone can atrophy and become weak from not being used. Physical therapy may be needed to restrengthen those muscles. Therefore, a multifaceted approach is often needed, even for uncomplicated conditions.
Mental pain often comes with physical pain, and this is an aspect of care that is often neglected. It can be quite devastating for patients to not be able to do the things they were previously able to do. While this is easily recognized in professional athletes when they can no longer play, it is not so readily apparent with a mother who is just trying to take care of her kids. As doctors, especially those of us in family medicine, we should be addressing more than just physical pain.
Patients can also do activities that exacerbate their pain. As doctors, we need to be asking questions that help us determine whether a patient’s pain is caused by a particular action. Maybe that increase in shoulder pain is due to nothing more than lifting something heavy rather than a failure in a prescribed medication. Pain diaries are helpful, and clinicians don’t use them often enough.
How pain affects mental health
Acute injuries can also lead to disability. Many patients become quite distressed about being unable to work. They often need Famiy & Medical Leave Act forms filled out, and this task usually falls to the primary care doctor. In addition to assessing the pain, we need to be evaluating, at each visit, a patient’s level of functioning and their ability to do their job.
Every patient responds to pain differently, and it is important to evaluate patients’ mindsets regarding theirs. A patient may be in severe pain and may try to ignore it for a variety of reasons. A patient may “catastrophize” their pain, believing only the worst outcome will happen to them. Helping patients set appropriate expectations and having a positive mindset can help.
Overall, the new recommendations are a great tool as a guideline, but they are not complete enough to be the only ones used in managing acute, non–low back, musculoskeletal pain in adults.
They are very important for clinicians who may be prescribing opioid medications for patients with this type of pain. Amid an opioid crisis, it is the responsibility of every doctor to prescribe these medications appropriately. The evidence clearly shows they provide little benefit and place patients at risk of addiction.
We should all be following these recommendations as the baseline of care for acute pain. However, we need to delve deeper and manage all the components involved. We would be ignoring very real suffering in our patients if we limited our focus to only the physical discomfort.
Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Rutgers RWJ Medical School.
SOURCE: Ann Intern Med. 2020 Aug 18. doi: 10.7326/M19-3602.
The American College of Physicians and the American Academy of Family Physicians recently authored a guideline regarding the treatment of acute, non–low back, musculoskeletal injuries in adults in the outpatient setting.
According to the authors, musculoskeletal injuries result in more than 65 million medical visits a year with an annual estimated cost of $176.1 billion in 2010.
In summary, the guideline, which was published in the Annals of Internal Medicine, is based on a review of the best available evidence. The research reviewed by the guideline authors showed favorable results with topical NSAIDs, oral NSAIDs, oral acetaminophen, acupressure, and transcutaneous electrical nerve stimulation in reducing pain and/or improving function. The guideline authors “recommend that clinicians treat patients with acute pain from non–low back, musculoskeletal injuries with topical [NSAIDs] with or without gel as first-line therapy to reduce or relieve symptoms, including pain; improve physical function; and improve the patient’s treatment satisfaction (Grade: strong recommendation; moderate-certainty evidence).” Additionally, the guideline recommends against treating acute pain from non–low back, musculoskeletal injuries with opioids, including tramadol (Grade: conditional recommendation; low-certainty evidence).
The guideline also mentions improving function in relation to decreasing pain, which can be multifactorial.
Treating pain requires a multipronged approach. Many patients require more than one therapy to treat their pain, such as NSAIDs plus physical therapy. The ACP and AAFP did not make any recommendations for combination therapies in this guideline.
When physical therapy is needed
Nonopioid pain medications can do a great job of reducing a patient’s physical discomfort, which the evidence for these guideline demonstrates. However, much of the dysfunction caused by musculoskeletal injuries will not improve by reducing the pain alone. Physical therapy, exercise, and mobilization did not show a significant benefit in reducing symptoms in the systematic review and meta-analysis of randomized trials that appeared alongside the guideline. The type of pain, however, was not evaluated in relation to the effectiveness of these treatments. A fractured bone, for example, may heal just fine with casting and pain management, without the need for additional therapies. However, the muscles surrounding that bone can atrophy and become weak from not being used. Physical therapy may be needed to restrengthen those muscles. Therefore, a multifaceted approach is often needed, even for uncomplicated conditions.
Mental pain often comes with physical pain, and this is an aspect of care that is often neglected. It can be quite devastating for patients to not be able to do the things they were previously able to do. While this is easily recognized in professional athletes when they can no longer play, it is not so readily apparent with a mother who is just trying to take care of her kids. As doctors, especially those of us in family medicine, we should be addressing more than just physical pain.
Patients can also do activities that exacerbate their pain. As doctors, we need to be asking questions that help us determine whether a patient’s pain is caused by a particular action. Maybe that increase in shoulder pain is due to nothing more than lifting something heavy rather than a failure in a prescribed medication. Pain diaries are helpful, and clinicians don’t use them often enough.
How pain affects mental health
Acute injuries can also lead to disability. Many patients become quite distressed about being unable to work. They often need Famiy & Medical Leave Act forms filled out, and this task usually falls to the primary care doctor. In addition to assessing the pain, we need to be evaluating, at each visit, a patient’s level of functioning and their ability to do their job.
Every patient responds to pain differently, and it is important to evaluate patients’ mindsets regarding theirs. A patient may be in severe pain and may try to ignore it for a variety of reasons. A patient may “catastrophize” their pain, believing only the worst outcome will happen to them. Helping patients set appropriate expectations and having a positive mindset can help.
Overall, the new recommendations are a great tool as a guideline, but they are not complete enough to be the only ones used in managing acute, non–low back, musculoskeletal pain in adults.
They are very important for clinicians who may be prescribing opioid medications for patients with this type of pain. Amid an opioid crisis, it is the responsibility of every doctor to prescribe these medications appropriately. The evidence clearly shows they provide little benefit and place patients at risk of addiction.
We should all be following these recommendations as the baseline of care for acute pain. However, we need to delve deeper and manage all the components involved. We would be ignoring very real suffering in our patients if we limited our focus to only the physical discomfort.
Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Rutgers RWJ Medical School.
SOURCE: Ann Intern Med. 2020 Aug 18. doi: 10.7326/M19-3602.
ECG promising for predicting major depression, treatment response
Individuals with major depressive disorder (MDD) have an increased heart rate – a finding that may have the potential to identify individuals at risk for the disorder and predict treatment response, early research suggests.
Using the rapid-action of the novel antidepressant ketamine and the latest wearable 24-hour electrocardiogram (ECG) technology, investigators found that heart rate could distinguish MDD patients from healthy individuals.
They also found that patients with MDD with the highest resting heart rate had a greater treatment response. In fact, on average, depressed patients had a heart rate that was roughly 10-15 beats per minute higher than healthy controls.
The innovative design of the proof-of-concept study “allowed us to see that average resting heart rate may change quite suddenly to reflect the change in mood,” lead investigator Carmen Schiweck, PhD, Goethe University, Frankfurt am Main, Germany, said in an interview.
These results could have “exciting implications for treatment selection,” and the researchers plan to assess the potential for heart rate to act as an early warning system for depression, they noted.
The findings were presented at the 33rd European College of Neuropsychopharmacology (ECNP) Congress, which was held online this year because of the COVID-19 pandemic.
Identifying trait markers
There have been recent attempts to assess heart rate or heart rate variability (HRV) in patients with MDD to identify trait markers, which are present regardless of the disease phase, or state markers, which are present only during a depressive phase.
However, heart rate and HRV are “highly variable” over a 24-hour cycle, a fact that has been ignored by recent classification efforts, the researchers noted. Moreover, most commonly used antidepressants have a long onset of action, which makes studying their impact on the heart rate challenging.
The researchers’ goal was to determine whether heart rate and HRV could be used as trait markers to distinguish MDD patients from healthy individuals and, through the use of ketamine, whether they can also act as state markers for depression.
For the study, 16 treatment-resistant patients with MDD and 16 age- and sex-matched healthy controls wore a portable ECG device for 4 consecutive days and 3 nights. Heart rate and HRV data were subsequently averaged to obtain a 24-hour ECG.
Participants then received a single infusion of intravenous ketamine for 40 minutes. After waiting for 1 hour, the patients resumed ECG recording for an additional 4 days, with changes in mood assessed using the Hamilton Rating Scale for Depression (HAM-D).
Results showed that, compared with the control group, patients with MDD had a significantly higher 24-hour heart rate (P < .001) and a significantly lower HRV, as measured by the root mean square of successive differences (P < .001).
The investigators also found a reduction in heart rate amplitude, which indicates “significant blunting of circadian rhythm variation throughout the day and less recovery at night.”
Ninety percent accuracy
Harmonic and binary regression showed that heart rate was able to identify those with MDD versus those in the control group, particularly using nighttime readings, with 90.6% accuracy. The data correctly identified 14 (87.5%) patients and 15 (93.8%) members of the control group.
Following treatment, heart rate decreased significantly among the MDD group (P < .001), but there was no significant change in HRV (P = .295).
There was a significant positive association between baseline heart rate and response to treatment on the HAM-D (r = .55; P = .046), which suggested better outcomes in patients with a higher heart rate.
Interestingly, while heart rate was positively correlated with depression severity before treatment (r = .59; P = .03), this relationship disappeared following treatment (r = –0.04; P = .90), suggesting heart rate changes were not linked to depression states.
While heart rate levels may be useful as a trait marker and, potentially, for predicting response to antidepressant treatment, they did not show potential as a state marker, the investigators noted.
They suggested that, while the results need to be confirmed in longitudinal studies, approval of a ketamine nasal spray “may open up new avenues to conceive treatment paradigms, as explored in this study.”
However, “this is a small proof-of-concept study,” the investigators acknowledged. They also point out that only six of the patients with MDD had a reduction in HAM-D scores of at least 30% in response to treatment.
Future research plans
Dr. Schiweck said in an interview that her team was able to identify differences in heart rate and HRV in MDD patients that were not observed in other studies because portable at-home devices allowed them to monitor heart rate continuously over days.
The use of ketamine may also have been advantageous because the Netherlands Study of Depression and Anxiety (NESDA), which was published in 2010, clearly showed that “traditional antidepressants,” in particular tricyclic antidepressants, have a strong influence on heart rate and HRV, Dr. Schiweck said.
because most of the recent studies “just assess patients who are remitted and patients who are currently depressed, but it’s a cross-sectional study design,” said Schiweck.
“If we can follow up the same patients over time then we might really know if it is possible to use heart rate as a state marker for depression,” she added. “That’s what we tried to do with ketamine, but our study was very, very small.”
She noted that the investigators would also like to assess individuals who are “very stressed” and may show some depressive symptoms but don’t yet have a diagnosis of depression.
Mind-body link
Commenting on the findings, Brenda W.J.H. Penninx, MD, PhD, professor of psychiatric epidemiology at the VU University Medical Center in Amsterdam, said the concept of higher heart rate and lower HRV in depression “is indicative of more sympathetic drive and less parasympathetic drive of the autonomic nervous system.”
“That fits with the overall thought that depression is a state with more continuous exposure to stress overactivation of the body, which can be reflected in the [hypothalamic-pituitary-adrenal] axis, leading to higher levels of cortisol stress hormone. But it can also be reflected in the parasympathetic and sympathetic activation of the autonomic nervous system,” she said.
Dr. Penninx, who was also the principal investigator of the NESDA study, was not involved with the current research.
She noted that the NESDA study showed that, when patients with depressive disorder are compared with a healthy controls group, they have a higher heart rate and lower HRV. “But if we then divide people into medicated and nonmedicated people ... then we see that these deviations are only seen in people using medication,” she added.
“Our findings indicate that at least the use of antidepressants is having quite a large impact on autonomic nervous system dysregulation,” Dr. Penninx said. The difference with the current study, she pointed out, is that “it examines the problem over a completely different time scale.”
Although this offers advantages, the current study did not have the large patient numbers that were included in the NESDA study and “they were not clearly able to distinguish the effect of disease from medication,” noted Dr. Penninx.
In addition, this is not an easy area to investigate because there are multiple factors that can mitigate results, including the psychiatric state of the patient, use of medications for both mental illness and cardiometabolic disease, and a patient’s age and gender.
Still, the study clearly illustrates the importance of the interplay between mental health and somatic health and that there is “a very clear indication that we don’t need to separate those,” Dr. Penninx said.
The study was funded by a TGO-IWT Grant from Belgium. The study authors and Dr. Penninx have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Individuals with major depressive disorder (MDD) have an increased heart rate – a finding that may have the potential to identify individuals at risk for the disorder and predict treatment response, early research suggests.
Using the rapid-action of the novel antidepressant ketamine and the latest wearable 24-hour electrocardiogram (ECG) technology, investigators found that heart rate could distinguish MDD patients from healthy individuals.
They also found that patients with MDD with the highest resting heart rate had a greater treatment response. In fact, on average, depressed patients had a heart rate that was roughly 10-15 beats per minute higher than healthy controls.
The innovative design of the proof-of-concept study “allowed us to see that average resting heart rate may change quite suddenly to reflect the change in mood,” lead investigator Carmen Schiweck, PhD, Goethe University, Frankfurt am Main, Germany, said in an interview.
These results could have “exciting implications for treatment selection,” and the researchers plan to assess the potential for heart rate to act as an early warning system for depression, they noted.
The findings were presented at the 33rd European College of Neuropsychopharmacology (ECNP) Congress, which was held online this year because of the COVID-19 pandemic.
Identifying trait markers
There have been recent attempts to assess heart rate or heart rate variability (HRV) in patients with MDD to identify trait markers, which are present regardless of the disease phase, or state markers, which are present only during a depressive phase.
However, heart rate and HRV are “highly variable” over a 24-hour cycle, a fact that has been ignored by recent classification efforts, the researchers noted. Moreover, most commonly used antidepressants have a long onset of action, which makes studying their impact on the heart rate challenging.
The researchers’ goal was to determine whether heart rate and HRV could be used as trait markers to distinguish MDD patients from healthy individuals and, through the use of ketamine, whether they can also act as state markers for depression.
For the study, 16 treatment-resistant patients with MDD and 16 age- and sex-matched healthy controls wore a portable ECG device for 4 consecutive days and 3 nights. Heart rate and HRV data were subsequently averaged to obtain a 24-hour ECG.
Participants then received a single infusion of intravenous ketamine for 40 minutes. After waiting for 1 hour, the patients resumed ECG recording for an additional 4 days, with changes in mood assessed using the Hamilton Rating Scale for Depression (HAM-D).
Results showed that, compared with the control group, patients with MDD had a significantly higher 24-hour heart rate (P < .001) and a significantly lower HRV, as measured by the root mean square of successive differences (P < .001).
The investigators also found a reduction in heart rate amplitude, which indicates “significant blunting of circadian rhythm variation throughout the day and less recovery at night.”
Ninety percent accuracy
Harmonic and binary regression showed that heart rate was able to identify those with MDD versus those in the control group, particularly using nighttime readings, with 90.6% accuracy. The data correctly identified 14 (87.5%) patients and 15 (93.8%) members of the control group.
Following treatment, heart rate decreased significantly among the MDD group (P < .001), but there was no significant change in HRV (P = .295).
There was a significant positive association between baseline heart rate and response to treatment on the HAM-D (r = .55; P = .046), which suggested better outcomes in patients with a higher heart rate.
Interestingly, while heart rate was positively correlated with depression severity before treatment (r = .59; P = .03), this relationship disappeared following treatment (r = –0.04; P = .90), suggesting heart rate changes were not linked to depression states.
While heart rate levels may be useful as a trait marker and, potentially, for predicting response to antidepressant treatment, they did not show potential as a state marker, the investigators noted.
They suggested that, while the results need to be confirmed in longitudinal studies, approval of a ketamine nasal spray “may open up new avenues to conceive treatment paradigms, as explored in this study.”
However, “this is a small proof-of-concept study,” the investigators acknowledged. They also point out that only six of the patients with MDD had a reduction in HAM-D scores of at least 30% in response to treatment.
Future research plans
Dr. Schiweck said in an interview that her team was able to identify differences in heart rate and HRV in MDD patients that were not observed in other studies because portable at-home devices allowed them to monitor heart rate continuously over days.
The use of ketamine may also have been advantageous because the Netherlands Study of Depression and Anxiety (NESDA), which was published in 2010, clearly showed that “traditional antidepressants,” in particular tricyclic antidepressants, have a strong influence on heart rate and HRV, Dr. Schiweck said.
because most of the recent studies “just assess patients who are remitted and patients who are currently depressed, but it’s a cross-sectional study design,” said Schiweck.
“If we can follow up the same patients over time then we might really know if it is possible to use heart rate as a state marker for depression,” she added. “That’s what we tried to do with ketamine, but our study was very, very small.”
She noted that the investigators would also like to assess individuals who are “very stressed” and may show some depressive symptoms but don’t yet have a diagnosis of depression.
Mind-body link
Commenting on the findings, Brenda W.J.H. Penninx, MD, PhD, professor of psychiatric epidemiology at the VU University Medical Center in Amsterdam, said the concept of higher heart rate and lower HRV in depression “is indicative of more sympathetic drive and less parasympathetic drive of the autonomic nervous system.”
“That fits with the overall thought that depression is a state with more continuous exposure to stress overactivation of the body, which can be reflected in the [hypothalamic-pituitary-adrenal] axis, leading to higher levels of cortisol stress hormone. But it can also be reflected in the parasympathetic and sympathetic activation of the autonomic nervous system,” she said.
Dr. Penninx, who was also the principal investigator of the NESDA study, was not involved with the current research.
She noted that the NESDA study showed that, when patients with depressive disorder are compared with a healthy controls group, they have a higher heart rate and lower HRV. “But if we then divide people into medicated and nonmedicated people ... then we see that these deviations are only seen in people using medication,” she added.
“Our findings indicate that at least the use of antidepressants is having quite a large impact on autonomic nervous system dysregulation,” Dr. Penninx said. The difference with the current study, she pointed out, is that “it examines the problem over a completely different time scale.”
Although this offers advantages, the current study did not have the large patient numbers that were included in the NESDA study and “they were not clearly able to distinguish the effect of disease from medication,” noted Dr. Penninx.
In addition, this is not an easy area to investigate because there are multiple factors that can mitigate results, including the psychiatric state of the patient, use of medications for both mental illness and cardiometabolic disease, and a patient’s age and gender.
Still, the study clearly illustrates the importance of the interplay between mental health and somatic health and that there is “a very clear indication that we don’t need to separate those,” Dr. Penninx said.
The study was funded by a TGO-IWT Grant from Belgium. The study authors and Dr. Penninx have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Individuals with major depressive disorder (MDD) have an increased heart rate – a finding that may have the potential to identify individuals at risk for the disorder and predict treatment response, early research suggests.
Using the rapid-action of the novel antidepressant ketamine and the latest wearable 24-hour electrocardiogram (ECG) technology, investigators found that heart rate could distinguish MDD patients from healthy individuals.
They also found that patients with MDD with the highest resting heart rate had a greater treatment response. In fact, on average, depressed patients had a heart rate that was roughly 10-15 beats per minute higher than healthy controls.
The innovative design of the proof-of-concept study “allowed us to see that average resting heart rate may change quite suddenly to reflect the change in mood,” lead investigator Carmen Schiweck, PhD, Goethe University, Frankfurt am Main, Germany, said in an interview.
These results could have “exciting implications for treatment selection,” and the researchers plan to assess the potential for heart rate to act as an early warning system for depression, they noted.
The findings were presented at the 33rd European College of Neuropsychopharmacology (ECNP) Congress, which was held online this year because of the COVID-19 pandemic.
Identifying trait markers
There have been recent attempts to assess heart rate or heart rate variability (HRV) in patients with MDD to identify trait markers, which are present regardless of the disease phase, or state markers, which are present only during a depressive phase.
However, heart rate and HRV are “highly variable” over a 24-hour cycle, a fact that has been ignored by recent classification efforts, the researchers noted. Moreover, most commonly used antidepressants have a long onset of action, which makes studying their impact on the heart rate challenging.
The researchers’ goal was to determine whether heart rate and HRV could be used as trait markers to distinguish MDD patients from healthy individuals and, through the use of ketamine, whether they can also act as state markers for depression.
For the study, 16 treatment-resistant patients with MDD and 16 age- and sex-matched healthy controls wore a portable ECG device for 4 consecutive days and 3 nights. Heart rate and HRV data were subsequently averaged to obtain a 24-hour ECG.
Participants then received a single infusion of intravenous ketamine for 40 minutes. After waiting for 1 hour, the patients resumed ECG recording for an additional 4 days, with changes in mood assessed using the Hamilton Rating Scale for Depression (HAM-D).
Results showed that, compared with the control group, patients with MDD had a significantly higher 24-hour heart rate (P < .001) and a significantly lower HRV, as measured by the root mean square of successive differences (P < .001).
The investigators also found a reduction in heart rate amplitude, which indicates “significant blunting of circadian rhythm variation throughout the day and less recovery at night.”
Ninety percent accuracy
Harmonic and binary regression showed that heart rate was able to identify those with MDD versus those in the control group, particularly using nighttime readings, with 90.6% accuracy. The data correctly identified 14 (87.5%) patients and 15 (93.8%) members of the control group.
Following treatment, heart rate decreased significantly among the MDD group (P < .001), but there was no significant change in HRV (P = .295).
There was a significant positive association between baseline heart rate and response to treatment on the HAM-D (r = .55; P = .046), which suggested better outcomes in patients with a higher heart rate.
Interestingly, while heart rate was positively correlated with depression severity before treatment (r = .59; P = .03), this relationship disappeared following treatment (r = –0.04; P = .90), suggesting heart rate changes were not linked to depression states.
While heart rate levels may be useful as a trait marker and, potentially, for predicting response to antidepressant treatment, they did not show potential as a state marker, the investigators noted.
They suggested that, while the results need to be confirmed in longitudinal studies, approval of a ketamine nasal spray “may open up new avenues to conceive treatment paradigms, as explored in this study.”
However, “this is a small proof-of-concept study,” the investigators acknowledged. They also point out that only six of the patients with MDD had a reduction in HAM-D scores of at least 30% in response to treatment.
Future research plans
Dr. Schiweck said in an interview that her team was able to identify differences in heart rate and HRV in MDD patients that were not observed in other studies because portable at-home devices allowed them to monitor heart rate continuously over days.
The use of ketamine may also have been advantageous because the Netherlands Study of Depression and Anxiety (NESDA), which was published in 2010, clearly showed that “traditional antidepressants,” in particular tricyclic antidepressants, have a strong influence on heart rate and HRV, Dr. Schiweck said.
because most of the recent studies “just assess patients who are remitted and patients who are currently depressed, but it’s a cross-sectional study design,” said Schiweck.
“If we can follow up the same patients over time then we might really know if it is possible to use heart rate as a state marker for depression,” she added. “That’s what we tried to do with ketamine, but our study was very, very small.”
She noted that the investigators would also like to assess individuals who are “very stressed” and may show some depressive symptoms but don’t yet have a diagnosis of depression.
Mind-body link
Commenting on the findings, Brenda W.J.H. Penninx, MD, PhD, professor of psychiatric epidemiology at the VU University Medical Center in Amsterdam, said the concept of higher heart rate and lower HRV in depression “is indicative of more sympathetic drive and less parasympathetic drive of the autonomic nervous system.”
“That fits with the overall thought that depression is a state with more continuous exposure to stress overactivation of the body, which can be reflected in the [hypothalamic-pituitary-adrenal] axis, leading to higher levels of cortisol stress hormone. But it can also be reflected in the parasympathetic and sympathetic activation of the autonomic nervous system,” she said.
Dr. Penninx, who was also the principal investigator of the NESDA study, was not involved with the current research.
She noted that the NESDA study showed that, when patients with depressive disorder are compared with a healthy controls group, they have a higher heart rate and lower HRV. “But if we then divide people into medicated and nonmedicated people ... then we see that these deviations are only seen in people using medication,” she added.
“Our findings indicate that at least the use of antidepressants is having quite a large impact on autonomic nervous system dysregulation,” Dr. Penninx said. The difference with the current study, she pointed out, is that “it examines the problem over a completely different time scale.”
Although this offers advantages, the current study did not have the large patient numbers that were included in the NESDA study and “they were not clearly able to distinguish the effect of disease from medication,” noted Dr. Penninx.
In addition, this is not an easy area to investigate because there are multiple factors that can mitigate results, including the psychiatric state of the patient, use of medications for both mental illness and cardiometabolic disease, and a patient’s age and gender.
Still, the study clearly illustrates the importance of the interplay between mental health and somatic health and that there is “a very clear indication that we don’t need to separate those,” Dr. Penninx said.
The study was funded by a TGO-IWT Grant from Belgium. The study authors and Dr. Penninx have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
All about puberty blockers!
While many transgender individuals develop their gender identity early on in life, medically there may not be any intervention until they hit puberty. For prepubertal children, providing a supportive environment and letting them explore gender expression with haircut, clothing, toys, name, and pronouns may be the main “interventions.” Ensure a safe bathroom and safe spaces at school (and home), and perhaps find an experienced therapist comfortable navigating gender concerns. Supporting the family supports the child and can make all the difference in the world. Often clinics specializing in gender care will see young children to provide this support and follow the child into puberty.
Once puberty starts, however, medical interventions can be discussed and puberty blockers are a great place to start, given their reversibility. Having an understanding of how puberty blockers work, the side effects, and timing of blocker use is important to the average pediatric provider as you may see some of these children and be able to intervene by sending them to a specialist early!
How do puberty blockers work?
One of the first hormonal signals of puberty is the pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary. LH and FSH then stimulate sex steroidogenesis (production of estradiol or testosterone) and gametogenesis in the gonads. The most common choice for puberty blockers are GnRH agonists, such as leuprolide (a series of shots) or histrelin (an implantable rod), which have been studied extensively for the treatment of children with central precocious puberty, and more recently gender dysphoria. Interestingly, these medicines actually stimulate gonadotropin release and the overproduction makes the gonadotropin receptors less sensitive.1 Gradually the production of sex steroids decreases. allowing one to proceed with natal puberty if one so desires. Gender specialists always start with the most reversible intervention, especially at such a young age. Puberty blockers are like a pause button that gives everyone – patient, clinicians, therapists – time to process, explore, and ensure transition is the right path.
Sexual development should stop on puberty blockers. For those born with ovaries, breasts will not continue to develop and menses will not start if premenarchal or stop soon if postmenarchal. For those born with testicles, testicular and penile enlargement will not proceed, the voice will not deepen, hands will not grow in size, and an “Adam’s apple” will not develop. Preventing these changes may not only prevent future surgeries (mastectomy, tracheal shaving, etc.) but may also be lifesaving given the lack of development as secondary sex characteristics may not develop, thus avoiding telltale signs that one has transitioned physically, particularly for transwomen.
What are the side effects of puberty blockers?
Whenever an adolescent is started on puberty blockers, it is important to discuss both the main effects (i.e., cessation of puberty and sexual development) as well as the side effects. There are four main side effect areas that are important to cover: bone health and height, brain development, fertility, and surgical implications.
- Bone health & height. Adolescence is an important time for growth. During adolescence, bones grow both in length, which determines an individual’s height, and in density, which can affect risk of osteoporosis later on in life. Sex steroids are an important factor for both of these issues. Estradiol is responsible for closure of the growth plates and, in general, those born with ovaries enter puberty earlier than those born with testicles, therefore they see higher rates of estradiol earlier, which causes cessation of growth, hence why females are typically shorter than males. Delaying these high levels of estrogen may give transmales (female to male individuals) more time to grow. Conversely, decreasing release of testosterone in transfemales (male to female individuals) and then introducing estradiol at higher levels earlier than they would experience with their natal puberty may stop transfemales from growing much taller than the average cisgender woman. Bone density also is a major concern as the sex steroids are very important for bone mass accretion.1,2 Studies in transgender individuals using dual-energy x-ray absorptiometry show that, for transmale patients, z scores do decrease but they tend to catch up once gender-affirming hormones are started. For transfemale patients, the z scores don’t decrease as much but also don’t increase as much once estrogen is started.1,3 It is for these reasons that the Endocrine Society guidelines recommend monitoring bone density both before and while on puberty blockers.4,5
- Brain development. Adolescence also is an important time for brain development, particularly the areas that focus on executive function. Studies comparing transgender patients on GnRH agonists noted no detrimental effects on higher-order cognitive process associated with a specific task meant to test executive function.6 Although not performed on transgender individuals, a study examining girls with central precocious puberty on GnRH agonists found no difference with the control group on auditory and visual memory, response inhibition, spatial ability, behavioral problems, or social competence.7
- Fertility. Suspending puberty at an early Sexual Maturity Rating (such as stage 2 or 3) may make it difficult to harvest mature oocytes or spermatozoa, thus compromising long-term fertility, especially once they start on gender-affirming hormones. While some patients may choose to delay starting puberty blockers for the sake of cryopreservation, others may be in too much distress at their pubertal changes to wait. Fertility counseling is thus an important aspect of the discussion with transgender patients considering puberty blockers and/or gender-affirming hormones.
- Surgical implications. The most common “bottom surgery” performed in transfemales is called penile inversion vaginoplasty, which uses the penile and scrotal skin to create a neovagina.8 However, one has to have enough penile and scrotal development for this surgery to be successful, which may mean waiting until a patient has reached Sexual Maturity Rating stage 4 before starting blockers. There are alternative surgical options, but one must discuss the risks and benefits of waiting to start blockers with the patient and family.
When can puberty blockers be started?
Patients must meet criteria for gender dysphoria with emergence or worsening with puberty.9 Any coexisting conditions (psychological, medical, social) that could interfere with treatment have to be addressed, and both the patient and their guardian must undergo informed consent for treatment.4,5,10 Puberty blockers cannot be used until after puberty has started, so at least Sexual Maturity Rating stage 2. In the early stages of puberty, hormonally one will see LH rise followed by rise in estradiol and/or testosterone. Consideration for both the development of secondary sex characteristics and associated increased distress or dysphoria as well as surgical implications must be weighed in each individual case. The bottom line is that these medications can be life saving and are reversible, so if a patient and/or family decides to stop them, the effects will wear off and natal puberty will resume.
Dr. Lawlis is an assistant professor of pediatrics at the University of Oklahoma Health Sciences Center, Oklahoma City, and an adolescent medicine specialist at OU Children’s. She has no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Lancet Diabetes Endocrinol. 2017 Oct. doi: 10.1016/S2213-8587(17)30099-2.
2. Bone. 2010 Feb. doi: 10.1016/j.bone.2009.10.005.
3. J Clin Endocrinol Metab. 2015 Feb. doi: 10.1210/jc.2014-2439.
4. J Clin Endocrinol Metab. 2009 Sep. doi: 10.1210/jc.2009-0345.
5. J Clin Endocrinol Metab. 2017 Nov. doi: 10.1210/jc.2017-01658.
6. Psychoneuroendocrinology. 2015 Jun. doi: 10.1016/j.psyneuen.2015.03.007.
7. Front Psychol. 2016 Jul. doi: 10.3389/fpsyg.2016.01053.
8. Sex Med Rev. 2017 Jan. doi: 10.1016/j.sxmr.2016.08.001.
9. “Diagnostic and Statistical Manual of Mental Disorders,” 5th ed. (Arlington, Va.: American Psychiatric Association, 2013).
10. Int J Transgend. 2012. doi: 10.1080/15532739.2011.700873.
While many transgender individuals develop their gender identity early on in life, medically there may not be any intervention until they hit puberty. For prepubertal children, providing a supportive environment and letting them explore gender expression with haircut, clothing, toys, name, and pronouns may be the main “interventions.” Ensure a safe bathroom and safe spaces at school (and home), and perhaps find an experienced therapist comfortable navigating gender concerns. Supporting the family supports the child and can make all the difference in the world. Often clinics specializing in gender care will see young children to provide this support and follow the child into puberty.
Once puberty starts, however, medical interventions can be discussed and puberty blockers are a great place to start, given their reversibility. Having an understanding of how puberty blockers work, the side effects, and timing of blocker use is important to the average pediatric provider as you may see some of these children and be able to intervene by sending them to a specialist early!
How do puberty blockers work?
One of the first hormonal signals of puberty is the pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary. LH and FSH then stimulate sex steroidogenesis (production of estradiol or testosterone) and gametogenesis in the gonads. The most common choice for puberty blockers are GnRH agonists, such as leuprolide (a series of shots) or histrelin (an implantable rod), which have been studied extensively for the treatment of children with central precocious puberty, and more recently gender dysphoria. Interestingly, these medicines actually stimulate gonadotropin release and the overproduction makes the gonadotropin receptors less sensitive.1 Gradually the production of sex steroids decreases. allowing one to proceed with natal puberty if one so desires. Gender specialists always start with the most reversible intervention, especially at such a young age. Puberty blockers are like a pause button that gives everyone – patient, clinicians, therapists – time to process, explore, and ensure transition is the right path.
Sexual development should stop on puberty blockers. For those born with ovaries, breasts will not continue to develop and menses will not start if premenarchal or stop soon if postmenarchal. For those born with testicles, testicular and penile enlargement will not proceed, the voice will not deepen, hands will not grow in size, and an “Adam’s apple” will not develop. Preventing these changes may not only prevent future surgeries (mastectomy, tracheal shaving, etc.) but may also be lifesaving given the lack of development as secondary sex characteristics may not develop, thus avoiding telltale signs that one has transitioned physically, particularly for transwomen.
What are the side effects of puberty blockers?
Whenever an adolescent is started on puberty blockers, it is important to discuss both the main effects (i.e., cessation of puberty and sexual development) as well as the side effects. There are four main side effect areas that are important to cover: bone health and height, brain development, fertility, and surgical implications.
- Bone health & height. Adolescence is an important time for growth. During adolescence, bones grow both in length, which determines an individual’s height, and in density, which can affect risk of osteoporosis later on in life. Sex steroids are an important factor for both of these issues. Estradiol is responsible for closure of the growth plates and, in general, those born with ovaries enter puberty earlier than those born with testicles, therefore they see higher rates of estradiol earlier, which causes cessation of growth, hence why females are typically shorter than males. Delaying these high levels of estrogen may give transmales (female to male individuals) more time to grow. Conversely, decreasing release of testosterone in transfemales (male to female individuals) and then introducing estradiol at higher levels earlier than they would experience with their natal puberty may stop transfemales from growing much taller than the average cisgender woman. Bone density also is a major concern as the sex steroids are very important for bone mass accretion.1,2 Studies in transgender individuals using dual-energy x-ray absorptiometry show that, for transmale patients, z scores do decrease but they tend to catch up once gender-affirming hormones are started. For transfemale patients, the z scores don’t decrease as much but also don’t increase as much once estrogen is started.1,3 It is for these reasons that the Endocrine Society guidelines recommend monitoring bone density both before and while on puberty blockers.4,5
- Brain development. Adolescence also is an important time for brain development, particularly the areas that focus on executive function. Studies comparing transgender patients on GnRH agonists noted no detrimental effects on higher-order cognitive process associated with a specific task meant to test executive function.6 Although not performed on transgender individuals, a study examining girls with central precocious puberty on GnRH agonists found no difference with the control group on auditory and visual memory, response inhibition, spatial ability, behavioral problems, or social competence.7
- Fertility. Suspending puberty at an early Sexual Maturity Rating (such as stage 2 or 3) may make it difficult to harvest mature oocytes or spermatozoa, thus compromising long-term fertility, especially once they start on gender-affirming hormones. While some patients may choose to delay starting puberty blockers for the sake of cryopreservation, others may be in too much distress at their pubertal changes to wait. Fertility counseling is thus an important aspect of the discussion with transgender patients considering puberty blockers and/or gender-affirming hormones.
- Surgical implications. The most common “bottom surgery” performed in transfemales is called penile inversion vaginoplasty, which uses the penile and scrotal skin to create a neovagina.8 However, one has to have enough penile and scrotal development for this surgery to be successful, which may mean waiting until a patient has reached Sexual Maturity Rating stage 4 before starting blockers. There are alternative surgical options, but one must discuss the risks and benefits of waiting to start blockers with the patient and family.
When can puberty blockers be started?
Patients must meet criteria for gender dysphoria with emergence or worsening with puberty.9 Any coexisting conditions (psychological, medical, social) that could interfere with treatment have to be addressed, and both the patient and their guardian must undergo informed consent for treatment.4,5,10 Puberty blockers cannot be used until after puberty has started, so at least Sexual Maturity Rating stage 2. In the early stages of puberty, hormonally one will see LH rise followed by rise in estradiol and/or testosterone. Consideration for both the development of secondary sex characteristics and associated increased distress or dysphoria as well as surgical implications must be weighed in each individual case. The bottom line is that these medications can be life saving and are reversible, so if a patient and/or family decides to stop them, the effects will wear off and natal puberty will resume.
Dr. Lawlis is an assistant professor of pediatrics at the University of Oklahoma Health Sciences Center, Oklahoma City, and an adolescent medicine specialist at OU Children’s. She has no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Lancet Diabetes Endocrinol. 2017 Oct. doi: 10.1016/S2213-8587(17)30099-2.
2. Bone. 2010 Feb. doi: 10.1016/j.bone.2009.10.005.
3. J Clin Endocrinol Metab. 2015 Feb. doi: 10.1210/jc.2014-2439.
4. J Clin Endocrinol Metab. 2009 Sep. doi: 10.1210/jc.2009-0345.
5. J Clin Endocrinol Metab. 2017 Nov. doi: 10.1210/jc.2017-01658.
6. Psychoneuroendocrinology. 2015 Jun. doi: 10.1016/j.psyneuen.2015.03.007.
7. Front Psychol. 2016 Jul. doi: 10.3389/fpsyg.2016.01053.
8. Sex Med Rev. 2017 Jan. doi: 10.1016/j.sxmr.2016.08.001.
9. “Diagnostic and Statistical Manual of Mental Disorders,” 5th ed. (Arlington, Va.: American Psychiatric Association, 2013).
10. Int J Transgend. 2012. doi: 10.1080/15532739.2011.700873.
While many transgender individuals develop their gender identity early on in life, medically there may not be any intervention until they hit puberty. For prepubertal children, providing a supportive environment and letting them explore gender expression with haircut, clothing, toys, name, and pronouns may be the main “interventions.” Ensure a safe bathroom and safe spaces at school (and home), and perhaps find an experienced therapist comfortable navigating gender concerns. Supporting the family supports the child and can make all the difference in the world. Often clinics specializing in gender care will see young children to provide this support and follow the child into puberty.
Once puberty starts, however, medical interventions can be discussed and puberty blockers are a great place to start, given their reversibility. Having an understanding of how puberty blockers work, the side effects, and timing of blocker use is important to the average pediatric provider as you may see some of these children and be able to intervene by sending them to a specialist early!
How do puberty blockers work?
One of the first hormonal signals of puberty is the pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary. LH and FSH then stimulate sex steroidogenesis (production of estradiol or testosterone) and gametogenesis in the gonads. The most common choice for puberty blockers are GnRH agonists, such as leuprolide (a series of shots) or histrelin (an implantable rod), which have been studied extensively for the treatment of children with central precocious puberty, and more recently gender dysphoria. Interestingly, these medicines actually stimulate gonadotropin release and the overproduction makes the gonadotropin receptors less sensitive.1 Gradually the production of sex steroids decreases. allowing one to proceed with natal puberty if one so desires. Gender specialists always start with the most reversible intervention, especially at such a young age. Puberty blockers are like a pause button that gives everyone – patient, clinicians, therapists – time to process, explore, and ensure transition is the right path.
Sexual development should stop on puberty blockers. For those born with ovaries, breasts will not continue to develop and menses will not start if premenarchal or stop soon if postmenarchal. For those born with testicles, testicular and penile enlargement will not proceed, the voice will not deepen, hands will not grow in size, and an “Adam’s apple” will not develop. Preventing these changes may not only prevent future surgeries (mastectomy, tracheal shaving, etc.) but may also be lifesaving given the lack of development as secondary sex characteristics may not develop, thus avoiding telltale signs that one has transitioned physically, particularly for transwomen.
What are the side effects of puberty blockers?
Whenever an adolescent is started on puberty blockers, it is important to discuss both the main effects (i.e., cessation of puberty and sexual development) as well as the side effects. There are four main side effect areas that are important to cover: bone health and height, brain development, fertility, and surgical implications.
- Bone health & height. Adolescence is an important time for growth. During adolescence, bones grow both in length, which determines an individual’s height, and in density, which can affect risk of osteoporosis later on in life. Sex steroids are an important factor for both of these issues. Estradiol is responsible for closure of the growth plates and, in general, those born with ovaries enter puberty earlier than those born with testicles, therefore they see higher rates of estradiol earlier, which causes cessation of growth, hence why females are typically shorter than males. Delaying these high levels of estrogen may give transmales (female to male individuals) more time to grow. Conversely, decreasing release of testosterone in transfemales (male to female individuals) and then introducing estradiol at higher levels earlier than they would experience with their natal puberty may stop transfemales from growing much taller than the average cisgender woman. Bone density also is a major concern as the sex steroids are very important for bone mass accretion.1,2 Studies in transgender individuals using dual-energy x-ray absorptiometry show that, for transmale patients, z scores do decrease but they tend to catch up once gender-affirming hormones are started. For transfemale patients, the z scores don’t decrease as much but also don’t increase as much once estrogen is started.1,3 It is for these reasons that the Endocrine Society guidelines recommend monitoring bone density both before and while on puberty blockers.4,5
- Brain development. Adolescence also is an important time for brain development, particularly the areas that focus on executive function. Studies comparing transgender patients on GnRH agonists noted no detrimental effects on higher-order cognitive process associated with a specific task meant to test executive function.6 Although not performed on transgender individuals, a study examining girls with central precocious puberty on GnRH agonists found no difference with the control group on auditory and visual memory, response inhibition, spatial ability, behavioral problems, or social competence.7
- Fertility. Suspending puberty at an early Sexual Maturity Rating (such as stage 2 or 3) may make it difficult to harvest mature oocytes or spermatozoa, thus compromising long-term fertility, especially once they start on gender-affirming hormones. While some patients may choose to delay starting puberty blockers for the sake of cryopreservation, others may be in too much distress at their pubertal changes to wait. Fertility counseling is thus an important aspect of the discussion with transgender patients considering puberty blockers and/or gender-affirming hormones.
- Surgical implications. The most common “bottom surgery” performed in transfemales is called penile inversion vaginoplasty, which uses the penile and scrotal skin to create a neovagina.8 However, one has to have enough penile and scrotal development for this surgery to be successful, which may mean waiting until a patient has reached Sexual Maturity Rating stage 4 before starting blockers. There are alternative surgical options, but one must discuss the risks and benefits of waiting to start blockers with the patient and family.
When can puberty blockers be started?
Patients must meet criteria for gender dysphoria with emergence or worsening with puberty.9 Any coexisting conditions (psychological, medical, social) that could interfere with treatment have to be addressed, and both the patient and their guardian must undergo informed consent for treatment.4,5,10 Puberty blockers cannot be used until after puberty has started, so at least Sexual Maturity Rating stage 2. In the early stages of puberty, hormonally one will see LH rise followed by rise in estradiol and/or testosterone. Consideration for both the development of secondary sex characteristics and associated increased distress or dysphoria as well as surgical implications must be weighed in each individual case. The bottom line is that these medications can be life saving and are reversible, so if a patient and/or family decides to stop them, the effects will wear off and natal puberty will resume.
Dr. Lawlis is an assistant professor of pediatrics at the University of Oklahoma Health Sciences Center, Oklahoma City, and an adolescent medicine specialist at OU Children’s. She has no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Lancet Diabetes Endocrinol. 2017 Oct. doi: 10.1016/S2213-8587(17)30099-2.
2. Bone. 2010 Feb. doi: 10.1016/j.bone.2009.10.005.
3. J Clin Endocrinol Metab. 2015 Feb. doi: 10.1210/jc.2014-2439.
4. J Clin Endocrinol Metab. 2009 Sep. doi: 10.1210/jc.2009-0345.
5. J Clin Endocrinol Metab. 2017 Nov. doi: 10.1210/jc.2017-01658.
6. Psychoneuroendocrinology. 2015 Jun. doi: 10.1016/j.psyneuen.2015.03.007.
7. Front Psychol. 2016 Jul. doi: 10.3389/fpsyg.2016.01053.
8. Sex Med Rev. 2017 Jan. doi: 10.1016/j.sxmr.2016.08.001.
9. “Diagnostic and Statistical Manual of Mental Disorders,” 5th ed. (Arlington, Va.: American Psychiatric Association, 2013).
10. Int J Transgend. 2012. doi: 10.1080/15532739.2011.700873.
Reassuring findings on SSRIs and diabetes risk in children
SSRIs are associated with a much lower risk of type 2 diabetes (T2D) in children and adolescents than previously reported, new research shows.
Investigators found publicly insured patients treated with SSRIs had a 13% increased risk for T2D, compared with those not treated with these agents. In addition, those taking SSRIs continuously (defined as receiving one or more prescriptions every 3 months) had a 33% increased risk of T2D.
On the other hand, privately insured youth had a much lower increased risk – a finding that may be attributable to a lower prevalence of risk factors for T2D in this group.
“We cannot exclude that children and adolescents treated with SSRIs may be at a small increased risk of developing T2D, particularly publicly insured patients, but the magnitude of association was weaker than previous thought and much smaller than other known risk factors for T2DM, such as obesity, race, and poverty,” lead investigator Jenny Sun, PhD, said in an interview.
“When weighing the known benefits and risks of SSRI treatment in children and adolescents, our findings provide reassurance that the risk of T2DM is not as substantial as initially reported,” said Dr. Sun, a postdoctoral research fellow in the department of population medicine at Harvard Medical School’s Harvard Pilgrim Health Care Institute, Boston.
The study was published online Sept. 2 in JAMA Psychiatry.
Limited evidence
Previous research suggested that SSRIs increase the risk of T2D by up to 90% in children and adolescents.
However, the investigators noted, the study reporting this finding was too small to draw conclusions about the SSRI class as a whole also did not examine specific SSRIs.
In addition, although “several studies have reported that antidepressant use may be a risk factor for T2D in adults, evidence was limited in children and adolescents,” said Dr. Sun.
“Rapid changes in growth during childhood and adolescents can alter drugs’ pharmacokinetics and pharmacodynamics, so high-quality, age-specific data are needed to inform prescribing decisions,” she said.
For the current study, the researchers analyzed claims data on almost 1.6 million patients aged 10-19 years (58.3% female; mean age, 15.1 years) from two large claims databases.
The analysis focused on those with a diagnosis warranting treatment with an SSRI, including depression, generalized or social anxiety disorder, obsessive compulsive disorder, PTSD, panic disorder, or bulimia nervosa.
The Medicaid Analytic Extract database consisted of 316,178 patients insured through Medicaid or the Children’s Health Insurance Program. The IBM MarketScan database consisted of 211,460 privately insured patients. Patients were followed up for a mean of 2.3 and 2.2 years, respectively.
Patients who initiated SSRI treatment were compared with those with a similar indication but who were not taking an SSRI. Secondary analyses compared new SSRI users with patients who recently initiated treatment with bupropion, which has no metabolic side effects, or with patients who recently initiated psychotherapy.
“In observational data, it is difficult to mimic a placebo group, often used in RCTs [randomized, controlled trials], therefore several comparator groups were explored to broaden our understanding,” said Dr. Sun.
In addition, the researchers compared the individual SSRI medications, using fluoxetine as a comparator.
A wide range of more than 100 potential confounders or “proxies of confounders,” were taken into account, including demographic characteristics, psychiatric diagnoses, metabolic conditions, concomitant medications, and use of health care services.
The researchers conducted two analyses. They included an intention-to-treat (ITT) analysis that was restricted to patients with one or more additional SSRI prescriptions during the 6 months following the index exposure assessment period.
Close monitoring required
An as-treated analysis estimated the association of continuous SSRI treatment (vs. untreated, bupropion treatment, and psychotherapy), with adherence assessed at 3-month intervals.
Initiation and continuation of SSRI treatment in publicly insured patients were both associated with a considerably higher risk of T2D, compared with untreated patients, and a steeper risk, compared with their privately insured counterparts.
For newly treated publicly insured patients initiated on SSRI treatment, the ITT adjusted hazard ratio was 1.13 (95% confidence interval, 1.04-1.22).
There was an even stronger association among continuously treated publicly insured patients, with an as-treated aHR of 1.33 (95% CI, 1.21-1.47). The authors noted that this corresponds to 6.6 additional T2D cases per 10,000 patients continuously treated for at least 2 years.
The association was weaker in privately insured patients (ITT aHR, 1.01; 95% CI, 0.84-1.23; as-treated aHR, 1.10; 95% CI, 0.88-1.36).
The secondary analyses yielded similar findings: When SSRI treatment was compared with psychotherapy, the as-treated aHR for publicly insured patients was 1.44 (95% CI, 1.25-1.65), whereas the aHR for privately insured patients was lower at 1.21 (95% CI, 0.93-1.57)
The investigators found no increased risk when SSRIs were compared with bupropion, and the within-class analysis showed that none of the SSRIs carried an increased hazard of T2D, compared with fluoxetine.
“Publicly insured patients are enrolled in Medicaid and the Children’s Health Insurance Program, whereas privately insured patients are generally covered by their parent’s employer-sponsored insurance,” said Dr. Sun.
“Publicly insured patients are of lower socioeconomic status and represent a population with greater overall medical burden, more comorbidities, and a higher prevalence of risk factors for T2D, such as obesity, at the time of treatment initiation,” she said.
She added that high-risk children and youth should be closely monitored and clinicians should also consider recommending dietary modifications and increased exercise to offset T2D risk.
Useful ‘real-world data’
William Cooper, MD, MPH, professor of pediatrics and health policy at Vanderbilt University Medical Center in Nashville, Tenn., said that the study “provides a fascinating look at risks of SSRI medications in children and adolescents.”
Dr. Cooper, who was not involved with the study, said that the authors “draw from real-world data representing two different populations and carefully consider factors which might confound the associations.”
The results, he said, “provide important benefits for patients, families, and clinicians as they weigh the risks and benefits of using SSRIs for children who need treatment for depression and anxiety disorders.
The study was supported by a training grant from the program in pharmacoepidemiology at the Harvard School of Public Health. Dr. Sun disclosed no relevant financial relationships. Dr. Cooper disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
SSRIs are associated with a much lower risk of type 2 diabetes (T2D) in children and adolescents than previously reported, new research shows.
Investigators found publicly insured patients treated with SSRIs had a 13% increased risk for T2D, compared with those not treated with these agents. In addition, those taking SSRIs continuously (defined as receiving one or more prescriptions every 3 months) had a 33% increased risk of T2D.
On the other hand, privately insured youth had a much lower increased risk – a finding that may be attributable to a lower prevalence of risk factors for T2D in this group.
“We cannot exclude that children and adolescents treated with SSRIs may be at a small increased risk of developing T2D, particularly publicly insured patients, but the magnitude of association was weaker than previous thought and much smaller than other known risk factors for T2DM, such as obesity, race, and poverty,” lead investigator Jenny Sun, PhD, said in an interview.
“When weighing the known benefits and risks of SSRI treatment in children and adolescents, our findings provide reassurance that the risk of T2DM is not as substantial as initially reported,” said Dr. Sun, a postdoctoral research fellow in the department of population medicine at Harvard Medical School’s Harvard Pilgrim Health Care Institute, Boston.
The study was published online Sept. 2 in JAMA Psychiatry.
Limited evidence
Previous research suggested that SSRIs increase the risk of T2D by up to 90% in children and adolescents.
However, the investigators noted, the study reporting this finding was too small to draw conclusions about the SSRI class as a whole also did not examine specific SSRIs.
In addition, although “several studies have reported that antidepressant use may be a risk factor for T2D in adults, evidence was limited in children and adolescents,” said Dr. Sun.
“Rapid changes in growth during childhood and adolescents can alter drugs’ pharmacokinetics and pharmacodynamics, so high-quality, age-specific data are needed to inform prescribing decisions,” she said.
For the current study, the researchers analyzed claims data on almost 1.6 million patients aged 10-19 years (58.3% female; mean age, 15.1 years) from two large claims databases.
The analysis focused on those with a diagnosis warranting treatment with an SSRI, including depression, generalized or social anxiety disorder, obsessive compulsive disorder, PTSD, panic disorder, or bulimia nervosa.
The Medicaid Analytic Extract database consisted of 316,178 patients insured through Medicaid or the Children’s Health Insurance Program. The IBM MarketScan database consisted of 211,460 privately insured patients. Patients were followed up for a mean of 2.3 and 2.2 years, respectively.
Patients who initiated SSRI treatment were compared with those with a similar indication but who were not taking an SSRI. Secondary analyses compared new SSRI users with patients who recently initiated treatment with bupropion, which has no metabolic side effects, or with patients who recently initiated psychotherapy.
“In observational data, it is difficult to mimic a placebo group, often used in RCTs [randomized, controlled trials], therefore several comparator groups were explored to broaden our understanding,” said Dr. Sun.
In addition, the researchers compared the individual SSRI medications, using fluoxetine as a comparator.
A wide range of more than 100 potential confounders or “proxies of confounders,” were taken into account, including demographic characteristics, psychiatric diagnoses, metabolic conditions, concomitant medications, and use of health care services.
The researchers conducted two analyses. They included an intention-to-treat (ITT) analysis that was restricted to patients with one or more additional SSRI prescriptions during the 6 months following the index exposure assessment period.
Close monitoring required
An as-treated analysis estimated the association of continuous SSRI treatment (vs. untreated, bupropion treatment, and psychotherapy), with adherence assessed at 3-month intervals.
Initiation and continuation of SSRI treatment in publicly insured patients were both associated with a considerably higher risk of T2D, compared with untreated patients, and a steeper risk, compared with their privately insured counterparts.
For newly treated publicly insured patients initiated on SSRI treatment, the ITT adjusted hazard ratio was 1.13 (95% confidence interval, 1.04-1.22).
There was an even stronger association among continuously treated publicly insured patients, with an as-treated aHR of 1.33 (95% CI, 1.21-1.47). The authors noted that this corresponds to 6.6 additional T2D cases per 10,000 patients continuously treated for at least 2 years.
The association was weaker in privately insured patients (ITT aHR, 1.01; 95% CI, 0.84-1.23; as-treated aHR, 1.10; 95% CI, 0.88-1.36).
The secondary analyses yielded similar findings: When SSRI treatment was compared with psychotherapy, the as-treated aHR for publicly insured patients was 1.44 (95% CI, 1.25-1.65), whereas the aHR for privately insured patients was lower at 1.21 (95% CI, 0.93-1.57)
The investigators found no increased risk when SSRIs were compared with bupropion, and the within-class analysis showed that none of the SSRIs carried an increased hazard of T2D, compared with fluoxetine.
“Publicly insured patients are enrolled in Medicaid and the Children’s Health Insurance Program, whereas privately insured patients are generally covered by their parent’s employer-sponsored insurance,” said Dr. Sun.
“Publicly insured patients are of lower socioeconomic status and represent a population with greater overall medical burden, more comorbidities, and a higher prevalence of risk factors for T2D, such as obesity, at the time of treatment initiation,” she said.
She added that high-risk children and youth should be closely monitored and clinicians should also consider recommending dietary modifications and increased exercise to offset T2D risk.
Useful ‘real-world data’
William Cooper, MD, MPH, professor of pediatrics and health policy at Vanderbilt University Medical Center in Nashville, Tenn., said that the study “provides a fascinating look at risks of SSRI medications in children and adolescents.”
Dr. Cooper, who was not involved with the study, said that the authors “draw from real-world data representing two different populations and carefully consider factors which might confound the associations.”
The results, he said, “provide important benefits for patients, families, and clinicians as they weigh the risks and benefits of using SSRIs for children who need treatment for depression and anxiety disorders.
The study was supported by a training grant from the program in pharmacoepidemiology at the Harvard School of Public Health. Dr. Sun disclosed no relevant financial relationships. Dr. Cooper disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
SSRIs are associated with a much lower risk of type 2 diabetes (T2D) in children and adolescents than previously reported, new research shows.
Investigators found publicly insured patients treated with SSRIs had a 13% increased risk for T2D, compared with those not treated with these agents. In addition, those taking SSRIs continuously (defined as receiving one or more prescriptions every 3 months) had a 33% increased risk of T2D.
On the other hand, privately insured youth had a much lower increased risk – a finding that may be attributable to a lower prevalence of risk factors for T2D in this group.
“We cannot exclude that children and adolescents treated with SSRIs may be at a small increased risk of developing T2D, particularly publicly insured patients, but the magnitude of association was weaker than previous thought and much smaller than other known risk factors for T2DM, such as obesity, race, and poverty,” lead investigator Jenny Sun, PhD, said in an interview.
“When weighing the known benefits and risks of SSRI treatment in children and adolescents, our findings provide reassurance that the risk of T2DM is not as substantial as initially reported,” said Dr. Sun, a postdoctoral research fellow in the department of population medicine at Harvard Medical School’s Harvard Pilgrim Health Care Institute, Boston.
The study was published online Sept. 2 in JAMA Psychiatry.
Limited evidence
Previous research suggested that SSRIs increase the risk of T2D by up to 90% in children and adolescents.
However, the investigators noted, the study reporting this finding was too small to draw conclusions about the SSRI class as a whole also did not examine specific SSRIs.
In addition, although “several studies have reported that antidepressant use may be a risk factor for T2D in adults, evidence was limited in children and adolescents,” said Dr. Sun.
“Rapid changes in growth during childhood and adolescents can alter drugs’ pharmacokinetics and pharmacodynamics, so high-quality, age-specific data are needed to inform prescribing decisions,” she said.
For the current study, the researchers analyzed claims data on almost 1.6 million patients aged 10-19 years (58.3% female; mean age, 15.1 years) from two large claims databases.
The analysis focused on those with a diagnosis warranting treatment with an SSRI, including depression, generalized or social anxiety disorder, obsessive compulsive disorder, PTSD, panic disorder, or bulimia nervosa.
The Medicaid Analytic Extract database consisted of 316,178 patients insured through Medicaid or the Children’s Health Insurance Program. The IBM MarketScan database consisted of 211,460 privately insured patients. Patients were followed up for a mean of 2.3 and 2.2 years, respectively.
Patients who initiated SSRI treatment were compared with those with a similar indication but who were not taking an SSRI. Secondary analyses compared new SSRI users with patients who recently initiated treatment with bupropion, which has no metabolic side effects, or with patients who recently initiated psychotherapy.
“In observational data, it is difficult to mimic a placebo group, often used in RCTs [randomized, controlled trials], therefore several comparator groups were explored to broaden our understanding,” said Dr. Sun.
In addition, the researchers compared the individual SSRI medications, using fluoxetine as a comparator.
A wide range of more than 100 potential confounders or “proxies of confounders,” were taken into account, including demographic characteristics, psychiatric diagnoses, metabolic conditions, concomitant medications, and use of health care services.
The researchers conducted two analyses. They included an intention-to-treat (ITT) analysis that was restricted to patients with one or more additional SSRI prescriptions during the 6 months following the index exposure assessment period.
Close monitoring required
An as-treated analysis estimated the association of continuous SSRI treatment (vs. untreated, bupropion treatment, and psychotherapy), with adherence assessed at 3-month intervals.
Initiation and continuation of SSRI treatment in publicly insured patients were both associated with a considerably higher risk of T2D, compared with untreated patients, and a steeper risk, compared with their privately insured counterparts.
For newly treated publicly insured patients initiated on SSRI treatment, the ITT adjusted hazard ratio was 1.13 (95% confidence interval, 1.04-1.22).
There was an even stronger association among continuously treated publicly insured patients, with an as-treated aHR of 1.33 (95% CI, 1.21-1.47). The authors noted that this corresponds to 6.6 additional T2D cases per 10,000 patients continuously treated for at least 2 years.
The association was weaker in privately insured patients (ITT aHR, 1.01; 95% CI, 0.84-1.23; as-treated aHR, 1.10; 95% CI, 0.88-1.36).
The secondary analyses yielded similar findings: When SSRI treatment was compared with psychotherapy, the as-treated aHR for publicly insured patients was 1.44 (95% CI, 1.25-1.65), whereas the aHR for privately insured patients was lower at 1.21 (95% CI, 0.93-1.57)
The investigators found no increased risk when SSRIs were compared with bupropion, and the within-class analysis showed that none of the SSRIs carried an increased hazard of T2D, compared with fluoxetine.
“Publicly insured patients are enrolled in Medicaid and the Children’s Health Insurance Program, whereas privately insured patients are generally covered by their parent’s employer-sponsored insurance,” said Dr. Sun.
“Publicly insured patients are of lower socioeconomic status and represent a population with greater overall medical burden, more comorbidities, and a higher prevalence of risk factors for T2D, such as obesity, at the time of treatment initiation,” she said.
She added that high-risk children and youth should be closely monitored and clinicians should also consider recommending dietary modifications and increased exercise to offset T2D risk.
Useful ‘real-world data’
William Cooper, MD, MPH, professor of pediatrics and health policy at Vanderbilt University Medical Center in Nashville, Tenn., said that the study “provides a fascinating look at risks of SSRI medications in children and adolescents.”
Dr. Cooper, who was not involved with the study, said that the authors “draw from real-world data representing two different populations and carefully consider factors which might confound the associations.”
The results, he said, “provide important benefits for patients, families, and clinicians as they weigh the risks and benefits of using SSRIs for children who need treatment for depression and anxiety disorders.
The study was supported by a training grant from the program in pharmacoepidemiology at the Harvard School of Public Health. Dr. Sun disclosed no relevant financial relationships. Dr. Cooper disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The gut a new therapeutic target for major depression?
The gut microbiota differs significantly between patients with major depressive disorder (MDD) and healthy individuals and may be modifiable with a probiotic diet to improve stress and depression scores, two new studies suggest.
In one study, investigators compared stool samples between patients with MDD and healthy controls. They found significant differences in bacterial profiles between the two groups, as well as between patients who responded vs those who were resistant to treatment.
“This finding further supports the relevance of an altered composition of the gut microbiota in the etiopathogenesis of MDD and suggests a role in response to antidepressants,” coinvestigator Andrea Fontana, MSc, Fondazione IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy, said in an interview.
Results from the second study showed significant improvements in self-reported stress, anxiety, and depression scores in healthy individuals following a “psychobiotic” diet (using probiotics or prebiotics to manipulate the microbiota to improve mental health) that was rich in fruit, vegetables, and fermented foods vs. those who received dietary advice alone.
The investigators, led by Kirsten Berding, PhD, APC Microbiome Ireland, University College Cork, Ireland, now plan on testing their psychobiotic diet in patients with MDD and hope the findings could be helpful in “the development of adjuvant therapeutic opportunities” where pharmacologic treatment is not effective.
Both studies were presented at the virtual congress of the European College of Neuropsychopharmacology, held online this year because of the COVID-19 pandemic.
A “hallmark” of major depression
Mr. Fontana and colleagues note that the mostly suboptimal response to pharmacologic treatments among patients with MDD is one of the factors that “contributes to the large socioeconomic burden” of the disease.
Previous research shows patients with MDD have gut dysbiosis, or an imbalance in the natural flora; that antidepressants have antimicrobial properties; and that probiotics have an antibiotic effect. However, the correlation between the composition of the gut microbiota and antidepressant response is poorly understood.
The investigators recruited 34 patients with MDD (aged 18-70 years) who were in a euthymic phase and who did not have comorbid conditions that could affect the gut microbiota.
Eight patients were treatment resistant, defined as a poor response to at least two adequate trials of different antidepressant classes, while 19 were treatment responsive and seven were treatment naive.
The researchers also recruited 20 healthy individuals via word of mouth to act as the control group. There were no significant differences between patients and the control group in terms of baseline characteristics.
Genomic sequencing of bacteria obtained from stool samples showed that it was possible to distinguish between patients with MDD and the healthy individuals, especially at the family, genus, and species levels.
In particular, there were significant differences in the Paenibacillaceae and Flavobacteriaceaea families, for the genus Fenollaria, and the species Flintibacter butyricus, Christensenella timonensis, and Eisenbergiella massiliensis, among others.
Results also showed that the phyla Proteobacteria, Tenericutes, and the family Peptostreptococcaceae were more common in patients with treatment-resistant MDD, whereas the phylum Actinobacteria was more abundant in treatment responders.
Moreover, several bacteria were found only in the microbiota of patients with treatment-resistant MDD, while others were seen only in treatment-responsive patients. This made it possible to discriminate not only between treatment-resistant and -responsive patients but also between those two patient groups and healthy controls.
“The results of our study confirm that gut dysbiosis is a hallmark of MDD, and suggests that the gut microbiota of patients with treatment-resistant MDD significantly differs from responders to antidepressants,” Mr. Fontana said.
Psychobiotic diet
For the second study, Dr. Berding and colleagues note that “psychobiotics” has previously achieved “promising results.”
In addition, diet is both “one of the most influential modifying factors” for the gut microbiota and an easily accessible strategy, they wrote. However, there is also a paucity of studies in this area, they added.
The researchers randomly assigned healthy volunteers with relatively poor dietary habits to either a 4-week psychobiotic diet group (n = 21) or a control group (n = 19).
Individuals in the psychobiotic group were told to eat a diet rich in prebiotics, such as fruit and vegetables, fiber including whole grains and legumes, and fermented foods. The control group was educated on Irish healthy-eating guidelines.
Stool and saliva samples were collected and the participants completed several self-reported mental health questionnaires, as well as a 7-day food diary. They also took the socially evaluated cold-pressor test (SECPT) to measure acute stress responses.
Results showed that total daily energy intake decreased significantly in both the diet and control groups over the study period (P = .04 for both) but did not differ significantly between the groups.
In contrast, dietary fiber intake increased significantly in the diet group (P < .001) and was significantly higher than in the control group at the end of the intervention (P = .03).
Individuals in the diet group showed significant decreases in scores on the Perceived Stress Scale (P = .002) and the Beck Depression Inventory (P = .007) during the study, an effect that was not found in the control group.
Dietary intervention
There were no significant effects of diet on the acute stress response, but both groups showed improvements in self-concept, or perceived ability to cope, on the Primary Appraisal, Secondary Appraisal index (P = .03 for the diet group, P = .04 for the control group).
The results show that a dietary intervention targeted at the microbiota “can improve subjective feelings of stress and depression in a healthy population,” the investigators wrote.
However, elucidating the “contribution of the microbiota-gut-brain axis on the signaling response to dietary interventions” will require further studies on microbiota sequencing and biological measures of stress, they added.
This will “contribute to the understanding of the benefits of a psychobiotic diet on stress and anxiety,” wrote the researchers.
Dr. Berding said in an interview that while the consumption of dietary fiber changed the most in the diet group, “it would not be the only nutrient” that had an impact on the results, with fermented foods a likely candidate.
She said the next step is to test the dietary intervention in patients with MDD; however, “doing nutritional interventions in diseased populations is always difficult.”
Dr. Berding suggested that the best approach would be to study inpatients in a clinic, as “we would be able to provide every meal and only provide foods that are part of the dietary intervention.”
Although another option would be to conduct the study in outpatients, she noted that assessing inpatients “would give us the best control over compliance.”
“Brilliant ideas”
Commenting on the findings, Sergueï Fetissov, MD, PhD, professor of physiology at Rouen University, Mont-Saint-Aignan, France, said that although both studies bring attention to a possible role for the gut microbiota in MDD, neither “provide any experimental evidence of a causative nature.”
Dr. Fetissov, who was not involved in either study, noted that this topic has been the subject of clinical nutritional research for many years.
However, “we still need some strong evidence to prove that some bacteria can influence the regulation of mood and anxiety and stress,” he said.
In addition, researchers currently do not know what actually causes MDD. “How we can say the gut bacteria regulates something if we don’t know what really causes the altered mood?” said Dr. Fetissov.
He noted that over the last 50 years, there have been great advances in the development of drugs that alleviate depression and anxiety by regulating dopamine, serotonin, and other neurotransmitters. However, it is still unknown whether these reflect primary or secondary aspects of mood disorders.
Furthermore, it is not clear “how probiotics to bacteria can influence these neuronal pathways,” he said.
The research by Dr. Berding and colleagues is funded by a postdoctoral fellowship grant from the Irish Research Council. The study authors and Dr. Fetissov have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The gut microbiota differs significantly between patients with major depressive disorder (MDD) and healthy individuals and may be modifiable with a probiotic diet to improve stress and depression scores, two new studies suggest.
In one study, investigators compared stool samples between patients with MDD and healthy controls. They found significant differences in bacterial profiles between the two groups, as well as between patients who responded vs those who were resistant to treatment.
“This finding further supports the relevance of an altered composition of the gut microbiota in the etiopathogenesis of MDD and suggests a role in response to antidepressants,” coinvestigator Andrea Fontana, MSc, Fondazione IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy, said in an interview.
Results from the second study showed significant improvements in self-reported stress, anxiety, and depression scores in healthy individuals following a “psychobiotic” diet (using probiotics or prebiotics to manipulate the microbiota to improve mental health) that was rich in fruit, vegetables, and fermented foods vs. those who received dietary advice alone.
The investigators, led by Kirsten Berding, PhD, APC Microbiome Ireland, University College Cork, Ireland, now plan on testing their psychobiotic diet in patients with MDD and hope the findings could be helpful in “the development of adjuvant therapeutic opportunities” where pharmacologic treatment is not effective.
Both studies were presented at the virtual congress of the European College of Neuropsychopharmacology, held online this year because of the COVID-19 pandemic.
A “hallmark” of major depression
Mr. Fontana and colleagues note that the mostly suboptimal response to pharmacologic treatments among patients with MDD is one of the factors that “contributes to the large socioeconomic burden” of the disease.
Previous research shows patients with MDD have gut dysbiosis, or an imbalance in the natural flora; that antidepressants have antimicrobial properties; and that probiotics have an antibiotic effect. However, the correlation between the composition of the gut microbiota and antidepressant response is poorly understood.
The investigators recruited 34 patients with MDD (aged 18-70 years) who were in a euthymic phase and who did not have comorbid conditions that could affect the gut microbiota.
Eight patients were treatment resistant, defined as a poor response to at least two adequate trials of different antidepressant classes, while 19 were treatment responsive and seven were treatment naive.
The researchers also recruited 20 healthy individuals via word of mouth to act as the control group. There were no significant differences between patients and the control group in terms of baseline characteristics.
Genomic sequencing of bacteria obtained from stool samples showed that it was possible to distinguish between patients with MDD and the healthy individuals, especially at the family, genus, and species levels.
In particular, there were significant differences in the Paenibacillaceae and Flavobacteriaceaea families, for the genus Fenollaria, and the species Flintibacter butyricus, Christensenella timonensis, and Eisenbergiella massiliensis, among others.
Results also showed that the phyla Proteobacteria, Tenericutes, and the family Peptostreptococcaceae were more common in patients with treatment-resistant MDD, whereas the phylum Actinobacteria was more abundant in treatment responders.
Moreover, several bacteria were found only in the microbiota of patients with treatment-resistant MDD, while others were seen only in treatment-responsive patients. This made it possible to discriminate not only between treatment-resistant and -responsive patients but also between those two patient groups and healthy controls.
“The results of our study confirm that gut dysbiosis is a hallmark of MDD, and suggests that the gut microbiota of patients with treatment-resistant MDD significantly differs from responders to antidepressants,” Mr. Fontana said.
Psychobiotic diet
For the second study, Dr. Berding and colleagues note that “psychobiotics” has previously achieved “promising results.”
In addition, diet is both “one of the most influential modifying factors” for the gut microbiota and an easily accessible strategy, they wrote. However, there is also a paucity of studies in this area, they added.
The researchers randomly assigned healthy volunteers with relatively poor dietary habits to either a 4-week psychobiotic diet group (n = 21) or a control group (n = 19).
Individuals in the psychobiotic group were told to eat a diet rich in prebiotics, such as fruit and vegetables, fiber including whole grains and legumes, and fermented foods. The control group was educated on Irish healthy-eating guidelines.
Stool and saliva samples were collected and the participants completed several self-reported mental health questionnaires, as well as a 7-day food diary. They also took the socially evaluated cold-pressor test (SECPT) to measure acute stress responses.
Results showed that total daily energy intake decreased significantly in both the diet and control groups over the study period (P = .04 for both) but did not differ significantly between the groups.
In contrast, dietary fiber intake increased significantly in the diet group (P < .001) and was significantly higher than in the control group at the end of the intervention (P = .03).
Individuals in the diet group showed significant decreases in scores on the Perceived Stress Scale (P = .002) and the Beck Depression Inventory (P = .007) during the study, an effect that was not found in the control group.
Dietary intervention
There were no significant effects of diet on the acute stress response, but both groups showed improvements in self-concept, or perceived ability to cope, on the Primary Appraisal, Secondary Appraisal index (P = .03 for the diet group, P = .04 for the control group).
The results show that a dietary intervention targeted at the microbiota “can improve subjective feelings of stress and depression in a healthy population,” the investigators wrote.
However, elucidating the “contribution of the microbiota-gut-brain axis on the signaling response to dietary interventions” will require further studies on microbiota sequencing and biological measures of stress, they added.
This will “contribute to the understanding of the benefits of a psychobiotic diet on stress and anxiety,” wrote the researchers.
Dr. Berding said in an interview that while the consumption of dietary fiber changed the most in the diet group, “it would not be the only nutrient” that had an impact on the results, with fermented foods a likely candidate.
She said the next step is to test the dietary intervention in patients with MDD; however, “doing nutritional interventions in diseased populations is always difficult.”
Dr. Berding suggested that the best approach would be to study inpatients in a clinic, as “we would be able to provide every meal and only provide foods that are part of the dietary intervention.”
Although another option would be to conduct the study in outpatients, she noted that assessing inpatients “would give us the best control over compliance.”
“Brilliant ideas”
Commenting on the findings, Sergueï Fetissov, MD, PhD, professor of physiology at Rouen University, Mont-Saint-Aignan, France, said that although both studies bring attention to a possible role for the gut microbiota in MDD, neither “provide any experimental evidence of a causative nature.”
Dr. Fetissov, who was not involved in either study, noted that this topic has been the subject of clinical nutritional research for many years.
However, “we still need some strong evidence to prove that some bacteria can influence the regulation of mood and anxiety and stress,” he said.
In addition, researchers currently do not know what actually causes MDD. “How we can say the gut bacteria regulates something if we don’t know what really causes the altered mood?” said Dr. Fetissov.
He noted that over the last 50 years, there have been great advances in the development of drugs that alleviate depression and anxiety by regulating dopamine, serotonin, and other neurotransmitters. However, it is still unknown whether these reflect primary or secondary aspects of mood disorders.
Furthermore, it is not clear “how probiotics to bacteria can influence these neuronal pathways,” he said.
The research by Dr. Berding and colleagues is funded by a postdoctoral fellowship grant from the Irish Research Council. The study authors and Dr. Fetissov have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The gut microbiota differs significantly between patients with major depressive disorder (MDD) and healthy individuals and may be modifiable with a probiotic diet to improve stress and depression scores, two new studies suggest.
In one study, investigators compared stool samples between patients with MDD and healthy controls. They found significant differences in bacterial profiles between the two groups, as well as between patients who responded vs those who were resistant to treatment.
“This finding further supports the relevance of an altered composition of the gut microbiota in the etiopathogenesis of MDD and suggests a role in response to antidepressants,” coinvestigator Andrea Fontana, MSc, Fondazione IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy, said in an interview.
Results from the second study showed significant improvements in self-reported stress, anxiety, and depression scores in healthy individuals following a “psychobiotic” diet (using probiotics or prebiotics to manipulate the microbiota to improve mental health) that was rich in fruit, vegetables, and fermented foods vs. those who received dietary advice alone.
The investigators, led by Kirsten Berding, PhD, APC Microbiome Ireland, University College Cork, Ireland, now plan on testing their psychobiotic diet in patients with MDD and hope the findings could be helpful in “the development of adjuvant therapeutic opportunities” where pharmacologic treatment is not effective.
Both studies were presented at the virtual congress of the European College of Neuropsychopharmacology, held online this year because of the COVID-19 pandemic.
A “hallmark” of major depression
Mr. Fontana and colleagues note that the mostly suboptimal response to pharmacologic treatments among patients with MDD is one of the factors that “contributes to the large socioeconomic burden” of the disease.
Previous research shows patients with MDD have gut dysbiosis, or an imbalance in the natural flora; that antidepressants have antimicrobial properties; and that probiotics have an antibiotic effect. However, the correlation between the composition of the gut microbiota and antidepressant response is poorly understood.
The investigators recruited 34 patients with MDD (aged 18-70 years) who were in a euthymic phase and who did not have comorbid conditions that could affect the gut microbiota.
Eight patients were treatment resistant, defined as a poor response to at least two adequate trials of different antidepressant classes, while 19 were treatment responsive and seven were treatment naive.
The researchers also recruited 20 healthy individuals via word of mouth to act as the control group. There were no significant differences between patients and the control group in terms of baseline characteristics.
Genomic sequencing of bacteria obtained from stool samples showed that it was possible to distinguish between patients with MDD and the healthy individuals, especially at the family, genus, and species levels.
In particular, there were significant differences in the Paenibacillaceae and Flavobacteriaceaea families, for the genus Fenollaria, and the species Flintibacter butyricus, Christensenella timonensis, and Eisenbergiella massiliensis, among others.
Results also showed that the phyla Proteobacteria, Tenericutes, and the family Peptostreptococcaceae were more common in patients with treatment-resistant MDD, whereas the phylum Actinobacteria was more abundant in treatment responders.
Moreover, several bacteria were found only in the microbiota of patients with treatment-resistant MDD, while others were seen only in treatment-responsive patients. This made it possible to discriminate not only between treatment-resistant and -responsive patients but also between those two patient groups and healthy controls.
“The results of our study confirm that gut dysbiosis is a hallmark of MDD, and suggests that the gut microbiota of patients with treatment-resistant MDD significantly differs from responders to antidepressants,” Mr. Fontana said.
Psychobiotic diet
For the second study, Dr. Berding and colleagues note that “psychobiotics” has previously achieved “promising results.”
In addition, diet is both “one of the most influential modifying factors” for the gut microbiota and an easily accessible strategy, they wrote. However, there is also a paucity of studies in this area, they added.
The researchers randomly assigned healthy volunteers with relatively poor dietary habits to either a 4-week psychobiotic diet group (n = 21) or a control group (n = 19).
Individuals in the psychobiotic group were told to eat a diet rich in prebiotics, such as fruit and vegetables, fiber including whole grains and legumes, and fermented foods. The control group was educated on Irish healthy-eating guidelines.
Stool and saliva samples were collected and the participants completed several self-reported mental health questionnaires, as well as a 7-day food diary. They also took the socially evaluated cold-pressor test (SECPT) to measure acute stress responses.
Results showed that total daily energy intake decreased significantly in both the diet and control groups over the study period (P = .04 for both) but did not differ significantly between the groups.
In contrast, dietary fiber intake increased significantly in the diet group (P < .001) and was significantly higher than in the control group at the end of the intervention (P = .03).
Individuals in the diet group showed significant decreases in scores on the Perceived Stress Scale (P = .002) and the Beck Depression Inventory (P = .007) during the study, an effect that was not found in the control group.
Dietary intervention
There were no significant effects of diet on the acute stress response, but both groups showed improvements in self-concept, or perceived ability to cope, on the Primary Appraisal, Secondary Appraisal index (P = .03 for the diet group, P = .04 for the control group).
The results show that a dietary intervention targeted at the microbiota “can improve subjective feelings of stress and depression in a healthy population,” the investigators wrote.
However, elucidating the “contribution of the microbiota-gut-brain axis on the signaling response to dietary interventions” will require further studies on microbiota sequencing and biological measures of stress, they added.
This will “contribute to the understanding of the benefits of a psychobiotic diet on stress and anxiety,” wrote the researchers.
Dr. Berding said in an interview that while the consumption of dietary fiber changed the most in the diet group, “it would not be the only nutrient” that had an impact on the results, with fermented foods a likely candidate.
She said the next step is to test the dietary intervention in patients with MDD; however, “doing nutritional interventions in diseased populations is always difficult.”
Dr. Berding suggested that the best approach would be to study inpatients in a clinic, as “we would be able to provide every meal and only provide foods that are part of the dietary intervention.”
Although another option would be to conduct the study in outpatients, she noted that assessing inpatients “would give us the best control over compliance.”
“Brilliant ideas”
Commenting on the findings, Sergueï Fetissov, MD, PhD, professor of physiology at Rouen University, Mont-Saint-Aignan, France, said that although both studies bring attention to a possible role for the gut microbiota in MDD, neither “provide any experimental evidence of a causative nature.”
Dr. Fetissov, who was not involved in either study, noted that this topic has been the subject of clinical nutritional research for many years.
However, “we still need some strong evidence to prove that some bacteria can influence the regulation of mood and anxiety and stress,” he said.
In addition, researchers currently do not know what actually causes MDD. “How we can say the gut bacteria regulates something if we don’t know what really causes the altered mood?” said Dr. Fetissov.
He noted that over the last 50 years, there have been great advances in the development of drugs that alleviate depression and anxiety by regulating dopamine, serotonin, and other neurotransmitters. However, it is still unknown whether these reflect primary or secondary aspects of mood disorders.
Furthermore, it is not clear “how probiotics to bacteria can influence these neuronal pathways,” he said.
The research by Dr. Berding and colleagues is funded by a postdoctoral fellowship grant from the Irish Research Council. The study authors and Dr. Fetissov have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
COVID-19 and the psychological side effects of PPE
A few months ago, I published a short thought piece on the use of “sitters” with patients who were COVID-19 positive, or patients under investigation. In it, I recommended the use of telesitters for those who normally would warrant a human sitter, to decrease the discomfort of sitting in full personal protective equipment (PPE) (gown, mask, gloves, etc.) while monitoring a suicidal patient.
I received several queries, which I want to address here. In addition, I want to draw from my Army days in terms of the claustrophobia often experienced with PPE.
The first of the questions was about evidence-based practices. The second was about the discomfort of having sitters sit for many hours in the full gear.
I do not know of any evidence-based practices, but I hope we will develop them.
I agree that spending many hours in full PPE can be discomforting, which is why I wrote the essay.
As far as lessons learned from the Army time, I briefly learned how to wear a “gas mask” or Mission-Oriented Protective Posture (MOPP gear) while at Fort Bragg. We were run through the “gas chamber,” where sergeants released tear gas while we had the mask on. We were then asked to lift it up, and then tearing and sputtering, we could leave the small wooden building.
We wore the mask as part of our Army gear, usually on the right leg. After that, I mainly used the protective mask in its bag as a pillow when I was in the field.
Fast forward to August 1990. I arrived at Camp Casey, near the Korean demilitarized zone. Four days later, Saddam Hussein invaded Kuwait. The gas mask moved from a pillow to something we had to wear while doing 12-mile road marches in “full ruck.” In full ruck, you have your uniform on, with TA-50, knapsack, and weapon. No, I do not remember any more what TA-50 stands for, but essentially it is the webbing that holds your bullets and bandages.
Many could not tolerate it. They developed claustrophobia – sweating, air hunger, and panic. If stationed in the Gulf for Operation Desert Storm, they were evacuated home.
I wrote a couple of short articles on treatment of gas mask phobia.1,2 I basically advised desensitization. Start by watching TV in it for 5 minutes. Graduate to ironing your uniform in the mask. Go then to shorter runs. Work up to the 12-mile road march.
In my second tour in Korea, we had exercises where we simulated being hit by nerve agents and had to operate the hospital for days at a time in partial or full PPE. It was tough but we did it, and felt more confident about surviving attacks from North Korea.
So back to the pandemic present. I have gotten more used to my constant wearing of a surgical mask. I get anxious when I see others with masks below their noses.
The pandemic is not going away anytime soon, in my opinion. Furthermore, there are other viruses that are worse, such as Ebola. It is only a matter of time.
So, let us train with our PPE. If health care workers cannot tolerate them, use desensitization- and anxiety-reducing techniques to help them.
There are no easy answers here, in the time of the COVID pandemic. However, we owe it to ourselves, our patients, and society to do the best we can.
References
1. Ritchie EC. Milit Med. 1992 Feb;157(2):104-6.
2. Ritchie EC. Milit Med. 2001 Dec;166. Suppl. 2(1)83-4.
Dr. Ritchie is chair of psychiatry at Medstar Washington Hospital Center and professor of psychiatry at Georgetown University, Washington. She has no disclosures and can be reached at cpnews@mdedge.com.
A few months ago, I published a short thought piece on the use of “sitters” with patients who were COVID-19 positive, or patients under investigation. In it, I recommended the use of telesitters for those who normally would warrant a human sitter, to decrease the discomfort of sitting in full personal protective equipment (PPE) (gown, mask, gloves, etc.) while monitoring a suicidal patient.
I received several queries, which I want to address here. In addition, I want to draw from my Army days in terms of the claustrophobia often experienced with PPE.
The first of the questions was about evidence-based practices. The second was about the discomfort of having sitters sit for many hours in the full gear.
I do not know of any evidence-based practices, but I hope we will develop them.
I agree that spending many hours in full PPE can be discomforting, which is why I wrote the essay.
As far as lessons learned from the Army time, I briefly learned how to wear a “gas mask” or Mission-Oriented Protective Posture (MOPP gear) while at Fort Bragg. We were run through the “gas chamber,” where sergeants released tear gas while we had the mask on. We were then asked to lift it up, and then tearing and sputtering, we could leave the small wooden building.
We wore the mask as part of our Army gear, usually on the right leg. After that, I mainly used the protective mask in its bag as a pillow when I was in the field.
Fast forward to August 1990. I arrived at Camp Casey, near the Korean demilitarized zone. Four days later, Saddam Hussein invaded Kuwait. The gas mask moved from a pillow to something we had to wear while doing 12-mile road marches in “full ruck.” In full ruck, you have your uniform on, with TA-50, knapsack, and weapon. No, I do not remember any more what TA-50 stands for, but essentially it is the webbing that holds your bullets and bandages.
Many could not tolerate it. They developed claustrophobia – sweating, air hunger, and panic. If stationed in the Gulf for Operation Desert Storm, they were evacuated home.
I wrote a couple of short articles on treatment of gas mask phobia.1,2 I basically advised desensitization. Start by watching TV in it for 5 minutes. Graduate to ironing your uniform in the mask. Go then to shorter runs. Work up to the 12-mile road march.
In my second tour in Korea, we had exercises where we simulated being hit by nerve agents and had to operate the hospital for days at a time in partial or full PPE. It was tough but we did it, and felt more confident about surviving attacks from North Korea.
So back to the pandemic present. I have gotten more used to my constant wearing of a surgical mask. I get anxious when I see others with masks below their noses.
The pandemic is not going away anytime soon, in my opinion. Furthermore, there are other viruses that are worse, such as Ebola. It is only a matter of time.
So, let us train with our PPE. If health care workers cannot tolerate them, use desensitization- and anxiety-reducing techniques to help them.
There are no easy answers here, in the time of the COVID pandemic. However, we owe it to ourselves, our patients, and society to do the best we can.
References
1. Ritchie EC. Milit Med. 1992 Feb;157(2):104-6.
2. Ritchie EC. Milit Med. 2001 Dec;166. Suppl. 2(1)83-4.
Dr. Ritchie is chair of psychiatry at Medstar Washington Hospital Center and professor of psychiatry at Georgetown University, Washington. She has no disclosures and can be reached at cpnews@mdedge.com.
A few months ago, I published a short thought piece on the use of “sitters” with patients who were COVID-19 positive, or patients under investigation. In it, I recommended the use of telesitters for those who normally would warrant a human sitter, to decrease the discomfort of sitting in full personal protective equipment (PPE) (gown, mask, gloves, etc.) while monitoring a suicidal patient.
I received several queries, which I want to address here. In addition, I want to draw from my Army days in terms of the claustrophobia often experienced with PPE.
The first of the questions was about evidence-based practices. The second was about the discomfort of having sitters sit for many hours in the full gear.
I do not know of any evidence-based practices, but I hope we will develop them.
I agree that spending many hours in full PPE can be discomforting, which is why I wrote the essay.
As far as lessons learned from the Army time, I briefly learned how to wear a “gas mask” or Mission-Oriented Protective Posture (MOPP gear) while at Fort Bragg. We were run through the “gas chamber,” where sergeants released tear gas while we had the mask on. We were then asked to lift it up, and then tearing and sputtering, we could leave the small wooden building.
We wore the mask as part of our Army gear, usually on the right leg. After that, I mainly used the protective mask in its bag as a pillow when I was in the field.
Fast forward to August 1990. I arrived at Camp Casey, near the Korean demilitarized zone. Four days later, Saddam Hussein invaded Kuwait. The gas mask moved from a pillow to something we had to wear while doing 12-mile road marches in “full ruck.” In full ruck, you have your uniform on, with TA-50, knapsack, and weapon. No, I do not remember any more what TA-50 stands for, but essentially it is the webbing that holds your bullets and bandages.
Many could not tolerate it. They developed claustrophobia – sweating, air hunger, and panic. If stationed in the Gulf for Operation Desert Storm, they were evacuated home.
I wrote a couple of short articles on treatment of gas mask phobia.1,2 I basically advised desensitization. Start by watching TV in it for 5 minutes. Graduate to ironing your uniform in the mask. Go then to shorter runs. Work up to the 12-mile road march.
In my second tour in Korea, we had exercises where we simulated being hit by nerve agents and had to operate the hospital for days at a time in partial or full PPE. It was tough but we did it, and felt more confident about surviving attacks from North Korea.
So back to the pandemic present. I have gotten more used to my constant wearing of a surgical mask. I get anxious when I see others with masks below their noses.
The pandemic is not going away anytime soon, in my opinion. Furthermore, there are other viruses that are worse, such as Ebola. It is only a matter of time.
So, let us train with our PPE. If health care workers cannot tolerate them, use desensitization- and anxiety-reducing techniques to help them.
There are no easy answers here, in the time of the COVID pandemic. However, we owe it to ourselves, our patients, and society to do the best we can.
References
1. Ritchie EC. Milit Med. 1992 Feb;157(2):104-6.
2. Ritchie EC. Milit Med. 2001 Dec;166. Suppl. 2(1)83-4.
Dr. Ritchie is chair of psychiatry at Medstar Washington Hospital Center and professor of psychiatry at Georgetown University, Washington. She has no disclosures and can be reached at cpnews@mdedge.com.