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LGBTQ+ teens in homophobic high schools
I am a psychiatrist now but had another life teaching English in public high school for 17 years. My teaching life, in which I was an openly gay teacher, spanned 2001-2018 and was divided between two urban California schools – in Berkeley and San Leandro. I came out by responding honestly to student questions about whether I had a girlfriend, and what I did over the weekend. At Berkeley High my openness wasn’t an issue at all. The school had a vibrant Gay Straight Alliance/GSA for years, there were many openly gay staff and many openly gay students. No students felt the need to come out to me in search of a gay mentor.
Two years later, I began teaching in San Leandro, 20 miles away, and it was a lesson in how even the San Francisco Bay Area, an LGBTQ+ bastion, could harbor homophobia. When I was hired in 2003, San Leandro High had one openly gay teacher, Q. I quickly realized how much braver his coming out was compared with mine in Berkeley.
In San Leandro, gay slurs were heard nonstop in the hallways, no students were out, and by the end of my first year Q had quit, confiding in me that he couldn’t handle the homophobic harassment from students anymore. There was no GSA. A few years ago, two lesbians had held hands during lunch and inspired the wrath of a group of parents who advocated for their expulsion. In response, a teacher tried to introduce gay sensitivity training into his class and the same group of parents tried to get him fired. He was reprimanded by the principal, he countersued in a case that went all the way to the California Supreme Court, and won. Comparing these two local high schools reinforced to me how visibility really matters in creating a childhood experience that is nurturing versus traumatizing.1
Two Chinese girls in love
N and T were two Chinese girls who grew up in San Leandro. They went to the same elementary school and had crushes on each other since then. In their junior year, they joined our first student GSA, becoming president and vice-president. They were out. And, of course, they must’ve known that their families, who would not have been supportive, would become aware. I remember sitting at an outdoor concert when I got a text from N warning me her father had found out and blamed me for having corrupted her. He planned on coming to school to demand I be fired. And such was the unrelenting pressure that N and T faced every time they went home from school and sat at their dinner tables. Eventually, they broke up. They didn’t do so tearfully, but more wearily.
This story illustrates how difficult it is for love between two LGBTQ+ teens to be nurtured. Love in youth can already be volatile because of the lack of emotional regulation and experience. The questioning of identity and the threat of family disintegration at a time when these teens do not have the economic means to protect themselves makes love dangerous. It is no wonder that gay teens are at increased risk for homelessness.2
The family incident that led to the girls’ breakup reveals how culture affects homophobic pressure. N resisted her parents’ disapproval for months, but she capitulated when her father had a heart attack and blamed it on her. “And it’s true,” N confided. “After my parents found out, they were continually stressed. I could see it affect their health. And it breaks my heart to see my dad in the hospital.”
For N, she had not capitulated from fear, but perhaps because of filial piety, or one’s obligation to protect one’s parent. It was a choice between two heartbreaks. Double minorities, like N and T, face a double threat and often can find no safe place. One of my patients who is gay and Black put it best: “It’s like being beaten up at school only to come home to another beating.” This double threat is evidenced by the higher suicide risk of ethnicities who are LGBTQ+ relative to their white counterparts.3
The confusion of a gay athlete
R was a star point guard, a senior who had secured an athletic scholarship, and was recognized as the best athlete in our county. A popular boy, he flaunted his physique and flirted with all the girls. And then when he was enrolled in my class, he began flirting with all the boys, too. There was gossip that R was bisexual. Then one day, not unexpectedly, he came out to me as gay. He admitted he only flirted with girls for his reputation.
By this time many students had come out to me but he flirted with me with his revelation. I corrected him and warned him unequivocally that it was inappropriate but I was worried because I knew he had placed his trust in me. I also knew he came from a homophobic family that was violent – his father had attacked him physically at a school game and our coaches had to pull him off.
Instinctively, I felt I had to have a witness so I confided in another teacher and documented the situation meticulously. Then, one day, just as I feared, he went too far. He stayed after class and said he wanted to show me something on his phone. And that something turned out to be a picture of himself naked. I immediately confiscated the phone and reported it to the administration. This was not how I wanted him to come out: His family notified by the police that he had sexually harassed his teacher, expulsion pending, and scholarship inevitably revoked. Fortunately, we did find a resolution that restored R’s future.
Let’s examine the circumstances that could’ve informed his transgressive behavior. If we consider sexual harassment a form of bullying, R’s history of having a father who publicly bullied him – and may have bullied others in front of him – is a known risk factor.4 It is also common knowledge that organized team sports were and still are a bastion of homophobia and that gay athletes had to accept a culture of explicit homophobia.5
So, it is not hard to understand the constant public pressures that R faced in addition to those from his family. Let’s also consider that appropriate sexual behaviors are not something we are born with, but something that is learned. Of course, inappropriate sexual behavior also happens in the heterosexual world. But heterosexual sexual behavior often has more accepted paths of trial and error. Children experiment with these behaviors and are corrected by adults and older peers as they mature.
However, for homosexual behaviors, there is not usually the fine-tuning about what is appropriate.
Summary
An educational environment where LGBTQ+ persons are highly visible and accepted is a more nurturing environment for LGBTQ teens than one that is not. Specific subcultures within the LGBTQ population involving race, culture, gender, and athletics modulate the experience of coming out and the nature of homophobic oppression.
Dr. Nguyen is a first-year psychiatry resident at the University of San Francisco School of Medicine at Fresno.
References
1. Kosciw JG et al. The effect of negative school climate on academic outcomes for LGBT youth and the role of in-school supports. J Sch Violence. 2013;12(1):45-63.
2. Center for American Progress. Gay and Transgender Youth Homelessness by the Numbers. June 21, 2010).
3. O’Donnell S et al. Increased risk of suicide attempts among Black and Latino lesbians, gay men, and bisexuals. Am J Public Health. 2011;101(6):1055-9.
4. Farrington D and Baldry A. Individual risk factors for school bullying. J Aggress Confl Peace Res. 2010 Jan;2(1):4-16.
5. Anderson E. Openly gay athletes: Contesting hegemonic masculinity in a homophobic environment Gend Soc. 2002 Dec:16(6):860-77.
I am a psychiatrist now but had another life teaching English in public high school for 17 years. My teaching life, in which I was an openly gay teacher, spanned 2001-2018 and was divided between two urban California schools – in Berkeley and San Leandro. I came out by responding honestly to student questions about whether I had a girlfriend, and what I did over the weekend. At Berkeley High my openness wasn’t an issue at all. The school had a vibrant Gay Straight Alliance/GSA for years, there were many openly gay staff and many openly gay students. No students felt the need to come out to me in search of a gay mentor.
Two years later, I began teaching in San Leandro, 20 miles away, and it was a lesson in how even the San Francisco Bay Area, an LGBTQ+ bastion, could harbor homophobia. When I was hired in 2003, San Leandro High had one openly gay teacher, Q. I quickly realized how much braver his coming out was compared with mine in Berkeley.
In San Leandro, gay slurs were heard nonstop in the hallways, no students were out, and by the end of my first year Q had quit, confiding in me that he couldn’t handle the homophobic harassment from students anymore. There was no GSA. A few years ago, two lesbians had held hands during lunch and inspired the wrath of a group of parents who advocated for their expulsion. In response, a teacher tried to introduce gay sensitivity training into his class and the same group of parents tried to get him fired. He was reprimanded by the principal, he countersued in a case that went all the way to the California Supreme Court, and won. Comparing these two local high schools reinforced to me how visibility really matters in creating a childhood experience that is nurturing versus traumatizing.1
Two Chinese girls in love
N and T were two Chinese girls who grew up in San Leandro. They went to the same elementary school and had crushes on each other since then. In their junior year, they joined our first student GSA, becoming president and vice-president. They were out. And, of course, they must’ve known that their families, who would not have been supportive, would become aware. I remember sitting at an outdoor concert when I got a text from N warning me her father had found out and blamed me for having corrupted her. He planned on coming to school to demand I be fired. And such was the unrelenting pressure that N and T faced every time they went home from school and sat at their dinner tables. Eventually, they broke up. They didn’t do so tearfully, but more wearily.
This story illustrates how difficult it is for love between two LGBTQ+ teens to be nurtured. Love in youth can already be volatile because of the lack of emotional regulation and experience. The questioning of identity and the threat of family disintegration at a time when these teens do not have the economic means to protect themselves makes love dangerous. It is no wonder that gay teens are at increased risk for homelessness.2
The family incident that led to the girls’ breakup reveals how culture affects homophobic pressure. N resisted her parents’ disapproval for months, but she capitulated when her father had a heart attack and blamed it on her. “And it’s true,” N confided. “After my parents found out, they were continually stressed. I could see it affect their health. And it breaks my heart to see my dad in the hospital.”
For N, she had not capitulated from fear, but perhaps because of filial piety, or one’s obligation to protect one’s parent. It was a choice between two heartbreaks. Double minorities, like N and T, face a double threat and often can find no safe place. One of my patients who is gay and Black put it best: “It’s like being beaten up at school only to come home to another beating.” This double threat is evidenced by the higher suicide risk of ethnicities who are LGBTQ+ relative to their white counterparts.3
The confusion of a gay athlete
R was a star point guard, a senior who had secured an athletic scholarship, and was recognized as the best athlete in our county. A popular boy, he flaunted his physique and flirted with all the girls. And then when he was enrolled in my class, he began flirting with all the boys, too. There was gossip that R was bisexual. Then one day, not unexpectedly, he came out to me as gay. He admitted he only flirted with girls for his reputation.
By this time many students had come out to me but he flirted with me with his revelation. I corrected him and warned him unequivocally that it was inappropriate but I was worried because I knew he had placed his trust in me. I also knew he came from a homophobic family that was violent – his father had attacked him physically at a school game and our coaches had to pull him off.
Instinctively, I felt I had to have a witness so I confided in another teacher and documented the situation meticulously. Then, one day, just as I feared, he went too far. He stayed after class and said he wanted to show me something on his phone. And that something turned out to be a picture of himself naked. I immediately confiscated the phone and reported it to the administration. This was not how I wanted him to come out: His family notified by the police that he had sexually harassed his teacher, expulsion pending, and scholarship inevitably revoked. Fortunately, we did find a resolution that restored R’s future.
Let’s examine the circumstances that could’ve informed his transgressive behavior. If we consider sexual harassment a form of bullying, R’s history of having a father who publicly bullied him – and may have bullied others in front of him – is a known risk factor.4 It is also common knowledge that organized team sports were and still are a bastion of homophobia and that gay athletes had to accept a culture of explicit homophobia.5
So, it is not hard to understand the constant public pressures that R faced in addition to those from his family. Let’s also consider that appropriate sexual behaviors are not something we are born with, but something that is learned. Of course, inappropriate sexual behavior also happens in the heterosexual world. But heterosexual sexual behavior often has more accepted paths of trial and error. Children experiment with these behaviors and are corrected by adults and older peers as they mature.
However, for homosexual behaviors, there is not usually the fine-tuning about what is appropriate.
Summary
An educational environment where LGBTQ+ persons are highly visible and accepted is a more nurturing environment for LGBTQ teens than one that is not. Specific subcultures within the LGBTQ population involving race, culture, gender, and athletics modulate the experience of coming out and the nature of homophobic oppression.
Dr. Nguyen is a first-year psychiatry resident at the University of San Francisco School of Medicine at Fresno.
References
1. Kosciw JG et al. The effect of negative school climate on academic outcomes for LGBT youth and the role of in-school supports. J Sch Violence. 2013;12(1):45-63.
2. Center for American Progress. Gay and Transgender Youth Homelessness by the Numbers. June 21, 2010).
3. O’Donnell S et al. Increased risk of suicide attempts among Black and Latino lesbians, gay men, and bisexuals. Am J Public Health. 2011;101(6):1055-9.
4. Farrington D and Baldry A. Individual risk factors for school bullying. J Aggress Confl Peace Res. 2010 Jan;2(1):4-16.
5. Anderson E. Openly gay athletes: Contesting hegemonic masculinity in a homophobic environment Gend Soc. 2002 Dec:16(6):860-77.
I am a psychiatrist now but had another life teaching English in public high school for 17 years. My teaching life, in which I was an openly gay teacher, spanned 2001-2018 and was divided between two urban California schools – in Berkeley and San Leandro. I came out by responding honestly to student questions about whether I had a girlfriend, and what I did over the weekend. At Berkeley High my openness wasn’t an issue at all. The school had a vibrant Gay Straight Alliance/GSA for years, there were many openly gay staff and many openly gay students. No students felt the need to come out to me in search of a gay mentor.
Two years later, I began teaching in San Leandro, 20 miles away, and it was a lesson in how even the San Francisco Bay Area, an LGBTQ+ bastion, could harbor homophobia. When I was hired in 2003, San Leandro High had one openly gay teacher, Q. I quickly realized how much braver his coming out was compared with mine in Berkeley.
In San Leandro, gay slurs were heard nonstop in the hallways, no students were out, and by the end of my first year Q had quit, confiding in me that he couldn’t handle the homophobic harassment from students anymore. There was no GSA. A few years ago, two lesbians had held hands during lunch and inspired the wrath of a group of parents who advocated for their expulsion. In response, a teacher tried to introduce gay sensitivity training into his class and the same group of parents tried to get him fired. He was reprimanded by the principal, he countersued in a case that went all the way to the California Supreme Court, and won. Comparing these two local high schools reinforced to me how visibility really matters in creating a childhood experience that is nurturing versus traumatizing.1
Two Chinese girls in love
N and T were two Chinese girls who grew up in San Leandro. They went to the same elementary school and had crushes on each other since then. In their junior year, they joined our first student GSA, becoming president and vice-president. They were out. And, of course, they must’ve known that their families, who would not have been supportive, would become aware. I remember sitting at an outdoor concert when I got a text from N warning me her father had found out and blamed me for having corrupted her. He planned on coming to school to demand I be fired. And such was the unrelenting pressure that N and T faced every time they went home from school and sat at their dinner tables. Eventually, they broke up. They didn’t do so tearfully, but more wearily.
This story illustrates how difficult it is for love between two LGBTQ+ teens to be nurtured. Love in youth can already be volatile because of the lack of emotional regulation and experience. The questioning of identity and the threat of family disintegration at a time when these teens do not have the economic means to protect themselves makes love dangerous. It is no wonder that gay teens are at increased risk for homelessness.2
The family incident that led to the girls’ breakup reveals how culture affects homophobic pressure. N resisted her parents’ disapproval for months, but she capitulated when her father had a heart attack and blamed it on her. “And it’s true,” N confided. “After my parents found out, they were continually stressed. I could see it affect their health. And it breaks my heart to see my dad in the hospital.”
For N, she had not capitulated from fear, but perhaps because of filial piety, or one’s obligation to protect one’s parent. It was a choice between two heartbreaks. Double minorities, like N and T, face a double threat and often can find no safe place. One of my patients who is gay and Black put it best: “It’s like being beaten up at school only to come home to another beating.” This double threat is evidenced by the higher suicide risk of ethnicities who are LGBTQ+ relative to their white counterparts.3
The confusion of a gay athlete
R was a star point guard, a senior who had secured an athletic scholarship, and was recognized as the best athlete in our county. A popular boy, he flaunted his physique and flirted with all the girls. And then when he was enrolled in my class, he began flirting with all the boys, too. There was gossip that R was bisexual. Then one day, not unexpectedly, he came out to me as gay. He admitted he only flirted with girls for his reputation.
By this time many students had come out to me but he flirted with me with his revelation. I corrected him and warned him unequivocally that it was inappropriate but I was worried because I knew he had placed his trust in me. I also knew he came from a homophobic family that was violent – his father had attacked him physically at a school game and our coaches had to pull him off.
Instinctively, I felt I had to have a witness so I confided in another teacher and documented the situation meticulously. Then, one day, just as I feared, he went too far. He stayed after class and said he wanted to show me something on his phone. And that something turned out to be a picture of himself naked. I immediately confiscated the phone and reported it to the administration. This was not how I wanted him to come out: His family notified by the police that he had sexually harassed his teacher, expulsion pending, and scholarship inevitably revoked. Fortunately, we did find a resolution that restored R’s future.
Let’s examine the circumstances that could’ve informed his transgressive behavior. If we consider sexual harassment a form of bullying, R’s history of having a father who publicly bullied him – and may have bullied others in front of him – is a known risk factor.4 It is also common knowledge that organized team sports were and still are a bastion of homophobia and that gay athletes had to accept a culture of explicit homophobia.5
So, it is not hard to understand the constant public pressures that R faced in addition to those from his family. Let’s also consider that appropriate sexual behaviors are not something we are born with, but something that is learned. Of course, inappropriate sexual behavior also happens in the heterosexual world. But heterosexual sexual behavior often has more accepted paths of trial and error. Children experiment with these behaviors and are corrected by adults and older peers as they mature.
However, for homosexual behaviors, there is not usually the fine-tuning about what is appropriate.
Summary
An educational environment where LGBTQ+ persons are highly visible and accepted is a more nurturing environment for LGBTQ teens than one that is not. Specific subcultures within the LGBTQ population involving race, culture, gender, and athletics modulate the experience of coming out and the nature of homophobic oppression.
Dr. Nguyen is a first-year psychiatry resident at the University of San Francisco School of Medicine at Fresno.
References
1. Kosciw JG et al. The effect of negative school climate on academic outcomes for LGBT youth and the role of in-school supports. J Sch Violence. 2013;12(1):45-63.
2. Center for American Progress. Gay and Transgender Youth Homelessness by the Numbers. June 21, 2010).
3. O’Donnell S et al. Increased risk of suicide attempts among Black and Latino lesbians, gay men, and bisexuals. Am J Public Health. 2011;101(6):1055-9.
4. Farrington D and Baldry A. Individual risk factors for school bullying. J Aggress Confl Peace Res. 2010 Jan;2(1):4-16.
5. Anderson E. Openly gay athletes: Contesting hegemonic masculinity in a homophobic environment Gend Soc. 2002 Dec:16(6):860-77.
Spinosad: New kid on the block for treating scabies
HONOLULU – , Anthony J. Mancini, MD, said during a presentation at the Hawaii Dermatology Seminar provided by MedscapeLIVE!
In April 2021, spinosad topical suspension 0.9%, was approved by the Food and Drug Administration for treating scabies infestations in adult and pediatric patients 4 years of age and older – a first-in-class drug and the first new scabicide approved in 31 years. It was also approved for treating head lice in adults and children aged 6 months of age and older.
“Scabies has been described as the worst itch one can experience,” said Dr. Mancini, professor of pediatrics and dermatology at Northwestern University, Chicago. “It’s a hallmark of the disease, it can persist for weeks, it’s most intense at night, and patients report various sensations. It’s believed to be a both type I and type IV hypersensitivity reaction.”
The microscopic scabies mite burrows into the upper layer of the skin where it lives and lays its eggs. Besides intense itching, the classic presentation consists of a skin rash composed of inflammatory papules, linear burrows and crusted papules (especially on the hands, feet, and groin), and at times, larger red nodules. “Scabies nodules can persist for many months,” he said.
The Global Burden of Disease Study 2015 cited scabies as having the greatest burden of disease in tropical regions, especially among children, adolescents, and the elderly. The greatest burden of disability-adjusted life years (DALYs) occurred in East and Southeast Asia, Oceana, and tropical South America, but in North America, there was a 24% increase in the DALY rate between 1990 and 2015.
In addition, the World Health Organization designated scabies as a neglected tropical disease in 2017 and included it in its 10-year road map for neglected tropical diseases 2021-2030 with goals of promoting disease awareness and encouraging research and achieving global control.
“In our country, we typically see scabies treated successfully without complications, but there can be complications, especially in underdeveloped areas, like Staph aureus and Group A beta-hemolytic streptococcal infections,” which can be fatal, said Dr. Mancini, who is also head of pediatric dermatology at Ann & Robert H. Lurie Children’s Hospital of Chicago.
Permethrin 5% cream is typically offered as first-line topical therapy in the United States for the treatment of scabies. However, in vitro studies and small investigator-initiated in vivo studies have reported that efficacy appears to be decreasing. In one of the trials, Italian researchers enrolled 155 patients who were treated with permethrin 5% for 8 hours for 2 consecutive days and repeated the treatment 5 days later . Following the course of permethrin, only 34 responded, 96 failed treatment, and 25 were lost to follow-up.
“The study authors concluded that mite resistance to permethrin 5% seems to be increasing, following a path like other ectoparasite resistance,” said Dr. Mancini, who was not involved with the study. “We may even be seeing more ivermectin resistance in some geographic locations, as well.”
According to new scabicide efficacy criteria established by the FDA in 2016, complete cure is now defined as meeting both clinical and confirmatory criteria. A clinical cure means that all signs and symptoms of scabies have completely resolved, including burrows, inflammatory/noninflammatory lesions, and pruritus. A confirmatory cure means there is an absence of mites, eggs, scybala (feces), and burrows via microscopy or dermoscopy.
Enter spinosad, which is derived from a naturally occurring soil microorganism known as Saccharopolyspora spinosa and is composed of two active molecules: spinosyn A and spinosyn D. According to Dr. Mancini, spinosad’s mechanism of action is unique from other medications used to treat ectoparasites. It activates nicotinic and GABA-gated sodium channels, leads to sodium influx in the insect nerves, hyperexcitation, then paralysis and death. Cross-resistance to other insecticides has not been reported, he added, and there is no known evidence of resistance to its active compound.
Approval of the drug was based on data from two phase 3 randomized clinical trials involving 551 index cases and household contacts. In the intent-to-treat population, with the two trials combined, complete cure was achieved in 78.1% of the spinosad-treated group, compared with 39.6% in the vehicle group (P < .0001), clinical cure was achieved in 79.6% of the spinosad group, compared with 41.2% in the vehicle group (P < .001), and microscopic cure occurred in 85.9% of the spinosad group, compared with 52.6% in the vehicle group (P < .001).
Of the 306 participants in the study, the only adverse events reported by more than one patient each included abdominal pain, back pain, cough, headache, neck pain, and decreased weight in two patients each (0.8%), which investigators believed were not attributable to the study drug. Adverse events that investigators considered to be potentially related to the study drug included burning sensation in two participants (0.7%) and dry skin in another (0.3%). In clinical trials reported in the prescribing information, adverse events occurring in greater than 1% of subjects included application-site irritation (3% spinosad vs. 0% vehicle) and dry skin (2% spinosad vs. 0% vehicle).
“Spinosad met the FDA’s new stringent criteria, with all signs and symptoms of scabies completely resolved and confirmed via microscopy or dermoscopy,” said Dr. Mancini, who was not involved in the trials. “The patented formulation drives the active compound to the stratum corneum, where mites live and breed. It’s a single full-body application, without any resistance observed to date. This is an exciting newer option for treating our scabies patients.”
In an interview at the meeting, John S. Barbieri, MD, MBA, of the department of dermatology, Brigham and Women’s Hospital, Boston, said that, while he has no clinical experience with spinosad for scabies, he welcomes a new option for the condition. “The fact that it has a different mechanism of action than permethrin is a good thing,” he said.
Dr. Mancini disclosed that he is a consultant or an adviser for ParaPRO, the manufacturer of spinosad, and Cassiopea, Castle Creek, Novan, Novartis, and Verrica. He was not involved in clinical trials of spinosad. Dr. Barbieri disclosed that he receives consulting fees from Dexcel.
Medscape and this news organization are owned by the same parent company.
HONOLULU – , Anthony J. Mancini, MD, said during a presentation at the Hawaii Dermatology Seminar provided by MedscapeLIVE!
In April 2021, spinosad topical suspension 0.9%, was approved by the Food and Drug Administration for treating scabies infestations in adult and pediatric patients 4 years of age and older – a first-in-class drug and the first new scabicide approved in 31 years. It was also approved for treating head lice in adults and children aged 6 months of age and older.
“Scabies has been described as the worst itch one can experience,” said Dr. Mancini, professor of pediatrics and dermatology at Northwestern University, Chicago. “It’s a hallmark of the disease, it can persist for weeks, it’s most intense at night, and patients report various sensations. It’s believed to be a both type I and type IV hypersensitivity reaction.”
The microscopic scabies mite burrows into the upper layer of the skin where it lives and lays its eggs. Besides intense itching, the classic presentation consists of a skin rash composed of inflammatory papules, linear burrows and crusted papules (especially on the hands, feet, and groin), and at times, larger red nodules. “Scabies nodules can persist for many months,” he said.
The Global Burden of Disease Study 2015 cited scabies as having the greatest burden of disease in tropical regions, especially among children, adolescents, and the elderly. The greatest burden of disability-adjusted life years (DALYs) occurred in East and Southeast Asia, Oceana, and tropical South America, but in North America, there was a 24% increase in the DALY rate between 1990 and 2015.
In addition, the World Health Organization designated scabies as a neglected tropical disease in 2017 and included it in its 10-year road map for neglected tropical diseases 2021-2030 with goals of promoting disease awareness and encouraging research and achieving global control.
“In our country, we typically see scabies treated successfully without complications, but there can be complications, especially in underdeveloped areas, like Staph aureus and Group A beta-hemolytic streptococcal infections,” which can be fatal, said Dr. Mancini, who is also head of pediatric dermatology at Ann & Robert H. Lurie Children’s Hospital of Chicago.
Permethrin 5% cream is typically offered as first-line topical therapy in the United States for the treatment of scabies. However, in vitro studies and small investigator-initiated in vivo studies have reported that efficacy appears to be decreasing. In one of the trials, Italian researchers enrolled 155 patients who were treated with permethrin 5% for 8 hours for 2 consecutive days and repeated the treatment 5 days later . Following the course of permethrin, only 34 responded, 96 failed treatment, and 25 were lost to follow-up.
“The study authors concluded that mite resistance to permethrin 5% seems to be increasing, following a path like other ectoparasite resistance,” said Dr. Mancini, who was not involved with the study. “We may even be seeing more ivermectin resistance in some geographic locations, as well.”
According to new scabicide efficacy criteria established by the FDA in 2016, complete cure is now defined as meeting both clinical and confirmatory criteria. A clinical cure means that all signs and symptoms of scabies have completely resolved, including burrows, inflammatory/noninflammatory lesions, and pruritus. A confirmatory cure means there is an absence of mites, eggs, scybala (feces), and burrows via microscopy or dermoscopy.
Enter spinosad, which is derived from a naturally occurring soil microorganism known as Saccharopolyspora spinosa and is composed of two active molecules: spinosyn A and spinosyn D. According to Dr. Mancini, spinosad’s mechanism of action is unique from other medications used to treat ectoparasites. It activates nicotinic and GABA-gated sodium channels, leads to sodium influx in the insect nerves, hyperexcitation, then paralysis and death. Cross-resistance to other insecticides has not been reported, he added, and there is no known evidence of resistance to its active compound.
Approval of the drug was based on data from two phase 3 randomized clinical trials involving 551 index cases and household contacts. In the intent-to-treat population, with the two trials combined, complete cure was achieved in 78.1% of the spinosad-treated group, compared with 39.6% in the vehicle group (P < .0001), clinical cure was achieved in 79.6% of the spinosad group, compared with 41.2% in the vehicle group (P < .001), and microscopic cure occurred in 85.9% of the spinosad group, compared with 52.6% in the vehicle group (P < .001).
Of the 306 participants in the study, the only adverse events reported by more than one patient each included abdominal pain, back pain, cough, headache, neck pain, and decreased weight in two patients each (0.8%), which investigators believed were not attributable to the study drug. Adverse events that investigators considered to be potentially related to the study drug included burning sensation in two participants (0.7%) and dry skin in another (0.3%). In clinical trials reported in the prescribing information, adverse events occurring in greater than 1% of subjects included application-site irritation (3% spinosad vs. 0% vehicle) and dry skin (2% spinosad vs. 0% vehicle).
“Spinosad met the FDA’s new stringent criteria, with all signs and symptoms of scabies completely resolved and confirmed via microscopy or dermoscopy,” said Dr. Mancini, who was not involved in the trials. “The patented formulation drives the active compound to the stratum corneum, where mites live and breed. It’s a single full-body application, without any resistance observed to date. This is an exciting newer option for treating our scabies patients.”
In an interview at the meeting, John S. Barbieri, MD, MBA, of the department of dermatology, Brigham and Women’s Hospital, Boston, said that, while he has no clinical experience with spinosad for scabies, he welcomes a new option for the condition. “The fact that it has a different mechanism of action than permethrin is a good thing,” he said.
Dr. Mancini disclosed that he is a consultant or an adviser for ParaPRO, the manufacturer of spinosad, and Cassiopea, Castle Creek, Novan, Novartis, and Verrica. He was not involved in clinical trials of spinosad. Dr. Barbieri disclosed that he receives consulting fees from Dexcel.
Medscape and this news organization are owned by the same parent company.
HONOLULU – , Anthony J. Mancini, MD, said during a presentation at the Hawaii Dermatology Seminar provided by MedscapeLIVE!
In April 2021, spinosad topical suspension 0.9%, was approved by the Food and Drug Administration for treating scabies infestations in adult and pediatric patients 4 years of age and older – a first-in-class drug and the first new scabicide approved in 31 years. It was also approved for treating head lice in adults and children aged 6 months of age and older.
“Scabies has been described as the worst itch one can experience,” said Dr. Mancini, professor of pediatrics and dermatology at Northwestern University, Chicago. “It’s a hallmark of the disease, it can persist for weeks, it’s most intense at night, and patients report various sensations. It’s believed to be a both type I and type IV hypersensitivity reaction.”
The microscopic scabies mite burrows into the upper layer of the skin where it lives and lays its eggs. Besides intense itching, the classic presentation consists of a skin rash composed of inflammatory papules, linear burrows and crusted papules (especially on the hands, feet, and groin), and at times, larger red nodules. “Scabies nodules can persist for many months,” he said.
The Global Burden of Disease Study 2015 cited scabies as having the greatest burden of disease in tropical regions, especially among children, adolescents, and the elderly. The greatest burden of disability-adjusted life years (DALYs) occurred in East and Southeast Asia, Oceana, and tropical South America, but in North America, there was a 24% increase in the DALY rate between 1990 and 2015.
In addition, the World Health Organization designated scabies as a neglected tropical disease in 2017 and included it in its 10-year road map for neglected tropical diseases 2021-2030 with goals of promoting disease awareness and encouraging research and achieving global control.
“In our country, we typically see scabies treated successfully without complications, but there can be complications, especially in underdeveloped areas, like Staph aureus and Group A beta-hemolytic streptococcal infections,” which can be fatal, said Dr. Mancini, who is also head of pediatric dermatology at Ann & Robert H. Lurie Children’s Hospital of Chicago.
Permethrin 5% cream is typically offered as first-line topical therapy in the United States for the treatment of scabies. However, in vitro studies and small investigator-initiated in vivo studies have reported that efficacy appears to be decreasing. In one of the trials, Italian researchers enrolled 155 patients who were treated with permethrin 5% for 8 hours for 2 consecutive days and repeated the treatment 5 days later . Following the course of permethrin, only 34 responded, 96 failed treatment, and 25 were lost to follow-up.
“The study authors concluded that mite resistance to permethrin 5% seems to be increasing, following a path like other ectoparasite resistance,” said Dr. Mancini, who was not involved with the study. “We may even be seeing more ivermectin resistance in some geographic locations, as well.”
According to new scabicide efficacy criteria established by the FDA in 2016, complete cure is now defined as meeting both clinical and confirmatory criteria. A clinical cure means that all signs and symptoms of scabies have completely resolved, including burrows, inflammatory/noninflammatory lesions, and pruritus. A confirmatory cure means there is an absence of mites, eggs, scybala (feces), and burrows via microscopy or dermoscopy.
Enter spinosad, which is derived from a naturally occurring soil microorganism known as Saccharopolyspora spinosa and is composed of two active molecules: spinosyn A and spinosyn D. According to Dr. Mancini, spinosad’s mechanism of action is unique from other medications used to treat ectoparasites. It activates nicotinic and GABA-gated sodium channels, leads to sodium influx in the insect nerves, hyperexcitation, then paralysis and death. Cross-resistance to other insecticides has not been reported, he added, and there is no known evidence of resistance to its active compound.
Approval of the drug was based on data from two phase 3 randomized clinical trials involving 551 index cases and household contacts. In the intent-to-treat population, with the two trials combined, complete cure was achieved in 78.1% of the spinosad-treated group, compared with 39.6% in the vehicle group (P < .0001), clinical cure was achieved in 79.6% of the spinosad group, compared with 41.2% in the vehicle group (P < .001), and microscopic cure occurred in 85.9% of the spinosad group, compared with 52.6% in the vehicle group (P < .001).
Of the 306 participants in the study, the only adverse events reported by more than one patient each included abdominal pain, back pain, cough, headache, neck pain, and decreased weight in two patients each (0.8%), which investigators believed were not attributable to the study drug. Adverse events that investigators considered to be potentially related to the study drug included burning sensation in two participants (0.7%) and dry skin in another (0.3%). In clinical trials reported in the prescribing information, adverse events occurring in greater than 1% of subjects included application-site irritation (3% spinosad vs. 0% vehicle) and dry skin (2% spinosad vs. 0% vehicle).
“Spinosad met the FDA’s new stringent criteria, with all signs and symptoms of scabies completely resolved and confirmed via microscopy or dermoscopy,” said Dr. Mancini, who was not involved in the trials. “The patented formulation drives the active compound to the stratum corneum, where mites live and breed. It’s a single full-body application, without any resistance observed to date. This is an exciting newer option for treating our scabies patients.”
In an interview at the meeting, John S. Barbieri, MD, MBA, of the department of dermatology, Brigham and Women’s Hospital, Boston, said that, while he has no clinical experience with spinosad for scabies, he welcomes a new option for the condition. “The fact that it has a different mechanism of action than permethrin is a good thing,” he said.
Dr. Mancini disclosed that he is a consultant or an adviser for ParaPRO, the manufacturer of spinosad, and Cassiopea, Castle Creek, Novan, Novartis, and Verrica. He was not involved in clinical trials of spinosad. Dr. Barbieri disclosed that he receives consulting fees from Dexcel.
Medscape and this news organization are owned by the same parent company.
AT THE MEDSCAPELIVE! HAWAII DERMATOLOGY SEMINAR
Notes on direct admission of pediatric patients
Scenario: Yesterday you saw a 6-month-old infant with what appeared to be viral gastroenteritis and mild dehydration. When you called his parents today to check on his condition he was not improving despite your recommendations about his diet and oral rehydration. Should you have him brought to your office for a reevaluation, have his parents take him to the local emergency department for evaluation and probable hospital admission, or ask his parents to take him to the hospital telling them that you will call and arrange for a direct admission.
Obviously, I haven’t given you enough background information to allow you to give me an answer you are comfortable with. What time of day is it? Is it a holiday weekend? What’s the weather like? How far is it from the patient’s home to your office? To the emergency department? How is the local ED staffed? Are there hospitalists? What is their training?
Whether or not you choose to see the patient first in the office, is direct admission to the hospital an option that you are likely to choose? What steps do you take to see that it happens smoothly?
At least one-quarter of the unscheduled pediatric hospitalizations begin with a direct admission, meaning that the patients are not first evaluated in that hospital’s ED. In a recent policy statement, the American Academy of Pediatrics Committee on Hospital Care explored the pluses and minuses of direct admission and issued a list of seven recommendations. Among the concerns raised by the authors are “potential delays in initial evaluation and treatment, inconsistent admission processes, and difficulties in determining the appropriateness of patients for direct admission.” The committee makes it clear that they understand each community has it own strengths and challenges and the unique needs of each patient make it difficult to define a set of recommendations that fits all.
However, as I read through the committee’s seven recommendations, one leapt off the screen as a unifying concept that should apply in every situation. Recommendation No. 2 reads, “[There should be] clear systems of communication between members of the health care team and with families of children requiring admission.”
First, who is on this “health care team”? Are you a team member with the hospital folks – the ED nurses and doctors, the hospitalists, the floor nurses? Do you share an employer? Are you in the same town? Have your ever met them face to face? Do you do so regularly?
I assume you call the ED or the pediatric floor to arrange a direct admit? Maybe you don’t. I can recall working in situations where several infamous “local docs” would just send the patients in with a scribbled note (or not) and no phone call. Will you be speaking to folks who are even vaguely familiar with you or even your name? Do you get to speak with people who will be hands on with the patient?
Obviously, where I’m going with this is that, if you and the hospital staff are truly on the same health care team, communication should flow freely among the members and having some familiarity allows this to happen more smoothly. It can start on our end as the referring physician by making the call personally. Likewise, the receiving hospital must make frontline people available so you can speak with staff who will be working with the patient. Do you have enough information to tell the family what to expect?
Of course legible and complete records are a must. But nothing beats personal contact and a name. If you can tell a parent “I spoke to Martha, the nurse who will meet you on the floor,” that can be a giant first step forward in the healing process.
Most of us trained at hospitals that accepted direct admit patients and can remember the challenges. And most of us recall EDs that weren’t pediatric friendly. Whether our local situation favors direct admission or ED preadmission evaluation, it is our job to make the communication flow with the patient’s safety and the family’s comfort in mind.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Scenario: Yesterday you saw a 6-month-old infant with what appeared to be viral gastroenteritis and mild dehydration. When you called his parents today to check on his condition he was not improving despite your recommendations about his diet and oral rehydration. Should you have him brought to your office for a reevaluation, have his parents take him to the local emergency department for evaluation and probable hospital admission, or ask his parents to take him to the hospital telling them that you will call and arrange for a direct admission.
Obviously, I haven’t given you enough background information to allow you to give me an answer you are comfortable with. What time of day is it? Is it a holiday weekend? What’s the weather like? How far is it from the patient’s home to your office? To the emergency department? How is the local ED staffed? Are there hospitalists? What is their training?
Whether or not you choose to see the patient first in the office, is direct admission to the hospital an option that you are likely to choose? What steps do you take to see that it happens smoothly?
At least one-quarter of the unscheduled pediatric hospitalizations begin with a direct admission, meaning that the patients are not first evaluated in that hospital’s ED. In a recent policy statement, the American Academy of Pediatrics Committee on Hospital Care explored the pluses and minuses of direct admission and issued a list of seven recommendations. Among the concerns raised by the authors are “potential delays in initial evaluation and treatment, inconsistent admission processes, and difficulties in determining the appropriateness of patients for direct admission.” The committee makes it clear that they understand each community has it own strengths and challenges and the unique needs of each patient make it difficult to define a set of recommendations that fits all.
However, as I read through the committee’s seven recommendations, one leapt off the screen as a unifying concept that should apply in every situation. Recommendation No. 2 reads, “[There should be] clear systems of communication between members of the health care team and with families of children requiring admission.”
First, who is on this “health care team”? Are you a team member with the hospital folks – the ED nurses and doctors, the hospitalists, the floor nurses? Do you share an employer? Are you in the same town? Have your ever met them face to face? Do you do so regularly?
I assume you call the ED or the pediatric floor to arrange a direct admit? Maybe you don’t. I can recall working in situations where several infamous “local docs” would just send the patients in with a scribbled note (or not) and no phone call. Will you be speaking to folks who are even vaguely familiar with you or even your name? Do you get to speak with people who will be hands on with the patient?
Obviously, where I’m going with this is that, if you and the hospital staff are truly on the same health care team, communication should flow freely among the members and having some familiarity allows this to happen more smoothly. It can start on our end as the referring physician by making the call personally. Likewise, the receiving hospital must make frontline people available so you can speak with staff who will be working with the patient. Do you have enough information to tell the family what to expect?
Of course legible and complete records are a must. But nothing beats personal contact and a name. If you can tell a parent “I spoke to Martha, the nurse who will meet you on the floor,” that can be a giant first step forward in the healing process.
Most of us trained at hospitals that accepted direct admit patients and can remember the challenges. And most of us recall EDs that weren’t pediatric friendly. Whether our local situation favors direct admission or ED preadmission evaluation, it is our job to make the communication flow with the patient’s safety and the family’s comfort in mind.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Scenario: Yesterday you saw a 6-month-old infant with what appeared to be viral gastroenteritis and mild dehydration. When you called his parents today to check on his condition he was not improving despite your recommendations about his diet and oral rehydration. Should you have him brought to your office for a reevaluation, have his parents take him to the local emergency department for evaluation and probable hospital admission, or ask his parents to take him to the hospital telling them that you will call and arrange for a direct admission.
Obviously, I haven’t given you enough background information to allow you to give me an answer you are comfortable with. What time of day is it? Is it a holiday weekend? What’s the weather like? How far is it from the patient’s home to your office? To the emergency department? How is the local ED staffed? Are there hospitalists? What is their training?
Whether or not you choose to see the patient first in the office, is direct admission to the hospital an option that you are likely to choose? What steps do you take to see that it happens smoothly?
At least one-quarter of the unscheduled pediatric hospitalizations begin with a direct admission, meaning that the patients are not first evaluated in that hospital’s ED. In a recent policy statement, the American Academy of Pediatrics Committee on Hospital Care explored the pluses and minuses of direct admission and issued a list of seven recommendations. Among the concerns raised by the authors are “potential delays in initial evaluation and treatment, inconsistent admission processes, and difficulties in determining the appropriateness of patients for direct admission.” The committee makes it clear that they understand each community has it own strengths and challenges and the unique needs of each patient make it difficult to define a set of recommendations that fits all.
However, as I read through the committee’s seven recommendations, one leapt off the screen as a unifying concept that should apply in every situation. Recommendation No. 2 reads, “[There should be] clear systems of communication between members of the health care team and with families of children requiring admission.”
First, who is on this “health care team”? Are you a team member with the hospital folks – the ED nurses and doctors, the hospitalists, the floor nurses? Do you share an employer? Are you in the same town? Have your ever met them face to face? Do you do so regularly?
I assume you call the ED or the pediatric floor to arrange a direct admit? Maybe you don’t. I can recall working in situations where several infamous “local docs” would just send the patients in with a scribbled note (or not) and no phone call. Will you be speaking to folks who are even vaguely familiar with you or even your name? Do you get to speak with people who will be hands on with the patient?
Obviously, where I’m going with this is that, if you and the hospital staff are truly on the same health care team, communication should flow freely among the members and having some familiarity allows this to happen more smoothly. It can start on our end as the referring physician by making the call personally. Likewise, the receiving hospital must make frontline people available so you can speak with staff who will be working with the patient. Do you have enough information to tell the family what to expect?
Of course legible and complete records are a must. But nothing beats personal contact and a name. If you can tell a parent “I spoke to Martha, the nurse who will meet you on the floor,” that can be a giant first step forward in the healing process.
Most of us trained at hospitals that accepted direct admit patients and can remember the challenges. And most of us recall EDs that weren’t pediatric friendly. Whether our local situation favors direct admission or ED preadmission evaluation, it is our job to make the communication flow with the patient’s safety and the family’s comfort in mind.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Pandemic hit Black children harder, study shows
Black children had almost three times as many COVID-related deaths as White children and about twice as many hospitalizations, according to a new study.
The study said that 1,556 children have died from the start of the pandemic until Nov. 30, 2022, with 593 of those children being 4 and under. Black children died of COVID-related causes 2.7 times more often than White children and were hospitalized 2.2 times more often than White children, the study said.
Lower vaccination rates for Black people may be a factor. The study said 43.6% of White children have received two or more vaccinations, compared with 40.2% of Black children.
“First and foremost, this study repudiates the misunderstanding that COVID-19 has not been of consequence to children who have had more than 15.5 million reported cases, representing 18 percent of all cases in the United States,” Reed Tuckson, MD, a member of the Black Coalition Against COVID board of directors and former District of Columbia public health commissioner, said in a news release.
“And second, our research shows that like their adult counterparts, Black and other children of color have shouldered more of the burden of COVID-19 than the White population.”
The study was commissioned by BCAC and conducted by the Satcher Health Leadership Institute of the Morehouse School of Medicine, Atlanta. It’s based on studies conducted by other agencies over 2 years.
Black and Hispanic children also had more severe COVID cases, the study said. Among 281 pediatric patients in New York, New Jersey, and Connecticut, 23.3% of severe cases were Black and 51% of severe cases were Hispanic.
The study says 1 in 310 Black children lost a parent or caregiver to COVID between April 2020 and June 2012, compared with 1 in 738 White children.
Economic and health-related hardships were experienced by 31% of Black households, 29% of Latino households, and 16% of White households, the study said.
“Children with COVID-19 in communities of color were sicker, [were] hospitalized and died at higher rates than White children,” Sandra Harris-Hooker, the interim executive director at the Satcher Health Leadership Institute of Morehouse School, said in the release. “We can now fully understand the devastating impact the virus had on communities of color across generations.”
The study recommends several changes, such as modifying eligibility requirements for the Children’s Health Insurance Program to help more children who fall into coverage gaps and expanding the Child Tax Credit.
A version of this article first appeared on WebMD.com.
Black children had almost three times as many COVID-related deaths as White children and about twice as many hospitalizations, according to a new study.
The study said that 1,556 children have died from the start of the pandemic until Nov. 30, 2022, with 593 of those children being 4 and under. Black children died of COVID-related causes 2.7 times more often than White children and were hospitalized 2.2 times more often than White children, the study said.
Lower vaccination rates for Black people may be a factor. The study said 43.6% of White children have received two or more vaccinations, compared with 40.2% of Black children.
“First and foremost, this study repudiates the misunderstanding that COVID-19 has not been of consequence to children who have had more than 15.5 million reported cases, representing 18 percent of all cases in the United States,” Reed Tuckson, MD, a member of the Black Coalition Against COVID board of directors and former District of Columbia public health commissioner, said in a news release.
“And second, our research shows that like their adult counterparts, Black and other children of color have shouldered more of the burden of COVID-19 than the White population.”
The study was commissioned by BCAC and conducted by the Satcher Health Leadership Institute of the Morehouse School of Medicine, Atlanta. It’s based on studies conducted by other agencies over 2 years.
Black and Hispanic children also had more severe COVID cases, the study said. Among 281 pediatric patients in New York, New Jersey, and Connecticut, 23.3% of severe cases were Black and 51% of severe cases were Hispanic.
The study says 1 in 310 Black children lost a parent or caregiver to COVID between April 2020 and June 2012, compared with 1 in 738 White children.
Economic and health-related hardships were experienced by 31% of Black households, 29% of Latino households, and 16% of White households, the study said.
“Children with COVID-19 in communities of color were sicker, [were] hospitalized and died at higher rates than White children,” Sandra Harris-Hooker, the interim executive director at the Satcher Health Leadership Institute of Morehouse School, said in the release. “We can now fully understand the devastating impact the virus had on communities of color across generations.”
The study recommends several changes, such as modifying eligibility requirements for the Children’s Health Insurance Program to help more children who fall into coverage gaps and expanding the Child Tax Credit.
A version of this article first appeared on WebMD.com.
Black children had almost three times as many COVID-related deaths as White children and about twice as many hospitalizations, according to a new study.
The study said that 1,556 children have died from the start of the pandemic until Nov. 30, 2022, with 593 of those children being 4 and under. Black children died of COVID-related causes 2.7 times more often than White children and were hospitalized 2.2 times more often than White children, the study said.
Lower vaccination rates for Black people may be a factor. The study said 43.6% of White children have received two or more vaccinations, compared with 40.2% of Black children.
“First and foremost, this study repudiates the misunderstanding that COVID-19 has not been of consequence to children who have had more than 15.5 million reported cases, representing 18 percent of all cases in the United States,” Reed Tuckson, MD, a member of the Black Coalition Against COVID board of directors and former District of Columbia public health commissioner, said in a news release.
“And second, our research shows that like their adult counterparts, Black and other children of color have shouldered more of the burden of COVID-19 than the White population.”
The study was commissioned by BCAC and conducted by the Satcher Health Leadership Institute of the Morehouse School of Medicine, Atlanta. It’s based on studies conducted by other agencies over 2 years.
Black and Hispanic children also had more severe COVID cases, the study said. Among 281 pediatric patients in New York, New Jersey, and Connecticut, 23.3% of severe cases were Black and 51% of severe cases were Hispanic.
The study says 1 in 310 Black children lost a parent or caregiver to COVID between April 2020 and June 2012, compared with 1 in 738 White children.
Economic and health-related hardships were experienced by 31% of Black households, 29% of Latino households, and 16% of White households, the study said.
“Children with COVID-19 in communities of color were sicker, [were] hospitalized and died at higher rates than White children,” Sandra Harris-Hooker, the interim executive director at the Satcher Health Leadership Institute of Morehouse School, said in the release. “We can now fully understand the devastating impact the virus had on communities of color across generations.”
The study recommends several changes, such as modifying eligibility requirements for the Children’s Health Insurance Program to help more children who fall into coverage gaps and expanding the Child Tax Credit.
A version of this article first appeared on WebMD.com.
FDA OKs first drug for Rett syndrome
Rett syndrome is a rare, genetic neurodevelopmental disorder that affects about 6,000-9,000 people in the United States, mostly females.
Symptoms typically present between 6 and 18 months of age, with patients experiencing a rapid decline with loss of fine motor and communication skills.
Trofinetide is a synthetic analogue of the amino-terminal tripeptide of insulinlike growth factor-1 (IGF-1), which occurs naturally in the brain. The drug is designed to treat the core symptoms of Rett syndrome by potentially reducing neuroinflammation and supporting synaptic function.
The approval of trofinetide was supported by results from the pivotal phase 3 LAVENDER study that tested the efficacy and safety of trofinetide vs. placebo in 187 female patients with Rett syndrome, aged 5-20 years.
A total of 93 participants were randomly assigned to twice-daily oral trofinetide, and 94 received placebo for 12 weeks.
After 12 weeks, trofinetide showed a statistically significant improvement from baseline, compared with placebo, on both the caregiver-assessed Rett Syndrome Behavior Questionnaire (RSBQ) and 7-point Clinical Global Impression-Improvement (CGI-I) scale.
The drug also outperformed placebo at 12 weeks in a key secondary endpoint: the composite score on the Communication and Symbolic Behavior Scales Developmental Profile Infant-Toddler Checklist-Social (CSBS-DP-IT Social), a scale on which caregivers assess nonverbal communication.
The most common adverse events with trofinetide treatment were diarrhea and vomiting. Almost all these events were considered mild or moderate.
‘Historic day’
“This is a historic day for the Rett syndrome community and a meaningful moment for the patients and caregivers who have eagerly awaited the arrival of an approved treatment for this condition,” Melissa Kennedy, MHA, chief executive officer of the International Rett Syndrome Foundation, said in a news release issued by Acadia.
“Rett syndrome is a complicated, devastating disease that affects not only the individual patient, but whole families. With today’s FDA decision, those impacted by Rett have a promising new treatment option that has demonstrated benefit across a variety of Rett symptoms, including those that impact the daily lives of those living with Rett and their loved ones,” Ms. Kennedy said.
Trofinetide is expected to be available in the United States by the end of April.
A version of this article first appeared on Medscape.com.
Rett syndrome is a rare, genetic neurodevelopmental disorder that affects about 6,000-9,000 people in the United States, mostly females.
Symptoms typically present between 6 and 18 months of age, with patients experiencing a rapid decline with loss of fine motor and communication skills.
Trofinetide is a synthetic analogue of the amino-terminal tripeptide of insulinlike growth factor-1 (IGF-1), which occurs naturally in the brain. The drug is designed to treat the core symptoms of Rett syndrome by potentially reducing neuroinflammation and supporting synaptic function.
The approval of trofinetide was supported by results from the pivotal phase 3 LAVENDER study that tested the efficacy and safety of trofinetide vs. placebo in 187 female patients with Rett syndrome, aged 5-20 years.
A total of 93 participants were randomly assigned to twice-daily oral trofinetide, and 94 received placebo for 12 weeks.
After 12 weeks, trofinetide showed a statistically significant improvement from baseline, compared with placebo, on both the caregiver-assessed Rett Syndrome Behavior Questionnaire (RSBQ) and 7-point Clinical Global Impression-Improvement (CGI-I) scale.
The drug also outperformed placebo at 12 weeks in a key secondary endpoint: the composite score on the Communication and Symbolic Behavior Scales Developmental Profile Infant-Toddler Checklist-Social (CSBS-DP-IT Social), a scale on which caregivers assess nonverbal communication.
The most common adverse events with trofinetide treatment were diarrhea and vomiting. Almost all these events were considered mild or moderate.
‘Historic day’
“This is a historic day for the Rett syndrome community and a meaningful moment for the patients and caregivers who have eagerly awaited the arrival of an approved treatment for this condition,” Melissa Kennedy, MHA, chief executive officer of the International Rett Syndrome Foundation, said in a news release issued by Acadia.
“Rett syndrome is a complicated, devastating disease that affects not only the individual patient, but whole families. With today’s FDA decision, those impacted by Rett have a promising new treatment option that has demonstrated benefit across a variety of Rett symptoms, including those that impact the daily lives of those living with Rett and their loved ones,” Ms. Kennedy said.
Trofinetide is expected to be available in the United States by the end of April.
A version of this article first appeared on Medscape.com.
Rett syndrome is a rare, genetic neurodevelopmental disorder that affects about 6,000-9,000 people in the United States, mostly females.
Symptoms typically present between 6 and 18 months of age, with patients experiencing a rapid decline with loss of fine motor and communication skills.
Trofinetide is a synthetic analogue of the amino-terminal tripeptide of insulinlike growth factor-1 (IGF-1), which occurs naturally in the brain. The drug is designed to treat the core symptoms of Rett syndrome by potentially reducing neuroinflammation and supporting synaptic function.
The approval of trofinetide was supported by results from the pivotal phase 3 LAVENDER study that tested the efficacy and safety of trofinetide vs. placebo in 187 female patients with Rett syndrome, aged 5-20 years.
A total of 93 participants were randomly assigned to twice-daily oral trofinetide, and 94 received placebo for 12 weeks.
After 12 weeks, trofinetide showed a statistically significant improvement from baseline, compared with placebo, on both the caregiver-assessed Rett Syndrome Behavior Questionnaire (RSBQ) and 7-point Clinical Global Impression-Improvement (CGI-I) scale.
The drug also outperformed placebo at 12 weeks in a key secondary endpoint: the composite score on the Communication and Symbolic Behavior Scales Developmental Profile Infant-Toddler Checklist-Social (CSBS-DP-IT Social), a scale on which caregivers assess nonverbal communication.
The most common adverse events with trofinetide treatment were diarrhea and vomiting. Almost all these events were considered mild or moderate.
‘Historic day’
“This is a historic day for the Rett syndrome community and a meaningful moment for the patients and caregivers who have eagerly awaited the arrival of an approved treatment for this condition,” Melissa Kennedy, MHA, chief executive officer of the International Rett Syndrome Foundation, said in a news release issued by Acadia.
“Rett syndrome is a complicated, devastating disease that affects not only the individual patient, but whole families. With today’s FDA decision, those impacted by Rett have a promising new treatment option that has demonstrated benefit across a variety of Rett symptoms, including those that impact the daily lives of those living with Rett and their loved ones,” Ms. Kennedy said.
Trofinetide is expected to be available in the United States by the end of April.
A version of this article first appeared on Medscape.com.
Children and COVID: A look back as the fourth year begins
With 3 years of the COVID-19 experience now past, it’s safe to say that SARS-CoV-2 changed American society in ways that could not have been predicted when the first U.S. cases were reported in January of 2020.
Who would have guessed back then that not one but two vaccines would be developed, approved, and widely distributed before the end of the year? Or that those vaccines would be rejected by large segments of the population on ideological grounds? Could anyone have predicted in early 2020 that schools in 21 states would be forbidden by law to require COVID-19 vaccination in students?
Vaccination is generally considered to be an activity of childhood, but that practice has been turned upside down with COVID-19. Among Americans aged 65 years and older, 95% have received at least one dose of vaccine, versus 27.9% of children younger than 12 years old, according to the Centers for Disease Control and Prevention.
The vaccine situation for children mirrors that of the population as a whole. The oldest children have the highest vaccination rates, and the rates decline along with age: 72.0% of those aged 12-17 years have received at least one dose, compared with 39.8% of 5- to 11-year-olds, 10.5% of 2- to 4-year-olds, and 8.0% of children under age 2, the CDC said on its COVID Data Tracker.
The youngest children were, of course, the last ones to be eligible for the vaccine, but their uptake has been much slower since emergency use was authorized in June of 2022. In the nearly 9 months since then, 9.5% of children aged 4 and under have received at least one dose, versus 66% of children aged 12-15 years in the first 9 months (May 2021 to March 2022).
Altogether, a total of 31.7 million, or 43%, of all children under age 18 had received at least one dose of COVID-19 vaccine as of March 8, 2023, according to the most recent CDC data.
Incidence: Counting COVID
Vaccination and other prevention efforts have tried to stem the tide, but what has COVID actually done to children since the Trump administration declared a nationwide emergency on March 13, 2020?
- 16.6 million cases.
- 186,035 new hospital admissions.
- 2,122 deaths.
Even the proportion of total COVID cases in children, 17.2%, is less than might be expected, given their relatively undervaccinated status.
Seroprevalence estimates seem to support the undercounting of pediatric cases. A survey of commercial laboratories working with the CDC put the seroprevalance of SARS-CoV-2 antibodies in children at 96.3% as of late 2022, based on tests of almost 27,000 specimens performed over an 8-week period from mid-October to mid-December. That would put the number of infected children at 65.7 million children.
Since Omicron
There has not been another major COVID-19 surge since the winter of 2021-2022, when the weekly rate of new cases reached 1,900 per 100,000 population in children aged 16-17 years in early January 2022 – the highest seen among children of any of the CDC’s age groups (0-4, 5-11, 12-15, 16-17) during the entire pandemic. Since the Omicron surge, the highest weekly rate was 221 per 100,000 during the week of May 15-21, again in 16- to 17-year-olds, the CDC reports.
The widely anticipated surge of COVID in the fall and winter of 2022 and 2023 – the so-called “tripledemic” involving influenza and respiratory syncytial virus – did not occur, possibly because so many Americans were vaccinated or previously infected, experts suggested. New-case rates, emergency room visits, and hospitalizations in children have continued to drop as winter comes to a close, CDC data show.
With 3 years of the COVID-19 experience now past, it’s safe to say that SARS-CoV-2 changed American society in ways that could not have been predicted when the first U.S. cases were reported in January of 2020.
Who would have guessed back then that not one but two vaccines would be developed, approved, and widely distributed before the end of the year? Or that those vaccines would be rejected by large segments of the population on ideological grounds? Could anyone have predicted in early 2020 that schools in 21 states would be forbidden by law to require COVID-19 vaccination in students?
Vaccination is generally considered to be an activity of childhood, but that practice has been turned upside down with COVID-19. Among Americans aged 65 years and older, 95% have received at least one dose of vaccine, versus 27.9% of children younger than 12 years old, according to the Centers for Disease Control and Prevention.
The vaccine situation for children mirrors that of the population as a whole. The oldest children have the highest vaccination rates, and the rates decline along with age: 72.0% of those aged 12-17 years have received at least one dose, compared with 39.8% of 5- to 11-year-olds, 10.5% of 2- to 4-year-olds, and 8.0% of children under age 2, the CDC said on its COVID Data Tracker.
The youngest children were, of course, the last ones to be eligible for the vaccine, but their uptake has been much slower since emergency use was authorized in June of 2022. In the nearly 9 months since then, 9.5% of children aged 4 and under have received at least one dose, versus 66% of children aged 12-15 years in the first 9 months (May 2021 to March 2022).
Altogether, a total of 31.7 million, or 43%, of all children under age 18 had received at least one dose of COVID-19 vaccine as of March 8, 2023, according to the most recent CDC data.
Incidence: Counting COVID
Vaccination and other prevention efforts have tried to stem the tide, but what has COVID actually done to children since the Trump administration declared a nationwide emergency on March 13, 2020?
- 16.6 million cases.
- 186,035 new hospital admissions.
- 2,122 deaths.
Even the proportion of total COVID cases in children, 17.2%, is less than might be expected, given their relatively undervaccinated status.
Seroprevalence estimates seem to support the undercounting of pediatric cases. A survey of commercial laboratories working with the CDC put the seroprevalance of SARS-CoV-2 antibodies in children at 96.3% as of late 2022, based on tests of almost 27,000 specimens performed over an 8-week period from mid-October to mid-December. That would put the number of infected children at 65.7 million children.
Since Omicron
There has not been another major COVID-19 surge since the winter of 2021-2022, when the weekly rate of new cases reached 1,900 per 100,000 population in children aged 16-17 years in early January 2022 – the highest seen among children of any of the CDC’s age groups (0-4, 5-11, 12-15, 16-17) during the entire pandemic. Since the Omicron surge, the highest weekly rate was 221 per 100,000 during the week of May 15-21, again in 16- to 17-year-olds, the CDC reports.
The widely anticipated surge of COVID in the fall and winter of 2022 and 2023 – the so-called “tripledemic” involving influenza and respiratory syncytial virus – did not occur, possibly because so many Americans were vaccinated or previously infected, experts suggested. New-case rates, emergency room visits, and hospitalizations in children have continued to drop as winter comes to a close, CDC data show.
With 3 years of the COVID-19 experience now past, it’s safe to say that SARS-CoV-2 changed American society in ways that could not have been predicted when the first U.S. cases were reported in January of 2020.
Who would have guessed back then that not one but two vaccines would be developed, approved, and widely distributed before the end of the year? Or that those vaccines would be rejected by large segments of the population on ideological grounds? Could anyone have predicted in early 2020 that schools in 21 states would be forbidden by law to require COVID-19 vaccination in students?
Vaccination is generally considered to be an activity of childhood, but that practice has been turned upside down with COVID-19. Among Americans aged 65 years and older, 95% have received at least one dose of vaccine, versus 27.9% of children younger than 12 years old, according to the Centers for Disease Control and Prevention.
The vaccine situation for children mirrors that of the population as a whole. The oldest children have the highest vaccination rates, and the rates decline along with age: 72.0% of those aged 12-17 years have received at least one dose, compared with 39.8% of 5- to 11-year-olds, 10.5% of 2- to 4-year-olds, and 8.0% of children under age 2, the CDC said on its COVID Data Tracker.
The youngest children were, of course, the last ones to be eligible for the vaccine, but their uptake has been much slower since emergency use was authorized in June of 2022. In the nearly 9 months since then, 9.5% of children aged 4 and under have received at least one dose, versus 66% of children aged 12-15 years in the first 9 months (May 2021 to March 2022).
Altogether, a total of 31.7 million, or 43%, of all children under age 18 had received at least one dose of COVID-19 vaccine as of March 8, 2023, according to the most recent CDC data.
Incidence: Counting COVID
Vaccination and other prevention efforts have tried to stem the tide, but what has COVID actually done to children since the Trump administration declared a nationwide emergency on March 13, 2020?
- 16.6 million cases.
- 186,035 new hospital admissions.
- 2,122 deaths.
Even the proportion of total COVID cases in children, 17.2%, is less than might be expected, given their relatively undervaccinated status.
Seroprevalence estimates seem to support the undercounting of pediatric cases. A survey of commercial laboratories working with the CDC put the seroprevalance of SARS-CoV-2 antibodies in children at 96.3% as of late 2022, based on tests of almost 27,000 specimens performed over an 8-week period from mid-October to mid-December. That would put the number of infected children at 65.7 million children.
Since Omicron
There has not been another major COVID-19 surge since the winter of 2021-2022, when the weekly rate of new cases reached 1,900 per 100,000 population in children aged 16-17 years in early January 2022 – the highest seen among children of any of the CDC’s age groups (0-4, 5-11, 12-15, 16-17) during the entire pandemic. Since the Omicron surge, the highest weekly rate was 221 per 100,000 during the week of May 15-21, again in 16- to 17-year-olds, the CDC reports.
The widely anticipated surge of COVID in the fall and winter of 2022 and 2023 – the so-called “tripledemic” involving influenza and respiratory syncytial virus – did not occur, possibly because so many Americans were vaccinated or previously infected, experts suggested. New-case rates, emergency room visits, and hospitalizations in children have continued to drop as winter comes to a close, CDC data show.
Will new guidelines widen the gap in treating childhood obesity?
In the United States, the Centers for Disease Control and Prevention estimates that nearly one in five children have obesity. Since the 1980s, the number of children with obesity has been increasing, with each generation reaching higher rates and greater weights at earlier ages. Even with extensive efforts from parents, clinicians, educators, and policymakers to limit the excessive weight gain among children, the number of obesity and severe obesity diagnoses keeps rising.
In response to this critical public health challenge, the American Academy of Pediatrics (AAP) introduced new clinical practice guidelines for the evaluation and management of obesity in children and adolescents. Developed by an expert panel, the new AAP guidelines present a departure in the conceptualization of obesity, recognizing the role that social determinants of health play in contributing to excessive weight gain.
As a community health researcher who investigates disparities in childhood obesity, I applaud the paradigm shift from the AAP. I specifically endorse the recognition that obesity is a very serious metabolic disease that won’t go away unless we introduce systemic changes and effective treatments.
However, I, like so many of my colleagues and anyone aware of the access barriers to the recommended treatments, worry about the consequences that the new guidelines will have in the context of current and future health disparities.
A recent study, published in Pediatrics, showed that childhood obesity disparities are widening. Younger generations of children are reaching higher weights at younger ages. These alarming trends are greater among Black children and children growing up with the greatest socioeconomic disadvantages. The new AAP guidelines – even while driven by good intentions – can exacerbate these differences and set children who are able to live healthy lives further apart from those with disproportionate obesity risks, who lack access to the treatments recommended by the AAP.
Rather than “watchful waiting,” to see if children outgrow obesity, the new guidelines call for “aggressive treatment,” as reported by this news organization. At least 26 hours of in-person intensive health behavior and lifestyle counseling and treatment are recommended for children aged 2 years old or older who meet the obesity criteria. For children aged 12 years or older, the AAP recommends complementing lifestyle counseling with pharmacotherapy. This breakthrough welcomes the use of promising antiobesity medications (for example, orlistat, Wegovy [semaglutide], Saxenda [liraglutide], Qsymia (phentermine and topiramate]) approved by the Food and Drug Administration for long-term use in children aged 12 and up. For children 13 years or older with severe obesity, bariatric surgery should be considered.
Will cost barriers continue to increase disparity?
The very promising semaglutide (Wegovy) is a GLP-1–based medication currently offered for about $1,000 per month. As with other chronic diseases, children should be prepared to take obesity medications for prolonged periods of time. A study conducted in adults found that when the medication is suspended, any weight loss can be regained. The costs of bariatric surgery total over $20,000.
In the U.S. health care system, at current prices, very few of the children in need of the medications or surgical treatments have access to them. Most private health insurance companies and Medicaid reject coverage for childhood obesity treatments. Barriers to treatment access are greater for Black and Hispanic children, children growing up in poverty, and children living in the U.S. South region, all of whom are more likely to develop obesity earlier in life than their White and wealthier counterparts.
The AAP recognized that a substantial time and financial commitment is required to follow the new treatment recommendations. Members of the AAP Expert Committee that developed the guidelines stated that they are “aware of the multitude of barriers to treatment that patients and their families face.”
Nevertheless, the recognition of the role of social determinants of health in the development of childhood obesity didn’t motivate the introduction of treatment options that aren’t unattainable for most U.S. families.
It’s important to step away from the conclusion that because of the price tag, at the population level, the new AAP guidelines will be inconsequential. This conclusion fails to recognize the potential harm that the guidelines may introduce. In the context of childhood obesity disparities, the new treatment recommendations probably will widen the childhood obesity prevalence gap between the haves – who will benefit from the options available to reduce childhood obesity – and the have-nots, whose obesity rates will continue with their growth.
We live in a world of the haves and have-nots. This applies to financial resources as well as obesity rates. In the long term, the optimists hope that the GLP-1 medications will become ubiquitous, generics will be developed, and insurance companies will expand coverage and grant access to most children in need of effective obesity treatment options. Until this happens, unless intentional policies are promptly introduced, childhood obesity disparities will continue to widen.
To avoid the increasing disparities, brave and intentional actions are required. A lack of attention dealt to this known problem will result in a lost opportunity for the AAP, legislators, and others in a position to help U.S. children.
Liliana Aguayo, PhD, MPH, is assistant professor, Clinical Research Track, Hubert Department of Global Health, Emory University, Atlanta. A version of this article first appeared on Medscape.com.
In the United States, the Centers for Disease Control and Prevention estimates that nearly one in five children have obesity. Since the 1980s, the number of children with obesity has been increasing, with each generation reaching higher rates and greater weights at earlier ages. Even with extensive efforts from parents, clinicians, educators, and policymakers to limit the excessive weight gain among children, the number of obesity and severe obesity diagnoses keeps rising.
In response to this critical public health challenge, the American Academy of Pediatrics (AAP) introduced new clinical practice guidelines for the evaluation and management of obesity in children and adolescents. Developed by an expert panel, the new AAP guidelines present a departure in the conceptualization of obesity, recognizing the role that social determinants of health play in contributing to excessive weight gain.
As a community health researcher who investigates disparities in childhood obesity, I applaud the paradigm shift from the AAP. I specifically endorse the recognition that obesity is a very serious metabolic disease that won’t go away unless we introduce systemic changes and effective treatments.
However, I, like so many of my colleagues and anyone aware of the access barriers to the recommended treatments, worry about the consequences that the new guidelines will have in the context of current and future health disparities.
A recent study, published in Pediatrics, showed that childhood obesity disparities are widening. Younger generations of children are reaching higher weights at younger ages. These alarming trends are greater among Black children and children growing up with the greatest socioeconomic disadvantages. The new AAP guidelines – even while driven by good intentions – can exacerbate these differences and set children who are able to live healthy lives further apart from those with disproportionate obesity risks, who lack access to the treatments recommended by the AAP.
Rather than “watchful waiting,” to see if children outgrow obesity, the new guidelines call for “aggressive treatment,” as reported by this news organization. At least 26 hours of in-person intensive health behavior and lifestyle counseling and treatment are recommended for children aged 2 years old or older who meet the obesity criteria. For children aged 12 years or older, the AAP recommends complementing lifestyle counseling with pharmacotherapy. This breakthrough welcomes the use of promising antiobesity medications (for example, orlistat, Wegovy [semaglutide], Saxenda [liraglutide], Qsymia (phentermine and topiramate]) approved by the Food and Drug Administration for long-term use in children aged 12 and up. For children 13 years or older with severe obesity, bariatric surgery should be considered.
Will cost barriers continue to increase disparity?
The very promising semaglutide (Wegovy) is a GLP-1–based medication currently offered for about $1,000 per month. As with other chronic diseases, children should be prepared to take obesity medications for prolonged periods of time. A study conducted in adults found that when the medication is suspended, any weight loss can be regained. The costs of bariatric surgery total over $20,000.
In the U.S. health care system, at current prices, very few of the children in need of the medications or surgical treatments have access to them. Most private health insurance companies and Medicaid reject coverage for childhood obesity treatments. Barriers to treatment access are greater for Black and Hispanic children, children growing up in poverty, and children living in the U.S. South region, all of whom are more likely to develop obesity earlier in life than their White and wealthier counterparts.
The AAP recognized that a substantial time and financial commitment is required to follow the new treatment recommendations. Members of the AAP Expert Committee that developed the guidelines stated that they are “aware of the multitude of barriers to treatment that patients and their families face.”
Nevertheless, the recognition of the role of social determinants of health in the development of childhood obesity didn’t motivate the introduction of treatment options that aren’t unattainable for most U.S. families.
It’s important to step away from the conclusion that because of the price tag, at the population level, the new AAP guidelines will be inconsequential. This conclusion fails to recognize the potential harm that the guidelines may introduce. In the context of childhood obesity disparities, the new treatment recommendations probably will widen the childhood obesity prevalence gap between the haves – who will benefit from the options available to reduce childhood obesity – and the have-nots, whose obesity rates will continue with their growth.
We live in a world of the haves and have-nots. This applies to financial resources as well as obesity rates. In the long term, the optimists hope that the GLP-1 medications will become ubiquitous, generics will be developed, and insurance companies will expand coverage and grant access to most children in need of effective obesity treatment options. Until this happens, unless intentional policies are promptly introduced, childhood obesity disparities will continue to widen.
To avoid the increasing disparities, brave and intentional actions are required. A lack of attention dealt to this known problem will result in a lost opportunity for the AAP, legislators, and others in a position to help U.S. children.
Liliana Aguayo, PhD, MPH, is assistant professor, Clinical Research Track, Hubert Department of Global Health, Emory University, Atlanta. A version of this article first appeared on Medscape.com.
In the United States, the Centers for Disease Control and Prevention estimates that nearly one in five children have obesity. Since the 1980s, the number of children with obesity has been increasing, with each generation reaching higher rates and greater weights at earlier ages. Even with extensive efforts from parents, clinicians, educators, and policymakers to limit the excessive weight gain among children, the number of obesity and severe obesity diagnoses keeps rising.
In response to this critical public health challenge, the American Academy of Pediatrics (AAP) introduced new clinical practice guidelines for the evaluation and management of obesity in children and adolescents. Developed by an expert panel, the new AAP guidelines present a departure in the conceptualization of obesity, recognizing the role that social determinants of health play in contributing to excessive weight gain.
As a community health researcher who investigates disparities in childhood obesity, I applaud the paradigm shift from the AAP. I specifically endorse the recognition that obesity is a very serious metabolic disease that won’t go away unless we introduce systemic changes and effective treatments.
However, I, like so many of my colleagues and anyone aware of the access barriers to the recommended treatments, worry about the consequences that the new guidelines will have in the context of current and future health disparities.
A recent study, published in Pediatrics, showed that childhood obesity disparities are widening. Younger generations of children are reaching higher weights at younger ages. These alarming trends are greater among Black children and children growing up with the greatest socioeconomic disadvantages. The new AAP guidelines – even while driven by good intentions – can exacerbate these differences and set children who are able to live healthy lives further apart from those with disproportionate obesity risks, who lack access to the treatments recommended by the AAP.
Rather than “watchful waiting,” to see if children outgrow obesity, the new guidelines call for “aggressive treatment,” as reported by this news organization. At least 26 hours of in-person intensive health behavior and lifestyle counseling and treatment are recommended for children aged 2 years old or older who meet the obesity criteria. For children aged 12 years or older, the AAP recommends complementing lifestyle counseling with pharmacotherapy. This breakthrough welcomes the use of promising antiobesity medications (for example, orlistat, Wegovy [semaglutide], Saxenda [liraglutide], Qsymia (phentermine and topiramate]) approved by the Food and Drug Administration for long-term use in children aged 12 and up. For children 13 years or older with severe obesity, bariatric surgery should be considered.
Will cost barriers continue to increase disparity?
The very promising semaglutide (Wegovy) is a GLP-1–based medication currently offered for about $1,000 per month. As with other chronic diseases, children should be prepared to take obesity medications for prolonged periods of time. A study conducted in adults found that when the medication is suspended, any weight loss can be regained. The costs of bariatric surgery total over $20,000.
In the U.S. health care system, at current prices, very few of the children in need of the medications or surgical treatments have access to them. Most private health insurance companies and Medicaid reject coverage for childhood obesity treatments. Barriers to treatment access are greater for Black and Hispanic children, children growing up in poverty, and children living in the U.S. South region, all of whom are more likely to develop obesity earlier in life than their White and wealthier counterparts.
The AAP recognized that a substantial time and financial commitment is required to follow the new treatment recommendations. Members of the AAP Expert Committee that developed the guidelines stated that they are “aware of the multitude of barriers to treatment that patients and their families face.”
Nevertheless, the recognition of the role of social determinants of health in the development of childhood obesity didn’t motivate the introduction of treatment options that aren’t unattainable for most U.S. families.
It’s important to step away from the conclusion that because of the price tag, at the population level, the new AAP guidelines will be inconsequential. This conclusion fails to recognize the potential harm that the guidelines may introduce. In the context of childhood obesity disparities, the new treatment recommendations probably will widen the childhood obesity prevalence gap between the haves – who will benefit from the options available to reduce childhood obesity – and the have-nots, whose obesity rates will continue with their growth.
We live in a world of the haves and have-nots. This applies to financial resources as well as obesity rates. In the long term, the optimists hope that the GLP-1 medications will become ubiquitous, generics will be developed, and insurance companies will expand coverage and grant access to most children in need of effective obesity treatment options. Until this happens, unless intentional policies are promptly introduced, childhood obesity disparities will continue to widen.
To avoid the increasing disparities, brave and intentional actions are required. A lack of attention dealt to this known problem will result in a lost opportunity for the AAP, legislators, and others in a position to help U.S. children.
Liliana Aguayo, PhD, MPH, is assistant professor, Clinical Research Track, Hubert Department of Global Health, Emory University, Atlanta. A version of this article first appeared on Medscape.com.
Can particles in dairy and beef cause cancer and MS?
In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?
However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.
In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.
Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
Acid radicals
However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.
According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
Viral progeny
In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.
The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
‘Breast milk is healthy’
Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.
The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
Colon cancer
To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.
The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
Institutional skepticism
When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?
The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.
BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.
Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
Association with MS?
Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”
However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.
Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?
However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.
In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.
Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
Acid radicals
However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.
According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
Viral progeny
In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.
The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
‘Breast milk is healthy’
Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.
The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
Colon cancer
To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.
The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
Institutional skepticism
When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?
The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.
BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.
Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
Association with MS?
Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”
However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.
Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
In Western diets, dairy and beef are ubiquitous: Milk goes with coffee, melted cheese with pizza, and chili with rice. But what if dairy products and beef contained a new kind of pathogen that could infect you as a child and trigger cancer or multiple sclerosis (MS) 40-70 years later?
However, in two joint statements, the German Federal Institute for Risk Assessment (BfR) and the Max Rubner Institute (MRI) have rejected such theories.
In 2008, Harald zur Hausen, MD, DSc, received the Nobel Prize in Medicine for his discovery that human papillomaviruses cause cervical cancer. His starting point was the observation that sexually abstinent women, such as nuns, rarely develop this cancer. So it was possible to draw the conclusion that pathogens are transmitted during sexual intercourse, explain Dr. zur Hausen and his wife Ethel-Michele de Villiers, PhD, both of DKFZ Heidelberg.
Papillomaviruses, as well as human herpes and Epstein-Barr viruses (EBV), polyomaviruses, and retroviruses, cause cancer in a direct way: by inserting their genes into the DNA of human cells. With a latency of a few years to a few decades, the proteins formed through expression stimulate malignant growth by altering the regulating host gene.
Acid radicals
However, viruses – just like bacteria and parasites – can also indirectly trigger cancer. One mechanism for this triggering is the disruption of immune defenses, as shown by the sometimes drastically increased tumor incidence with AIDS or with immunosuppressants after transplants. Chronic inflammation is a second mechanism that generates acid radicals and thereby causes random mutations in replicating cells. Examples include stomach cancer caused by Helicobacter pylori and liver cancer caused by Schistosoma, liver fluke, and hepatitis B and C viruses.
According to Dr. de Villiers and Dr. zur Hausen, there are good reasons to believe that other pathogens could cause chronic inflammation and thereby lead to cancer. Epidemiologic data suggest that dairy and meat products from European cows (Bos taurus) are a potential source. This is because colon cancer and breast cancer commonly occur in places where these foods are heavily consumed (that is, in North America, Argentina, Europe, and Australia). In contrast, the rate is low in India, where cows are revered as holy animals. Also noteworthy is that women with a lactose intolerance rarely develop breast cancer.
Viral progeny
In fact, the researchers found single-stranded DNA rings that originated in viruses, which they named bovine meat and milk factors (BMMF), in the intestines of patients with colon cancer. They reported, “This new class of pathogen deserves, in our opinion at least, to become the focus of cancer development and further chronic diseases.” They also detected elevated levels of acid radicals in these areas (that is, oxidative stress), which is typical for chronic inflammation.
The researchers assume that infants, whose immune system is not yet fully matured, ingest the BMMF as soon as they have dairy. Therefore, there is no need for adults to avoid dairy or beef because everyone is infected anyway, said Dr. zur Hausen.
‘Breast milk is healthy’
Dr. De Villiers and Dr. zur Hausen outlined more evidence of cancer-triggering pathogens. Mothers who have breastfed are less likely, especially after multiple pregnancies, to develop tumors in various organs or to have MS and type 2 diabetes. The authors attribute the protective effect to oligosaccharides in breast milk, which begin to be formed midway through the pregnancy. They bind to lectin receptors and, in so doing, mask the terminal molecule onto which the viruses need to dock. As a result, their port of entry into the cells is blocked.
The oligosaccharides also protect the baby against life-threatening infections by blocking access by rotaviruses and noroviruses. In this way, especially if breastfeeding lasts a long time – around 1 year – the period of incomplete immunocompetence is bridged.
Colon cancer
To date, it has been assumed that around 20% of all cancerous diseases globally are caused by infections, said the researchers. But if the suspected BMMF cases are included, this figure rises to 50%, even to around 80%, for colon cancer. If the suspicion is confirmed, the consequences for prevention and therapy would be significant.
The voice of a Nobel prize winner undoubtedly carries weight, but at the time, Dr. zur Hausen still had to convince a host of skeptics with his discovery that a viral infection is a major cause of cervical cancer. Nonetheless, some indicators suggest that he and his wife have found a dead end this time.
Institutional skepticism
When his working group made the results public in February 2019, the DKFZ felt the need to give an all-clear signal in response to alarmed press reports. There is no reason to see dairy and meat consumption as something negative. Similarly, in their first joint statement, the BfR and the MRI judged the data to be insufficient and called for further studies. Multiple research teams began to focus on BMMF as a result. In what foods can they be found? Are they more common in patients with cancer than in healthy people? Are they infectious? Do they cause inflammation and cancer?
The findings presented in a second statement by the BfR and MRI at the end of November 2022 contradicted the claims made by the DKFZ scientists across the board. In no way do BMMF represent new pathogens. They are variants of already known DNA sequences. In addition, they are present in numerous animal-based and plant-based foods, including pork, fish, fruit, vegetables, and nuts.
BMMF do not possess the ability to infect human cells, the institutes said. The proof that they are damaging to one’s health was also absent. It is true that the incidence of intestinal tumors correlates positively with the consumption of red and processed meat – which in no way signifies causality – but dairy products are linked to a reduced risk. On the other hand, breast cancer cannot be associated with the consumption of beef or dairy.
Therefore, both institutes recommend continuing to use these products as supplementary diet for infants because of their micronutrients. They further stated that the products are safe for people of all ages.
Association with MS?
Unperturbed, Dr. de Villiers and Dr. zur Hausen went one step further in their current article. They posited that MS is also associated with the consumption of dairy products and beef. Here too geographic distribution prompted the idea to look for BMMF in the brain lesions of patients with MS. The researchers isolated ring-shaped DNA molecules that proved to be closely related to BMMF from dairy and cattle blood. “The result was electrifying for us.”
However, there are several other factors to consider, such as vitamin D3 deficiency. This is because the incidence of MS decreases the further you travel from the poles toward the equator (that is, as solar radiation increases). Also, EBV clearly plays a role because patients with MS display increased titers of EBV antibodies. One study also showed that people in Antarctica excreted reactivated EBV in their saliva during winter and that vitamin D3 stopped the viral secretion.
Under these conditions, the researchers hypothesized that MS is caused by a double infection of brain cells by EBV and BMMF. EBV is reactivated by a lack of vitamin D3, and the BMMF multiply and are eventually converted into proteins. A focal immunoreaction causes the Schwann cells and oligodendrocytes to malfunction, which leads to the destruction of the myelin sheaths around the nerve fibers.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
Gestational diabetes affects fetal lung development
Lung development in the fetus may be adversely affected by a mother’s gestational diabetes, based on data from in vivo, in vitro, and ex vivo studies.
Gestational diabetes mellitus (GDM) has recently been associated with fetal lung underdevelopment (FLUD) and delayed lung maturation that may lead to immediate respiratory distress in newborns and later chronic lung disease, Pengzheng Chen, PhD, of Shandong University, Jinan, China, and colleagues wrote.
Antenatal corticosteroids are considered an effective treatment for gestational fetal lung underdevelopment, but recent studies have shown adverse effects of these medications, and therefore more research is needed to identify the etiology and pathogenesis of FLUD induced by GDM, they said.
In a study published in the International Journal of Nanomedicine, the researchers collected umbilical cord blood samples from patients with GDM and matched controls at a single hospital in China.
“Using an ex vivo exosome exposure model of fetal lung explants, we observed the morphological alteration of lung explants and evaluated the expression of molecules involved in lung development,” the researchers wrote.
Fetal lung underdevelopment was more common after exposure to exosomes from the umbilical cord plasma of individuals with gestational diabetes mellitus, compared with exosomes from healthy controls.
The researchers also used mouse models to examine the effects of exosomes on fetal lung development in vivo. They found that exosomes associated with GDM impeded the growth, branching morphogenesis, and maturation of fetal lungs in mouse models. In addition, the expression of the apoptotic biomarkers known as BAX, BIM, and cleaved CASPASE-3 was up-regulated in GDMUB-exosomes and HG-exos groups, but the antiapoptotic protein BCL-2 was down-regulated; this further supported the negative impact of GDM exomes on fetal lung development, the researchers said.
The researchers then conducted miRNA sequencing, which showed that the miRNA in placenta-derived exosomes from GDM pregnancies were distinct from the miRNA in exosomes from healthy control pregnancies.
The study findings were limited by several factors including the impurity of the isolated placenta-derived exosomes from the umbilical cord blood plasma, which were not placenta specific, the researchers noted. Other limitations included the lack of data on different stages of lung development, and more research is needed to validate miRNAs and to explore the signally pathways involved in fetal lung development.
However, the study is the first known to demonstrate an adverse effect of GDM on fetal lung development via in vitro, ex vivo, and in vitro models, they said.
“These data highlight an emerging role of placenta-derived exosomes in the pathogenesis of fetal lung underdevelopment in GDM pregnancies, and provide a novel strategy for maternal-fetal communication,” they concluded.
The study received no outside funding. The researchers had no financial conflicts to disclose.
Lung development in the fetus may be adversely affected by a mother’s gestational diabetes, based on data from in vivo, in vitro, and ex vivo studies.
Gestational diabetes mellitus (GDM) has recently been associated with fetal lung underdevelopment (FLUD) and delayed lung maturation that may lead to immediate respiratory distress in newborns and later chronic lung disease, Pengzheng Chen, PhD, of Shandong University, Jinan, China, and colleagues wrote.
Antenatal corticosteroids are considered an effective treatment for gestational fetal lung underdevelopment, but recent studies have shown adverse effects of these medications, and therefore more research is needed to identify the etiology and pathogenesis of FLUD induced by GDM, they said.
In a study published in the International Journal of Nanomedicine, the researchers collected umbilical cord blood samples from patients with GDM and matched controls at a single hospital in China.
“Using an ex vivo exosome exposure model of fetal lung explants, we observed the morphological alteration of lung explants and evaluated the expression of molecules involved in lung development,” the researchers wrote.
Fetal lung underdevelopment was more common after exposure to exosomes from the umbilical cord plasma of individuals with gestational diabetes mellitus, compared with exosomes from healthy controls.
The researchers also used mouse models to examine the effects of exosomes on fetal lung development in vivo. They found that exosomes associated with GDM impeded the growth, branching morphogenesis, and maturation of fetal lungs in mouse models. In addition, the expression of the apoptotic biomarkers known as BAX, BIM, and cleaved CASPASE-3 was up-regulated in GDMUB-exosomes and HG-exos groups, but the antiapoptotic protein BCL-2 was down-regulated; this further supported the negative impact of GDM exomes on fetal lung development, the researchers said.
The researchers then conducted miRNA sequencing, which showed that the miRNA in placenta-derived exosomes from GDM pregnancies were distinct from the miRNA in exosomes from healthy control pregnancies.
The study findings were limited by several factors including the impurity of the isolated placenta-derived exosomes from the umbilical cord blood plasma, which were not placenta specific, the researchers noted. Other limitations included the lack of data on different stages of lung development, and more research is needed to validate miRNAs and to explore the signally pathways involved in fetal lung development.
However, the study is the first known to demonstrate an adverse effect of GDM on fetal lung development via in vitro, ex vivo, and in vitro models, they said.
“These data highlight an emerging role of placenta-derived exosomes in the pathogenesis of fetal lung underdevelopment in GDM pregnancies, and provide a novel strategy for maternal-fetal communication,” they concluded.
The study received no outside funding. The researchers had no financial conflicts to disclose.
Lung development in the fetus may be adversely affected by a mother’s gestational diabetes, based on data from in vivo, in vitro, and ex vivo studies.
Gestational diabetes mellitus (GDM) has recently been associated with fetal lung underdevelopment (FLUD) and delayed lung maturation that may lead to immediate respiratory distress in newborns and later chronic lung disease, Pengzheng Chen, PhD, of Shandong University, Jinan, China, and colleagues wrote.
Antenatal corticosteroids are considered an effective treatment for gestational fetal lung underdevelopment, but recent studies have shown adverse effects of these medications, and therefore more research is needed to identify the etiology and pathogenesis of FLUD induced by GDM, they said.
In a study published in the International Journal of Nanomedicine, the researchers collected umbilical cord blood samples from patients with GDM and matched controls at a single hospital in China.
“Using an ex vivo exosome exposure model of fetal lung explants, we observed the morphological alteration of lung explants and evaluated the expression of molecules involved in lung development,” the researchers wrote.
Fetal lung underdevelopment was more common after exposure to exosomes from the umbilical cord plasma of individuals with gestational diabetes mellitus, compared with exosomes from healthy controls.
The researchers also used mouse models to examine the effects of exosomes on fetal lung development in vivo. They found that exosomes associated with GDM impeded the growth, branching morphogenesis, and maturation of fetal lungs in mouse models. In addition, the expression of the apoptotic biomarkers known as BAX, BIM, and cleaved CASPASE-3 was up-regulated in GDMUB-exosomes and HG-exos groups, but the antiapoptotic protein BCL-2 was down-regulated; this further supported the negative impact of GDM exomes on fetal lung development, the researchers said.
The researchers then conducted miRNA sequencing, which showed that the miRNA in placenta-derived exosomes from GDM pregnancies were distinct from the miRNA in exosomes from healthy control pregnancies.
The study findings were limited by several factors including the impurity of the isolated placenta-derived exosomes from the umbilical cord blood plasma, which were not placenta specific, the researchers noted. Other limitations included the lack of data on different stages of lung development, and more research is needed to validate miRNAs and to explore the signally pathways involved in fetal lung development.
However, the study is the first known to demonstrate an adverse effect of GDM on fetal lung development via in vitro, ex vivo, and in vitro models, they said.
“These data highlight an emerging role of placenta-derived exosomes in the pathogenesis of fetal lung underdevelopment in GDM pregnancies, and provide a novel strategy for maternal-fetal communication,” they concluded.
The study received no outside funding. The researchers had no financial conflicts to disclose.
FROM THE INTERNATIONAL JOURNAL OF NANOMEDICINE
Are early childhood viral infections linked with asthma?
MARSEILLE, France – It is well known that viral infections, especially respiratory syncytial virus (RSV) and rhinovirus (RV), exacerbate symptoms of asthma. But could they also play a part in triggering the onset of asthma?
The link between RSV and RV infections in early childhood and the development of asthma symptoms is well established, said Camille Taillé, MD, PhD, of the department of respiratory medicine and the rare diseases center of excellence at Bichat Hospital, Paris. But getting asthma is probably not just a matter of having a viral infection at a young age or of having a severe form of it. Gene polymorphisms, immune system disorders, and preexisting atopy are also associated with the risk of asthma. This was the focus of the 27th French-language respiratory medicine conference, held in Marseille, France.
RV and RSV
Persons with asthma are vulnerable to certain viral respiratory infections, in particular the flu and RV, which can exacerbate asthma symptoms. Inhaled corticosteroids have an overall protective effect against viral-induced exacerbations. For worsening asthma symptoms during an epidemic or pandemic, there is no contraindication to inhaled or oral corticosteroids.
Young children from the time of birth to 4 years of age are particularly susceptible to viral respiratory infections. According to data from France’s clinical surveillance network, Sentinelles, from the period covering winter 2021-2022, the rate of incidence per 100,000 inhabitants was systematically greater for the 0 to 4-year age range than for older age ranges.
Of the most common viruses that infect young children, RV, the virus that causes the common cold, is a nonenveloped RNA virus from the enterovirus family. There are 160 types, which are classified into three strains (A, B, and C). Of those strains, A and C confer the most severe infections. The virus is highly variable, which makes developing a vaccine challenging. The virus circulates year round, usually peaking in the fall and at the end of spring. RSV is an RNA virus that is classed as a respiratory virus. It comprises two serotypes: type A and B. Almost all children will have been infected with RSV by the time they are 2 years old. Epidemics occur each year during winter or in early spring in temperate climates. Vaccines are currently being developed and will soon be marketed. A monoclonal antibody (palivizumab), which targets fusion proteins of the virus, is available as prophylactic treatment for at-risk children.
RSV infection
During an RSV infection, the severe inflammation of the bronchial and alveolar wall causes acute respiratory distress. “But not all infants will develop severe forms of bronchiolitis,” said Dr. Taillé. “The risk factors for the severe form of the illness are well known: being under 6 months of age, prematurity, comorbidities (neurovascular, cardiovascular, respiratory, etc.), history of a stay in a neonatal intensive care unit at birth, living in low socioeconomic status towns, and exposure to smoking.”
Asthma development
The issue of whether or not viral diseases cause asthma has been the subject of intense debate. The studies are starting to stack up, however. They seem to show that RSV or RV infections are associated with the risk of subsequent asthma development. “For example, in a study published in 2022,” said Dr. Taillé, “in children admitted with an RSV infection, 60% of those who had been admitted to neonatal intensive care presented with symptoms of asthma between 3 and 6 years of age, compared with 18% of those who had had a milder case of RSV (admitted to nonintensive care settings). A serious RSV infection is a risk factor for later development of asthma.”
However, the link between RSV and later onset of asthma is also seen in milder cases of the infection. The American COAST study was designed to examine the effect of childhood respiratory infections on the risk of developing asthma. Researchers followed 259 newborns prospectively for 1, 3, and 6 years. To qualify, at least one parent was required to have respiratory allergies (defined as one or more positive aeroallergen skin tests) or a history of physician-diagnosed asthma. Regular samples taken during infectious episodes identified a virus in 90% of cases.
“We now know that RSV is not the only pathogen responsible for bronchiolitis. RV is often found, now that it can routinely be detected by PCR tests,” said Dr. Taillé. In the COAST study, the onset of wheezing during an RSV or RV infection in children aged 0-3 years was associated with an increased risk of asthma at 6 years of age. Globally, 28% of children infected by either virus were deemed to have asthma at 6 years of age. “There is clearly a link between having had a respiratory virus like RV or RSV and getting asthma symptoms at 6 years of age,” said Dr. Taillé. “What’s more, the effect of RV is not changed in this study by allergic sensitization.”
Many articles have been published on this topic. The results of cohort studies, from Japan to Finland and the United States, Italy, and Australia, are consistent with each other. Persons who have contracted RV or RSV are more likely to suffer from recurrent wheezing or asthma, especially if the infection is contracted in infancy or if it is severe. “Some studies even suggest that viral-induced asthma is more severe,” said Dr. Taillé. “For example, a Scottish study ... showed that children with a previous history of RSV infection had more hospital admissions and required more medication than asthmatics with no history of an RSV infection, suggesting the link between a previous history of RSV infection and the development of a more severe form of asthma.”
Reaching adulthood
Few longitudinal cohorts explore this issue in adulthood. A relatively old study reported an increased rate of asthma among adults who had required hospital admission for bronchiolitis in early childhood, as well as the effect on respiratory function. A 2023 study of the effects of respiratory illnesses in childhood reported similar findings. The authors evaluated lung structure and function via CT scans of 39 patients aged 26 years and concluded that participants who had been infected with RSV in childhood presented with increased air trapping, which is suggestive of airway abnormalities, possibly linked to a direct effect of viruses on lung development.
Mechanisms of action
“The real question is understanding if it’s the virus itself that causes asthma, or if the virus is simply uncovering underlying asthma in predisposed children,” said Dr. Taillé. From 30% to 40% of children who have had RSV will go on to develop wheezing or asthma in childhood. This observation suggests that there are factors favoring the development of asthma after infection with RSV. It has been shown that there is a genetic predisposition for RV. The roles of cigarette smoke, air pollution, environmental exposures to allergens, rapid urbanization, low vitamin D levels, low maternal omega-3 long-chain polyunsaturated fatty acid levels, maternal stress, and depression have also been highlighted.
It would seem that RSV and RV are a bit different. RV is thought to be associated with the development of asthma and wheezing, especially in people with a preexisting atopy or a reduced interferon immune response, while RSV, which occurs at a younger age and among the most vulnerable populations, seems to act independently of a person’s predisposition to allergies. RV stands out from other viral factors, owing to its tendency to create a Th2-biased inflammatory environment and its association with specific risk genes in people predisposed to asthma development (CDHR3).
Dr. Taillé has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
MARSEILLE, France – It is well known that viral infections, especially respiratory syncytial virus (RSV) and rhinovirus (RV), exacerbate symptoms of asthma. But could they also play a part in triggering the onset of asthma?
The link between RSV and RV infections in early childhood and the development of asthma symptoms is well established, said Camille Taillé, MD, PhD, of the department of respiratory medicine and the rare diseases center of excellence at Bichat Hospital, Paris. But getting asthma is probably not just a matter of having a viral infection at a young age or of having a severe form of it. Gene polymorphisms, immune system disorders, and preexisting atopy are also associated with the risk of asthma. This was the focus of the 27th French-language respiratory medicine conference, held in Marseille, France.
RV and RSV
Persons with asthma are vulnerable to certain viral respiratory infections, in particular the flu and RV, which can exacerbate asthma symptoms. Inhaled corticosteroids have an overall protective effect against viral-induced exacerbations. For worsening asthma symptoms during an epidemic or pandemic, there is no contraindication to inhaled or oral corticosteroids.
Young children from the time of birth to 4 years of age are particularly susceptible to viral respiratory infections. According to data from France’s clinical surveillance network, Sentinelles, from the period covering winter 2021-2022, the rate of incidence per 100,000 inhabitants was systematically greater for the 0 to 4-year age range than for older age ranges.
Of the most common viruses that infect young children, RV, the virus that causes the common cold, is a nonenveloped RNA virus from the enterovirus family. There are 160 types, which are classified into three strains (A, B, and C). Of those strains, A and C confer the most severe infections. The virus is highly variable, which makes developing a vaccine challenging. The virus circulates year round, usually peaking in the fall and at the end of spring. RSV is an RNA virus that is classed as a respiratory virus. It comprises two serotypes: type A and B. Almost all children will have been infected with RSV by the time they are 2 years old. Epidemics occur each year during winter or in early spring in temperate climates. Vaccines are currently being developed and will soon be marketed. A monoclonal antibody (palivizumab), which targets fusion proteins of the virus, is available as prophylactic treatment for at-risk children.
RSV infection
During an RSV infection, the severe inflammation of the bronchial and alveolar wall causes acute respiratory distress. “But not all infants will develop severe forms of bronchiolitis,” said Dr. Taillé. “The risk factors for the severe form of the illness are well known: being under 6 months of age, prematurity, comorbidities (neurovascular, cardiovascular, respiratory, etc.), history of a stay in a neonatal intensive care unit at birth, living in low socioeconomic status towns, and exposure to smoking.”
Asthma development
The issue of whether or not viral diseases cause asthma has been the subject of intense debate. The studies are starting to stack up, however. They seem to show that RSV or RV infections are associated with the risk of subsequent asthma development. “For example, in a study published in 2022,” said Dr. Taillé, “in children admitted with an RSV infection, 60% of those who had been admitted to neonatal intensive care presented with symptoms of asthma between 3 and 6 years of age, compared with 18% of those who had had a milder case of RSV (admitted to nonintensive care settings). A serious RSV infection is a risk factor for later development of asthma.”
However, the link between RSV and later onset of asthma is also seen in milder cases of the infection. The American COAST study was designed to examine the effect of childhood respiratory infections on the risk of developing asthma. Researchers followed 259 newborns prospectively for 1, 3, and 6 years. To qualify, at least one parent was required to have respiratory allergies (defined as one or more positive aeroallergen skin tests) or a history of physician-diagnosed asthma. Regular samples taken during infectious episodes identified a virus in 90% of cases.
“We now know that RSV is not the only pathogen responsible for bronchiolitis. RV is often found, now that it can routinely be detected by PCR tests,” said Dr. Taillé. In the COAST study, the onset of wheezing during an RSV or RV infection in children aged 0-3 years was associated with an increased risk of asthma at 6 years of age. Globally, 28% of children infected by either virus were deemed to have asthma at 6 years of age. “There is clearly a link between having had a respiratory virus like RV or RSV and getting asthma symptoms at 6 years of age,” said Dr. Taillé. “What’s more, the effect of RV is not changed in this study by allergic sensitization.”
Many articles have been published on this topic. The results of cohort studies, from Japan to Finland and the United States, Italy, and Australia, are consistent with each other. Persons who have contracted RV or RSV are more likely to suffer from recurrent wheezing or asthma, especially if the infection is contracted in infancy or if it is severe. “Some studies even suggest that viral-induced asthma is more severe,” said Dr. Taillé. “For example, a Scottish study ... showed that children with a previous history of RSV infection had more hospital admissions and required more medication than asthmatics with no history of an RSV infection, suggesting the link between a previous history of RSV infection and the development of a more severe form of asthma.”
Reaching adulthood
Few longitudinal cohorts explore this issue in adulthood. A relatively old study reported an increased rate of asthma among adults who had required hospital admission for bronchiolitis in early childhood, as well as the effect on respiratory function. A 2023 study of the effects of respiratory illnesses in childhood reported similar findings. The authors evaluated lung structure and function via CT scans of 39 patients aged 26 years and concluded that participants who had been infected with RSV in childhood presented with increased air trapping, which is suggestive of airway abnormalities, possibly linked to a direct effect of viruses on lung development.
Mechanisms of action
“The real question is understanding if it’s the virus itself that causes asthma, or if the virus is simply uncovering underlying asthma in predisposed children,” said Dr. Taillé. From 30% to 40% of children who have had RSV will go on to develop wheezing or asthma in childhood. This observation suggests that there are factors favoring the development of asthma after infection with RSV. It has been shown that there is a genetic predisposition for RV. The roles of cigarette smoke, air pollution, environmental exposures to allergens, rapid urbanization, low vitamin D levels, low maternal omega-3 long-chain polyunsaturated fatty acid levels, maternal stress, and depression have also been highlighted.
It would seem that RSV and RV are a bit different. RV is thought to be associated with the development of asthma and wheezing, especially in people with a preexisting atopy or a reduced interferon immune response, while RSV, which occurs at a younger age and among the most vulnerable populations, seems to act independently of a person’s predisposition to allergies. RV stands out from other viral factors, owing to its tendency to create a Th2-biased inflammatory environment and its association with specific risk genes in people predisposed to asthma development (CDHR3).
Dr. Taillé has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
MARSEILLE, France – It is well known that viral infections, especially respiratory syncytial virus (RSV) and rhinovirus (RV), exacerbate symptoms of asthma. But could they also play a part in triggering the onset of asthma?
The link between RSV and RV infections in early childhood and the development of asthma symptoms is well established, said Camille Taillé, MD, PhD, of the department of respiratory medicine and the rare diseases center of excellence at Bichat Hospital, Paris. But getting asthma is probably not just a matter of having a viral infection at a young age or of having a severe form of it. Gene polymorphisms, immune system disorders, and preexisting atopy are also associated with the risk of asthma. This was the focus of the 27th French-language respiratory medicine conference, held in Marseille, France.
RV and RSV
Persons with asthma are vulnerable to certain viral respiratory infections, in particular the flu and RV, which can exacerbate asthma symptoms. Inhaled corticosteroids have an overall protective effect against viral-induced exacerbations. For worsening asthma symptoms during an epidemic or pandemic, there is no contraindication to inhaled or oral corticosteroids.
Young children from the time of birth to 4 years of age are particularly susceptible to viral respiratory infections. According to data from France’s clinical surveillance network, Sentinelles, from the period covering winter 2021-2022, the rate of incidence per 100,000 inhabitants was systematically greater for the 0 to 4-year age range than for older age ranges.
Of the most common viruses that infect young children, RV, the virus that causes the common cold, is a nonenveloped RNA virus from the enterovirus family. There are 160 types, which are classified into three strains (A, B, and C). Of those strains, A and C confer the most severe infections. The virus is highly variable, which makes developing a vaccine challenging. The virus circulates year round, usually peaking in the fall and at the end of spring. RSV is an RNA virus that is classed as a respiratory virus. It comprises two serotypes: type A and B. Almost all children will have been infected with RSV by the time they are 2 years old. Epidemics occur each year during winter or in early spring in temperate climates. Vaccines are currently being developed and will soon be marketed. A monoclonal antibody (palivizumab), which targets fusion proteins of the virus, is available as prophylactic treatment for at-risk children.
RSV infection
During an RSV infection, the severe inflammation of the bronchial and alveolar wall causes acute respiratory distress. “But not all infants will develop severe forms of bronchiolitis,” said Dr. Taillé. “The risk factors for the severe form of the illness are well known: being under 6 months of age, prematurity, comorbidities (neurovascular, cardiovascular, respiratory, etc.), history of a stay in a neonatal intensive care unit at birth, living in low socioeconomic status towns, and exposure to smoking.”
Asthma development
The issue of whether or not viral diseases cause asthma has been the subject of intense debate. The studies are starting to stack up, however. They seem to show that RSV or RV infections are associated with the risk of subsequent asthma development. “For example, in a study published in 2022,” said Dr. Taillé, “in children admitted with an RSV infection, 60% of those who had been admitted to neonatal intensive care presented with symptoms of asthma between 3 and 6 years of age, compared with 18% of those who had had a milder case of RSV (admitted to nonintensive care settings). A serious RSV infection is a risk factor for later development of asthma.”
However, the link between RSV and later onset of asthma is also seen in milder cases of the infection. The American COAST study was designed to examine the effect of childhood respiratory infections on the risk of developing asthma. Researchers followed 259 newborns prospectively for 1, 3, and 6 years. To qualify, at least one parent was required to have respiratory allergies (defined as one or more positive aeroallergen skin tests) or a history of physician-diagnosed asthma. Regular samples taken during infectious episodes identified a virus in 90% of cases.
“We now know that RSV is not the only pathogen responsible for bronchiolitis. RV is often found, now that it can routinely be detected by PCR tests,” said Dr. Taillé. In the COAST study, the onset of wheezing during an RSV or RV infection in children aged 0-3 years was associated with an increased risk of asthma at 6 years of age. Globally, 28% of children infected by either virus were deemed to have asthma at 6 years of age. “There is clearly a link between having had a respiratory virus like RV or RSV and getting asthma symptoms at 6 years of age,” said Dr. Taillé. “What’s more, the effect of RV is not changed in this study by allergic sensitization.”
Many articles have been published on this topic. The results of cohort studies, from Japan to Finland and the United States, Italy, and Australia, are consistent with each other. Persons who have contracted RV or RSV are more likely to suffer from recurrent wheezing or asthma, especially if the infection is contracted in infancy or if it is severe. “Some studies even suggest that viral-induced asthma is more severe,” said Dr. Taillé. “For example, a Scottish study ... showed that children with a previous history of RSV infection had more hospital admissions and required more medication than asthmatics with no history of an RSV infection, suggesting the link between a previous history of RSV infection and the development of a more severe form of asthma.”
Reaching adulthood
Few longitudinal cohorts explore this issue in adulthood. A relatively old study reported an increased rate of asthma among adults who had required hospital admission for bronchiolitis in early childhood, as well as the effect on respiratory function. A 2023 study of the effects of respiratory illnesses in childhood reported similar findings. The authors evaluated lung structure and function via CT scans of 39 patients aged 26 years and concluded that participants who had been infected with RSV in childhood presented with increased air trapping, which is suggestive of airway abnormalities, possibly linked to a direct effect of viruses on lung development.
Mechanisms of action
“The real question is understanding if it’s the virus itself that causes asthma, or if the virus is simply uncovering underlying asthma in predisposed children,” said Dr. Taillé. From 30% to 40% of children who have had RSV will go on to develop wheezing or asthma in childhood. This observation suggests that there are factors favoring the development of asthma after infection with RSV. It has been shown that there is a genetic predisposition for RV. The roles of cigarette smoke, air pollution, environmental exposures to allergens, rapid urbanization, low vitamin D levels, low maternal omega-3 long-chain polyunsaturated fatty acid levels, maternal stress, and depression have also been highlighted.
It would seem that RSV and RV are a bit different. RV is thought to be associated with the development of asthma and wheezing, especially in people with a preexisting atopy or a reduced interferon immune response, while RSV, which occurs at a younger age and among the most vulnerable populations, seems to act independently of a person’s predisposition to allergies. RV stands out from other viral factors, owing to its tendency to create a Th2-biased inflammatory environment and its association with specific risk genes in people predisposed to asthma development (CDHR3).
Dr. Taillé has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.