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Sea buckthorn: What is it and what is it good for?
To avoid jumping on the bandwagon of another ingredient trend, we sought to examine the scientific background and properties of sea buckthorn oil and it’s utility for the skin.
Sea buckthorn (Hippophae rhamnoides) – also known as a Siberian pineapple tree, and as sandthorn, sallowthorn, or seaberry – is a thorny, dioecious shrub (or tree) in the oleaster family. It can grow up to 23 feet high and is found in coastal sea cliff areas and on mountain slopes of Western Europe, and in dry sandy areas of Asia Minor and Central Asia, Siberia, China, and Tibet. Common sea buckthorn flowers in late April and early May, producing a large number of small, green and brown flowers, turning into edible, usually yellow or orange round berries. The berries have a bitter, sour taste and have a mild aroma, resembling that of a pineapple. The fruit contains a small stone that covers an oily seed.
The berries are a source of antioxidant vitamins, flavonoids, and organic acids, and when pressed, produce a juice that separates into three layers: a thick cream (upper layer), a combination of saturated and unsaturated fatty acids (middle layer), and juice that is a source of fat (lower layer). The berries contain mainly vitamin C, but also vitamin A (alpha- and beta-carotene) and a mixture of other carotenoids, as well as varying concentrations of tocopherols (vitamin E), folic acid, and vitamin B complex–group vitamins.
In addition to flavonoids, the berries contain catechins and procyanidins, cyclitols, phospholipids, tannins, sugars (galactose, fructose, xylose), organic acids (maleic acid, oxalic acid, malic acid, tartaric acid), phenolic acids (such as ferulic acid), and fatty oil. The amount of vitamin C content varies with the variety of the plant and where it is found. The oil of sea buckthorn may be extracted from two parts of the plant, with mechanical cold pressing of seeds (up to 12.5% weight as oil content) and fruit pulp (8%-12% oil content).
Among vegetable oils, sea buckthorn fruit oil has the highest content of palmitoleic acid (omega-7).
Fruit and seed oils contain tocotrienols and plant sterols. Pulp sea buckthorn oil has a high carotenoid content, as opposed to seed oil, and in Mongolia, Russia, and China, is used as a topical therapy for skin burns.
Other significant fatty acids found in sea buckthorn oil are saturated fatty acids (palmitic acid and stearic acid) and polyunsaturated fatty acids, which include alpha-linolenic acid (omega-3), gamma-linolenic acid (omega-6), linolic acid (omega-6), oleic acid (omega-9), and eicosanoic acid (omega-9). Gamma-linoleic acid in particular is reduced in dry skin conditions, such as aging and atopic dermatitis. The human body can produce some gamma-linolenic acid, oleic acid, and palmitoleic acid, but not linolic acid and alpha-linolenic acid. The addition of these substances to diet or skin care has been found to be beneficial in improving dryness and the skin barrier.
In addition, linolic acid, a natural component of human sebum, has been noted to be decreased in the sebum of people with acne-prone skin. Preliminary evidence indicates that dietary supplements containing fatty acids such as docosahexaenoic acid, sea buckthorn oil, and hemp seed oil may decrease the severity of atopic dermatitis.
Besides use in topical skin care and cosmetic preparations, sea buckthorn has also been used successfully in the treatment of chronic gastric ulcer disease, inflammation of the vagina and cervix, and cervical erosion. The bark and leaves of sea buckthorn used to be applied to treat diarrhea and dermatologic conditions, while berry oil has been applied topically or taken orally to soften the skin.
In traditional Indian, Chinese, and Tibetan medicines, sea buckthorn berries are used for medicinal purposes, as their ingredients were thought to have a beneficial effect on the function of the alimentary, respiratory, and circulatory systems. Current studies and uses are now confirming their utility experienced over hundreds of years.
Harvesting sea buckthorn fruit is difficult because of dense thorn arrangement among the berries. Therefore, sometimes the only way to obtain fruit is to remove the entire branch of the shrub, which reduces future crops. For this reason berries can only be harvested once every 2 years.
Sea buckthorn has interesting properties and could be of benefit in topical skin care, as long as it is not overharvested or harvested in a way that has a detrimental impact on the environment.
Dr. Wesley and Lily Talakoub, MD, are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
United States Department of Agriculture. PLANTS Profile for Hippophae rhamnoides (seaberry). 2007.
Zielińska A and Nowak I. Lipids Health Dis. 2017 May 19;16(1):95.
Reynolds KA et al. Int J Dermatol. 2019 Dec;58(12):1371-6.
To avoid jumping on the bandwagon of another ingredient trend, we sought to examine the scientific background and properties of sea buckthorn oil and it’s utility for the skin.
Sea buckthorn (Hippophae rhamnoides) – also known as a Siberian pineapple tree, and as sandthorn, sallowthorn, or seaberry – is a thorny, dioecious shrub (or tree) in the oleaster family. It can grow up to 23 feet high and is found in coastal sea cliff areas and on mountain slopes of Western Europe, and in dry sandy areas of Asia Minor and Central Asia, Siberia, China, and Tibet. Common sea buckthorn flowers in late April and early May, producing a large number of small, green and brown flowers, turning into edible, usually yellow or orange round berries. The berries have a bitter, sour taste and have a mild aroma, resembling that of a pineapple. The fruit contains a small stone that covers an oily seed.
The berries are a source of antioxidant vitamins, flavonoids, and organic acids, and when pressed, produce a juice that separates into three layers: a thick cream (upper layer), a combination of saturated and unsaturated fatty acids (middle layer), and juice that is a source of fat (lower layer). The berries contain mainly vitamin C, but also vitamin A (alpha- and beta-carotene) and a mixture of other carotenoids, as well as varying concentrations of tocopherols (vitamin E), folic acid, and vitamin B complex–group vitamins.
In addition to flavonoids, the berries contain catechins and procyanidins, cyclitols, phospholipids, tannins, sugars (galactose, fructose, xylose), organic acids (maleic acid, oxalic acid, malic acid, tartaric acid), phenolic acids (such as ferulic acid), and fatty oil. The amount of vitamin C content varies with the variety of the plant and where it is found. The oil of sea buckthorn may be extracted from two parts of the plant, with mechanical cold pressing of seeds (up to 12.5% weight as oil content) and fruit pulp (8%-12% oil content).
Among vegetable oils, sea buckthorn fruit oil has the highest content of palmitoleic acid (omega-7).
Fruit and seed oils contain tocotrienols and plant sterols. Pulp sea buckthorn oil has a high carotenoid content, as opposed to seed oil, and in Mongolia, Russia, and China, is used as a topical therapy for skin burns.
Other significant fatty acids found in sea buckthorn oil are saturated fatty acids (palmitic acid and stearic acid) and polyunsaturated fatty acids, which include alpha-linolenic acid (omega-3), gamma-linolenic acid (omega-6), linolic acid (omega-6), oleic acid (omega-9), and eicosanoic acid (omega-9). Gamma-linoleic acid in particular is reduced in dry skin conditions, such as aging and atopic dermatitis. The human body can produce some gamma-linolenic acid, oleic acid, and palmitoleic acid, but not linolic acid and alpha-linolenic acid. The addition of these substances to diet or skin care has been found to be beneficial in improving dryness and the skin barrier.
In addition, linolic acid, a natural component of human sebum, has been noted to be decreased in the sebum of people with acne-prone skin. Preliminary evidence indicates that dietary supplements containing fatty acids such as docosahexaenoic acid, sea buckthorn oil, and hemp seed oil may decrease the severity of atopic dermatitis.
Besides use in topical skin care and cosmetic preparations, sea buckthorn has also been used successfully in the treatment of chronic gastric ulcer disease, inflammation of the vagina and cervix, and cervical erosion. The bark and leaves of sea buckthorn used to be applied to treat diarrhea and dermatologic conditions, while berry oil has been applied topically or taken orally to soften the skin.
In traditional Indian, Chinese, and Tibetan medicines, sea buckthorn berries are used for medicinal purposes, as their ingredients were thought to have a beneficial effect on the function of the alimentary, respiratory, and circulatory systems. Current studies and uses are now confirming their utility experienced over hundreds of years.
Harvesting sea buckthorn fruit is difficult because of dense thorn arrangement among the berries. Therefore, sometimes the only way to obtain fruit is to remove the entire branch of the shrub, which reduces future crops. For this reason berries can only be harvested once every 2 years.
Sea buckthorn has interesting properties and could be of benefit in topical skin care, as long as it is not overharvested or harvested in a way that has a detrimental impact on the environment.
Dr. Wesley and Lily Talakoub, MD, are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
United States Department of Agriculture. PLANTS Profile for Hippophae rhamnoides (seaberry). 2007.
Zielińska A and Nowak I. Lipids Health Dis. 2017 May 19;16(1):95.
Reynolds KA et al. Int J Dermatol. 2019 Dec;58(12):1371-6.
To avoid jumping on the bandwagon of another ingredient trend, we sought to examine the scientific background and properties of sea buckthorn oil and it’s utility for the skin.
Sea buckthorn (Hippophae rhamnoides) – also known as a Siberian pineapple tree, and as sandthorn, sallowthorn, or seaberry – is a thorny, dioecious shrub (or tree) in the oleaster family. It can grow up to 23 feet high and is found in coastal sea cliff areas and on mountain slopes of Western Europe, and in dry sandy areas of Asia Minor and Central Asia, Siberia, China, and Tibet. Common sea buckthorn flowers in late April and early May, producing a large number of small, green and brown flowers, turning into edible, usually yellow or orange round berries. The berries have a bitter, sour taste and have a mild aroma, resembling that of a pineapple. The fruit contains a small stone that covers an oily seed.
The berries are a source of antioxidant vitamins, flavonoids, and organic acids, and when pressed, produce a juice that separates into three layers: a thick cream (upper layer), a combination of saturated and unsaturated fatty acids (middle layer), and juice that is a source of fat (lower layer). The berries contain mainly vitamin C, but also vitamin A (alpha- and beta-carotene) and a mixture of other carotenoids, as well as varying concentrations of tocopherols (vitamin E), folic acid, and vitamin B complex–group vitamins.
In addition to flavonoids, the berries contain catechins and procyanidins, cyclitols, phospholipids, tannins, sugars (galactose, fructose, xylose), organic acids (maleic acid, oxalic acid, malic acid, tartaric acid), phenolic acids (such as ferulic acid), and fatty oil. The amount of vitamin C content varies with the variety of the plant and where it is found. The oil of sea buckthorn may be extracted from two parts of the plant, with mechanical cold pressing of seeds (up to 12.5% weight as oil content) and fruit pulp (8%-12% oil content).
Among vegetable oils, sea buckthorn fruit oil has the highest content of palmitoleic acid (omega-7).
Fruit and seed oils contain tocotrienols and plant sterols. Pulp sea buckthorn oil has a high carotenoid content, as opposed to seed oil, and in Mongolia, Russia, and China, is used as a topical therapy for skin burns.
Other significant fatty acids found in sea buckthorn oil are saturated fatty acids (palmitic acid and stearic acid) and polyunsaturated fatty acids, which include alpha-linolenic acid (omega-3), gamma-linolenic acid (omega-6), linolic acid (omega-6), oleic acid (omega-9), and eicosanoic acid (omega-9). Gamma-linoleic acid in particular is reduced in dry skin conditions, such as aging and atopic dermatitis. The human body can produce some gamma-linolenic acid, oleic acid, and palmitoleic acid, but not linolic acid and alpha-linolenic acid. The addition of these substances to diet or skin care has been found to be beneficial in improving dryness and the skin barrier.
In addition, linolic acid, a natural component of human sebum, has been noted to be decreased in the sebum of people with acne-prone skin. Preliminary evidence indicates that dietary supplements containing fatty acids such as docosahexaenoic acid, sea buckthorn oil, and hemp seed oil may decrease the severity of atopic dermatitis.
Besides use in topical skin care and cosmetic preparations, sea buckthorn has also been used successfully in the treatment of chronic gastric ulcer disease, inflammation of the vagina and cervix, and cervical erosion. The bark and leaves of sea buckthorn used to be applied to treat diarrhea and dermatologic conditions, while berry oil has been applied topically or taken orally to soften the skin.
In traditional Indian, Chinese, and Tibetan medicines, sea buckthorn berries are used for medicinal purposes, as their ingredients were thought to have a beneficial effect on the function of the alimentary, respiratory, and circulatory systems. Current studies and uses are now confirming their utility experienced over hundreds of years.
Harvesting sea buckthorn fruit is difficult because of dense thorn arrangement among the berries. Therefore, sometimes the only way to obtain fruit is to remove the entire branch of the shrub, which reduces future crops. For this reason berries can only be harvested once every 2 years.
Sea buckthorn has interesting properties and could be of benefit in topical skin care, as long as it is not overharvested or harvested in a way that has a detrimental impact on the environment.
Dr. Wesley and Lily Talakoub, MD, are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
United States Department of Agriculture. PLANTS Profile for Hippophae rhamnoides (seaberry). 2007.
Zielińska A and Nowak I. Lipids Health Dis. 2017 May 19;16(1):95.
Reynolds KA et al. Int J Dermatol. 2019 Dec;58(12):1371-6.
What is the diagnosis?
Numerous morphologies of skin rashes have been described in the setting of COVID-19, including pernio, livedoid rash, exanthem, and vasculitis. This classic constellation of symptoms (palpable purpura on buttocks/legs, abdominal pain, arthralgia, hematuria) is highly consistent with Henoch-Schonlein purpura (HSP). There are now multiple case reports of COVID-19–associated HSP.
HSP is the most common type of childhood systemic vasculitis. It is mediated by immunoglobulin A (IgA) immune complex deposition and has been associated with respiratory tract infections, streptococcal species, parainfluenza virus, and human parvovirus B19, medications, vaccinations, and malignancies. HSP is usually a self-limiting disease, with a course over 4-6 weeks, and can affect multiple organs, including the skin, gastrointestinal tract, joints, and the kidneys. The diagnostic criteria include palpable purpura in the presence of one or more of the following: diffuse abdominal pain, arthritis or arthralgia, any biopsy showing predominant IgA deposition, and renal involvement in the form of hematuria or proteinuria. Renal disease is variable and is the most significant indicator of long-term prognosis. This teenager was treated with oral corticosteroids because of the severe periarticular edema and responded rapidly. His subsequent urine analyses normalized.
What is on the differential?
Multisystem inflammatory syndrome in children (MIS-C) is a rare, potentially fatal, complication of COVID-19 infection that causes inflammation of multiple organs, including the heart, lungs, kidneys, brain, skin, eyes, or the gastrointestinal tract. It commonly affects children around ages 8-9 years. Initial symptoms include fever, rash, red eyes, diarrhea, and vomiting that appear 2-6 weeks post COVID-19 infection. Like HSP, MIS-C can present with edema of the extremities, worsening hand/foot pain, and hematuria; however, the absence of both fever and the pattern of system involvement seen with MIS-C and classic findings in this patient are more consistent with HSP.
Reactive infectious mucocutaneous eruption (RIME) was recently coined to encompass both infection-associated Stevens-Johnson eruptions including Mycoplasma pneumoniae-induced rash and mucositis (MIRM) and mucocutaneous eruptions caused by nonmycoplasma pathogens (including Chlamydia pneumoniae, human parainfluenza virus 2, rhinovirus, adenovirus, enterovirus, human metapneumovirus, influenza B virus, and COVID-19). It is usually seen in male children and adolescents. Prodromal symptoms include cough, fever, and malaise and they precede the prominent feature of mucositis. Our patient’s lack of mucosal involvement is not consistent with RIME.
Perniosis (chilblains) is characterized by localized edematous patches of erythema or cyanosis on exposed extremities, that may be associated with cold exposure. Lesions are usually symmetric and self-limiting, and symptoms can include numbness, tingling, pruritus, burning, or pain. Pernio-like skin lesions have been seen during the COVID-19 pandemic, though many patients have negative testing for infection by PCR and serology. Pernio may also be seen with autoimmune diseases or malignancy.
Meningococcemia is a rare disease caused by infection with gram-negative diplococci bacteria Neisseria meningitidis and spreads through saliva or respiratory secretions. Its clinical presentation can vary widely, from transient fever to fulminant disease. It is characterized by upper respiratory tract infection, fever, and petechial lesions associated with thrombocytopenia and coagulopathy.
Dr. Eichenfield is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Ms. Laborada is a pediatric dermatology research associate in the division of pediatric and adolescent dermatology at the University of California, San Diego, and Rady Children’s Hospital. Dr. Eichenfield and Ms. Laborada have no relevant financial disclosures.
References
AlGhoozi DA, AlKhayyat HM. BMJ Case Reports CP 2021;14:e239910.
Jacobi M et al. Pediatr Infect Dis J. 2021;40(2):e93-4.
Paller A, Mancini AJ. Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence. 4th ed. Philadelphia (PA): Elsevier Saunders; 2011.
Radia T et al. Paediatr Respir Rev. 2021;38:51-7.
Ramien ML. Clin Exp Dermatol. 2021;46(3):420-9.
Numerous morphologies of skin rashes have been described in the setting of COVID-19, including pernio, livedoid rash, exanthem, and vasculitis. This classic constellation of symptoms (palpable purpura on buttocks/legs, abdominal pain, arthralgia, hematuria) is highly consistent with Henoch-Schonlein purpura (HSP). There are now multiple case reports of COVID-19–associated HSP.
HSP is the most common type of childhood systemic vasculitis. It is mediated by immunoglobulin A (IgA) immune complex deposition and has been associated with respiratory tract infections, streptococcal species, parainfluenza virus, and human parvovirus B19, medications, vaccinations, and malignancies. HSP is usually a self-limiting disease, with a course over 4-6 weeks, and can affect multiple organs, including the skin, gastrointestinal tract, joints, and the kidneys. The diagnostic criteria include palpable purpura in the presence of one or more of the following: diffuse abdominal pain, arthritis or arthralgia, any biopsy showing predominant IgA deposition, and renal involvement in the form of hematuria or proteinuria. Renal disease is variable and is the most significant indicator of long-term prognosis. This teenager was treated with oral corticosteroids because of the severe periarticular edema and responded rapidly. His subsequent urine analyses normalized.
What is on the differential?
Multisystem inflammatory syndrome in children (MIS-C) is a rare, potentially fatal, complication of COVID-19 infection that causes inflammation of multiple organs, including the heart, lungs, kidneys, brain, skin, eyes, or the gastrointestinal tract. It commonly affects children around ages 8-9 years. Initial symptoms include fever, rash, red eyes, diarrhea, and vomiting that appear 2-6 weeks post COVID-19 infection. Like HSP, MIS-C can present with edema of the extremities, worsening hand/foot pain, and hematuria; however, the absence of both fever and the pattern of system involvement seen with MIS-C and classic findings in this patient are more consistent with HSP.
Reactive infectious mucocutaneous eruption (RIME) was recently coined to encompass both infection-associated Stevens-Johnson eruptions including Mycoplasma pneumoniae-induced rash and mucositis (MIRM) and mucocutaneous eruptions caused by nonmycoplasma pathogens (including Chlamydia pneumoniae, human parainfluenza virus 2, rhinovirus, adenovirus, enterovirus, human metapneumovirus, influenza B virus, and COVID-19). It is usually seen in male children and adolescents. Prodromal symptoms include cough, fever, and malaise and they precede the prominent feature of mucositis. Our patient’s lack of mucosal involvement is not consistent with RIME.
Perniosis (chilblains) is characterized by localized edematous patches of erythema or cyanosis on exposed extremities, that may be associated with cold exposure. Lesions are usually symmetric and self-limiting, and symptoms can include numbness, tingling, pruritus, burning, or pain. Pernio-like skin lesions have been seen during the COVID-19 pandemic, though many patients have negative testing for infection by PCR and serology. Pernio may also be seen with autoimmune diseases or malignancy.
Meningococcemia is a rare disease caused by infection with gram-negative diplococci bacteria Neisseria meningitidis and spreads through saliva or respiratory secretions. Its clinical presentation can vary widely, from transient fever to fulminant disease. It is characterized by upper respiratory tract infection, fever, and petechial lesions associated with thrombocytopenia and coagulopathy.
Dr. Eichenfield is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Ms. Laborada is a pediatric dermatology research associate in the division of pediatric and adolescent dermatology at the University of California, San Diego, and Rady Children’s Hospital. Dr. Eichenfield and Ms. Laborada have no relevant financial disclosures.
References
AlGhoozi DA, AlKhayyat HM. BMJ Case Reports CP 2021;14:e239910.
Jacobi M et al. Pediatr Infect Dis J. 2021;40(2):e93-4.
Paller A, Mancini AJ. Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence. 4th ed. Philadelphia (PA): Elsevier Saunders; 2011.
Radia T et al. Paediatr Respir Rev. 2021;38:51-7.
Ramien ML. Clin Exp Dermatol. 2021;46(3):420-9.
Numerous morphologies of skin rashes have been described in the setting of COVID-19, including pernio, livedoid rash, exanthem, and vasculitis. This classic constellation of symptoms (palpable purpura on buttocks/legs, abdominal pain, arthralgia, hematuria) is highly consistent with Henoch-Schonlein purpura (HSP). There are now multiple case reports of COVID-19–associated HSP.
HSP is the most common type of childhood systemic vasculitis. It is mediated by immunoglobulin A (IgA) immune complex deposition and has been associated with respiratory tract infections, streptococcal species, parainfluenza virus, and human parvovirus B19, medications, vaccinations, and malignancies. HSP is usually a self-limiting disease, with a course over 4-6 weeks, and can affect multiple organs, including the skin, gastrointestinal tract, joints, and the kidneys. The diagnostic criteria include palpable purpura in the presence of one or more of the following: diffuse abdominal pain, arthritis or arthralgia, any biopsy showing predominant IgA deposition, and renal involvement in the form of hematuria or proteinuria. Renal disease is variable and is the most significant indicator of long-term prognosis. This teenager was treated with oral corticosteroids because of the severe periarticular edema and responded rapidly. His subsequent urine analyses normalized.
What is on the differential?
Multisystem inflammatory syndrome in children (MIS-C) is a rare, potentially fatal, complication of COVID-19 infection that causes inflammation of multiple organs, including the heart, lungs, kidneys, brain, skin, eyes, or the gastrointestinal tract. It commonly affects children around ages 8-9 years. Initial symptoms include fever, rash, red eyes, diarrhea, and vomiting that appear 2-6 weeks post COVID-19 infection. Like HSP, MIS-C can present with edema of the extremities, worsening hand/foot pain, and hematuria; however, the absence of both fever and the pattern of system involvement seen with MIS-C and classic findings in this patient are more consistent with HSP.
Reactive infectious mucocutaneous eruption (RIME) was recently coined to encompass both infection-associated Stevens-Johnson eruptions including Mycoplasma pneumoniae-induced rash and mucositis (MIRM) and mucocutaneous eruptions caused by nonmycoplasma pathogens (including Chlamydia pneumoniae, human parainfluenza virus 2, rhinovirus, adenovirus, enterovirus, human metapneumovirus, influenza B virus, and COVID-19). It is usually seen in male children and adolescents. Prodromal symptoms include cough, fever, and malaise and they precede the prominent feature of mucositis. Our patient’s lack of mucosal involvement is not consistent with RIME.
Perniosis (chilblains) is characterized by localized edematous patches of erythema or cyanosis on exposed extremities, that may be associated with cold exposure. Lesions are usually symmetric and self-limiting, and symptoms can include numbness, tingling, pruritus, burning, or pain. Pernio-like skin lesions have been seen during the COVID-19 pandemic, though many patients have negative testing for infection by PCR and serology. Pernio may also be seen with autoimmune diseases or malignancy.
Meningococcemia is a rare disease caused by infection with gram-negative diplococci bacteria Neisseria meningitidis and spreads through saliva or respiratory secretions. Its clinical presentation can vary widely, from transient fever to fulminant disease. It is characterized by upper respiratory tract infection, fever, and petechial lesions associated with thrombocytopenia and coagulopathy.
Dr. Eichenfield is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Ms. Laborada is a pediatric dermatology research associate in the division of pediatric and adolescent dermatology at the University of California, San Diego, and Rady Children’s Hospital. Dr. Eichenfield and Ms. Laborada have no relevant financial disclosures.
References
AlGhoozi DA, AlKhayyat HM. BMJ Case Reports CP 2021;14:e239910.
Jacobi M et al. Pediatr Infect Dis J. 2021;40(2):e93-4.
Paller A, Mancini AJ. Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence. 4th ed. Philadelphia (PA): Elsevier Saunders; 2011.
Radia T et al. Paediatr Respir Rev. 2021;38:51-7.
Ramien ML. Clin Exp Dermatol. 2021;46(3):420-9.
Aaron Beck: An appreciation
He always dressed the same at conferences: dark suit, white shirt, bright red bow tie.
For all his fame, he was very kind, warmly greeting those who wanted to see him and immediately turning attention toward their research rather than his own. Aaron Beck actually didn’t lecture much; he preferred to roleplay cognitive therapy with an audience member acting as the patient. He would engage in what he called Socratic questioning, or more formally, cognitive restructuring, with warmth and true curiosity:
- What might be another explanation or viewpoint?
- What are the effects of thinking this way?
- Can you think of any evidence that supports the opposite view?
The audience member/patient would benefit not only from thinking about things differently, but also from the captivating interaction with the man, Aaron Temkin Beck, MD, (who went by Tim), youngest child of Jewish immigrants from the Ukraine.
When written up in treatment manuals, cognitive restructuring can seem cold and overly logical, but in person, Dr. Beck made it come to life. This ability to nurture curiosity was a special talent; his friend and fellow cognitive psychologist Donald Meichenbaum, PhD, recalls that even over lunch, he never stopped asking questions, personal and professional, on a wide range of topics.
It is widely accepted that Dr. Beck, who died Nov. 1 at the age of 100 in suburban Philadelphia, was the most important figure in the field of cognitive-behavioral therapy (CBT).
He didn’t invent the field. Behaviorism predated him by generations, founded by figures such as John Watson and B.F. Skinner. Those psychologists set up behaviorism as an alternative to the reigning power of Freudian psychoanalysis, but they ran a distant second.
It wasn’t until Dr. Beck added a new approach, cognitive therapy, to the behavioristic movement that the new mélange, CBT, began to gain traction with clinicians and researchers. Dr. Beck, who had trained in psychiatry, developed his ideas in the 1960s while observing what he believed were limitations in the classic Freudian methods. He recognized that patients had “automatic thoughts,” not just unconscious emotions, when they engaged in Freudian free association, saying whatever came to their minds.
These thoughts often distorted reality, he observed; they were “maladaptive beliefs,” and when they changed, patients’ emotional states improved.
Dr. Beck wasn’t alone. The psychologist Albert Ellis, PhD, in New York, had come to similar conclusions a decade earlier, though with a more coldly logical and challenging style. The prominent British psychologist Hans Eysenck, PhD, had argued strongly that Freudian psychoanalysis was ineffective and that behavioral approaches were better.
Dr. Beck turned the Freudian equation around: Instead of emotion as cause and thought as effect, it was thought which affected emotion, for better or worse. Once you connected behavior as the outcome, you had the essence of CBT: thought, emotion, and behavior – each affecting the other, with thought being the strongest axis of change.
The process wasn’t bloodless. Behaviorists defended their turf against cognitivists, just as much as Freudians rejected both. At one point the behaviorists in the Association for the Advancement of Behavior Therapy tried to expel the advocates of a cognitive approach. Dr. Beck responded by leading the cognitivists in creating a new journal; he emphasized the importance of research being the main mechanism to decide what treatments worked the best.
Putting these ideas out in the 1960s and 1970s, Dr. Beck garnered support from researchers when he manualized the approach. Freudian psychoanalysis was idiosyncratic; it was almost impossible to study empirically, because the therapist would be responding to the unpredictable dreams and memories of patients engaged in free association. Each case was unique.
But CBT was systematic: The same general approach was taken to all patients; the same negative cognitions were found in depression, for instance, like all-or-nothing thinking or overgeneralization. Once manualized, CBT became the standard method of psychotherapy studied with the newly developed method of randomized controlled trials (RCTs).
By the 1980s, RCTs had proven the efficacy of CBT in depression, and the approach took off.
Dr. Beck already had developed a series of rating scales: the Beck Depression Inventory, the Beck Scale for Suicidal Ideation, the Beck Anxiety Inventory, the Beck Hopelessness Scale. Widely used, these scales extended his influence enormously. Copyrighted, they created a new industry of psychological research.
Dr. Beck’s own work was mainly in depression, but his followers extended it everywhere else: anxiety disorders and phobias, eating disorders, substance abuse, bipolar illness, even schizophrenia. Meanwhile, Freudian psychoanalysis fell into a steep decline from which it never recovered.
Some argued that it was abetted by insurance restrictions on psychotherapy, which favored shorter-term CBT; others that its research was biased in its favor because psychotherapy treatments, unlike medications, cannot be blinded; others that its efficacy could not be shown to be specific to its theory, as opposed to the interpersonal relationship between therapist and client.
Still, CBT has transformed psychotherapy and continues to expand its influence. Computer-based CBT has been proven effective, and digital CBT has become a standard approach in many smartphone applications and is central to the claims of multiple new biotechnology companies advocating for digital psychotherapy.
Aaron Beck continued publishing scientific articles to age 98. His last papers reviewed his life’s work. He characteristically gave credit to others, calmly recollected how he traveled away from psychoanalysis, described how his work started and ended in schizophrenia, and noted that the “working relationship with the therapist” remained a key factor for the success of CBT.
That parting comment reminds us that behind all the technology and research stands the kindly man in the dark suit, white shirt, and bright red bow tie, looking at you warmly, asking about your thoughts, and curiously wondering what might be another explanation or viewpoint you hadn’t considered.
Nassir Ghaemi, MD, MPH, is a professor of psychiatry at Tufts Medical Center and a lecturer in psychiatry at Harvard Medical School. He is the author of several general-interest books on psychiatry. A version of this article first appeared on Medscape.com.
He always dressed the same at conferences: dark suit, white shirt, bright red bow tie.
For all his fame, he was very kind, warmly greeting those who wanted to see him and immediately turning attention toward their research rather than his own. Aaron Beck actually didn’t lecture much; he preferred to roleplay cognitive therapy with an audience member acting as the patient. He would engage in what he called Socratic questioning, or more formally, cognitive restructuring, with warmth and true curiosity:
- What might be another explanation or viewpoint?
- What are the effects of thinking this way?
- Can you think of any evidence that supports the opposite view?
The audience member/patient would benefit not only from thinking about things differently, but also from the captivating interaction with the man, Aaron Temkin Beck, MD, (who went by Tim), youngest child of Jewish immigrants from the Ukraine.
When written up in treatment manuals, cognitive restructuring can seem cold and overly logical, but in person, Dr. Beck made it come to life. This ability to nurture curiosity was a special talent; his friend and fellow cognitive psychologist Donald Meichenbaum, PhD, recalls that even over lunch, he never stopped asking questions, personal and professional, on a wide range of topics.
It is widely accepted that Dr. Beck, who died Nov. 1 at the age of 100 in suburban Philadelphia, was the most important figure in the field of cognitive-behavioral therapy (CBT).
He didn’t invent the field. Behaviorism predated him by generations, founded by figures such as John Watson and B.F. Skinner. Those psychologists set up behaviorism as an alternative to the reigning power of Freudian psychoanalysis, but they ran a distant second.
It wasn’t until Dr. Beck added a new approach, cognitive therapy, to the behavioristic movement that the new mélange, CBT, began to gain traction with clinicians and researchers. Dr. Beck, who had trained in psychiatry, developed his ideas in the 1960s while observing what he believed were limitations in the classic Freudian methods. He recognized that patients had “automatic thoughts,” not just unconscious emotions, when they engaged in Freudian free association, saying whatever came to their minds.
These thoughts often distorted reality, he observed; they were “maladaptive beliefs,” and when they changed, patients’ emotional states improved.
Dr. Beck wasn’t alone. The psychologist Albert Ellis, PhD, in New York, had come to similar conclusions a decade earlier, though with a more coldly logical and challenging style. The prominent British psychologist Hans Eysenck, PhD, had argued strongly that Freudian psychoanalysis was ineffective and that behavioral approaches were better.
Dr. Beck turned the Freudian equation around: Instead of emotion as cause and thought as effect, it was thought which affected emotion, for better or worse. Once you connected behavior as the outcome, you had the essence of CBT: thought, emotion, and behavior – each affecting the other, with thought being the strongest axis of change.
The process wasn’t bloodless. Behaviorists defended their turf against cognitivists, just as much as Freudians rejected both. At one point the behaviorists in the Association for the Advancement of Behavior Therapy tried to expel the advocates of a cognitive approach. Dr. Beck responded by leading the cognitivists in creating a new journal; he emphasized the importance of research being the main mechanism to decide what treatments worked the best.
Putting these ideas out in the 1960s and 1970s, Dr. Beck garnered support from researchers when he manualized the approach. Freudian psychoanalysis was idiosyncratic; it was almost impossible to study empirically, because the therapist would be responding to the unpredictable dreams and memories of patients engaged in free association. Each case was unique.
But CBT was systematic: The same general approach was taken to all patients; the same negative cognitions were found in depression, for instance, like all-or-nothing thinking or overgeneralization. Once manualized, CBT became the standard method of psychotherapy studied with the newly developed method of randomized controlled trials (RCTs).
By the 1980s, RCTs had proven the efficacy of CBT in depression, and the approach took off.
Dr. Beck already had developed a series of rating scales: the Beck Depression Inventory, the Beck Scale for Suicidal Ideation, the Beck Anxiety Inventory, the Beck Hopelessness Scale. Widely used, these scales extended his influence enormously. Copyrighted, they created a new industry of psychological research.
Dr. Beck’s own work was mainly in depression, but his followers extended it everywhere else: anxiety disorders and phobias, eating disorders, substance abuse, bipolar illness, even schizophrenia. Meanwhile, Freudian psychoanalysis fell into a steep decline from which it never recovered.
Some argued that it was abetted by insurance restrictions on psychotherapy, which favored shorter-term CBT; others that its research was biased in its favor because psychotherapy treatments, unlike medications, cannot be blinded; others that its efficacy could not be shown to be specific to its theory, as opposed to the interpersonal relationship between therapist and client.
Still, CBT has transformed psychotherapy and continues to expand its influence. Computer-based CBT has been proven effective, and digital CBT has become a standard approach in many smartphone applications and is central to the claims of multiple new biotechnology companies advocating for digital psychotherapy.
Aaron Beck continued publishing scientific articles to age 98. His last papers reviewed his life’s work. He characteristically gave credit to others, calmly recollected how he traveled away from psychoanalysis, described how his work started and ended in schizophrenia, and noted that the “working relationship with the therapist” remained a key factor for the success of CBT.
That parting comment reminds us that behind all the technology and research stands the kindly man in the dark suit, white shirt, and bright red bow tie, looking at you warmly, asking about your thoughts, and curiously wondering what might be another explanation or viewpoint you hadn’t considered.
Nassir Ghaemi, MD, MPH, is a professor of psychiatry at Tufts Medical Center and a lecturer in psychiatry at Harvard Medical School. He is the author of several general-interest books on psychiatry. A version of this article first appeared on Medscape.com.
He always dressed the same at conferences: dark suit, white shirt, bright red bow tie.
For all his fame, he was very kind, warmly greeting those who wanted to see him and immediately turning attention toward their research rather than his own. Aaron Beck actually didn’t lecture much; he preferred to roleplay cognitive therapy with an audience member acting as the patient. He would engage in what he called Socratic questioning, or more formally, cognitive restructuring, with warmth and true curiosity:
- What might be another explanation or viewpoint?
- What are the effects of thinking this way?
- Can you think of any evidence that supports the opposite view?
The audience member/patient would benefit not only from thinking about things differently, but also from the captivating interaction with the man, Aaron Temkin Beck, MD, (who went by Tim), youngest child of Jewish immigrants from the Ukraine.
When written up in treatment manuals, cognitive restructuring can seem cold and overly logical, but in person, Dr. Beck made it come to life. This ability to nurture curiosity was a special talent; his friend and fellow cognitive psychologist Donald Meichenbaum, PhD, recalls that even over lunch, he never stopped asking questions, personal and professional, on a wide range of topics.
It is widely accepted that Dr. Beck, who died Nov. 1 at the age of 100 in suburban Philadelphia, was the most important figure in the field of cognitive-behavioral therapy (CBT).
He didn’t invent the field. Behaviorism predated him by generations, founded by figures such as John Watson and B.F. Skinner. Those psychologists set up behaviorism as an alternative to the reigning power of Freudian psychoanalysis, but they ran a distant second.
It wasn’t until Dr. Beck added a new approach, cognitive therapy, to the behavioristic movement that the new mélange, CBT, began to gain traction with clinicians and researchers. Dr. Beck, who had trained in psychiatry, developed his ideas in the 1960s while observing what he believed were limitations in the classic Freudian methods. He recognized that patients had “automatic thoughts,” not just unconscious emotions, when they engaged in Freudian free association, saying whatever came to their minds.
These thoughts often distorted reality, he observed; they were “maladaptive beliefs,” and when they changed, patients’ emotional states improved.
Dr. Beck wasn’t alone. The psychologist Albert Ellis, PhD, in New York, had come to similar conclusions a decade earlier, though with a more coldly logical and challenging style. The prominent British psychologist Hans Eysenck, PhD, had argued strongly that Freudian psychoanalysis was ineffective and that behavioral approaches were better.
Dr. Beck turned the Freudian equation around: Instead of emotion as cause and thought as effect, it was thought which affected emotion, for better or worse. Once you connected behavior as the outcome, you had the essence of CBT: thought, emotion, and behavior – each affecting the other, with thought being the strongest axis of change.
The process wasn’t bloodless. Behaviorists defended their turf against cognitivists, just as much as Freudians rejected both. At one point the behaviorists in the Association for the Advancement of Behavior Therapy tried to expel the advocates of a cognitive approach. Dr. Beck responded by leading the cognitivists in creating a new journal; he emphasized the importance of research being the main mechanism to decide what treatments worked the best.
Putting these ideas out in the 1960s and 1970s, Dr. Beck garnered support from researchers when he manualized the approach. Freudian psychoanalysis was idiosyncratic; it was almost impossible to study empirically, because the therapist would be responding to the unpredictable dreams and memories of patients engaged in free association. Each case was unique.
But CBT was systematic: The same general approach was taken to all patients; the same negative cognitions were found in depression, for instance, like all-or-nothing thinking or overgeneralization. Once manualized, CBT became the standard method of psychotherapy studied with the newly developed method of randomized controlled trials (RCTs).
By the 1980s, RCTs had proven the efficacy of CBT in depression, and the approach took off.
Dr. Beck already had developed a series of rating scales: the Beck Depression Inventory, the Beck Scale for Suicidal Ideation, the Beck Anxiety Inventory, the Beck Hopelessness Scale. Widely used, these scales extended his influence enormously. Copyrighted, they created a new industry of psychological research.
Dr. Beck’s own work was mainly in depression, but his followers extended it everywhere else: anxiety disorders and phobias, eating disorders, substance abuse, bipolar illness, even schizophrenia. Meanwhile, Freudian psychoanalysis fell into a steep decline from which it never recovered.
Some argued that it was abetted by insurance restrictions on psychotherapy, which favored shorter-term CBT; others that its research was biased in its favor because psychotherapy treatments, unlike medications, cannot be blinded; others that its efficacy could not be shown to be specific to its theory, as opposed to the interpersonal relationship between therapist and client.
Still, CBT has transformed psychotherapy and continues to expand its influence. Computer-based CBT has been proven effective, and digital CBT has become a standard approach in many smartphone applications and is central to the claims of multiple new biotechnology companies advocating for digital psychotherapy.
Aaron Beck continued publishing scientific articles to age 98. His last papers reviewed his life’s work. He characteristically gave credit to others, calmly recollected how he traveled away from psychoanalysis, described how his work started and ended in schizophrenia, and noted that the “working relationship with the therapist” remained a key factor for the success of CBT.
That parting comment reminds us that behind all the technology and research stands the kindly man in the dark suit, white shirt, and bright red bow tie, looking at you warmly, asking about your thoughts, and curiously wondering what might be another explanation or viewpoint you hadn’t considered.
Nassir Ghaemi, MD, MPH, is a professor of psychiatry at Tufts Medical Center and a lecturer in psychiatry at Harvard Medical School. He is the author of several general-interest books on psychiatry. A version of this article first appeared on Medscape.com.
Does the use of frankincense make sense in dermatology?
The Boswellia serrata exudate or gum (known in India as “guggulu”) that forms an aromatic resin traditionally used as incense – and known as frankincense (especially when retrieved from Boswellia species found in Eritrea and Somalia but also from the Indian variety) – has been considered for thousands of years to possess therapeutic properties. It is used in Ayurvedic medicine, as well as in traditional medicine in China and the Middle East, particularly for its anti-inflammatory effects to treat chronic conditions.1-8 In fact, such essential oils have been used since 2800 BC to treat various inflammatory conditions, including skin sores and wounds, as well as in perfumes and incense.2,9 In the West, use of frankincense dates back to thousands of years as well, more often found in the form of incense for religious and cultural ceremonies.7 Over the past 2 decades, .3 This column focuses on some of the emerging data on this ancient botanical agent.
Chemical constituents
Terpenoids and essential oils are the primary components of frankincense and are known to impart anti-inflammatory and anticancer activity. The same is true for myrrh, which has been combined with frankincense in traditional Chinese medicine as a single medication for millennia, with the two acting synergistically and considered still to be a potent combination in conferring various biological benefits.7
In 2010, in a systematic review of the anti-inflammatory and anticancer activities of Boswellia species and their chemical ingredients, Efferth and Oesch found that frankincense blocks the production of leukotrienes, cyclooxygenase (COX) 1 and 2, as well as 5-lipoxygenase; and oxidative stress. It also contributes to regulation of immune cells from the innate and acquired immune systems and exerts anticancer activity by influencing signaling transduction responsible for cell cycle arrest, as well as inhibition of proliferation, angiogenesis, invasion, and metastasis. The investigators also reported on clinical trial results that have found efficacy of frankincense and its constituents in ameliorating symptoms of psoriasis and erythematous eczema, among other disorders.3
Anti-inflammatory activity
Li et al. completed a study in 2016 to identify the active ingredients responsible for the anti-inflammatory and analgesic effects of frankincense. They found that alpha-pinene, linalool, and 1-octanol were key contributors. These constituents were noted for suppressing COX-2 overexpression in mice, as well as nociceptive stimulus-induced inflammatory infiltrates.10
Noting the increasing popularity of frankincense essential oil in skin care, despite a paucity of data, in 2017, Han et al. evaluated the biological activities of the essential oil in pre-inflamed human dermal fibroblasts using 17 key protein biomarkers. Frankincense essential oil displayed significant antiproliferative activity and suppressed collagen III, interferon gamma-induced protein 10, and intracellular adhesion molecule 1. The investigators referred to the overall encouraging potential of frankincense essential oil to exert influence over inflammation and tissue remodeling in human skin and called for additional research into its mechanisms of action and active constituents.11
Anticancer activity
The main active ingredient in frankincense, boswellic acid, has been shown to promote apoptosis, suppress matrix metalloproteinase secretion, and hinder migration in metastatic melanoma cell lines in mice.6,12
In 2019, Hakkim et al. demonstrated that frankincense essential oil yielded substantial antimelanoma activity in vitro and in vivo and ameliorated hepatotoxicity caused by acetaminophen.13
There is one case report in the literature on the use of frankincense as a treatment for skin cancer. A 56-year-old man received frankincense oil multiple times a day for 4 months to treat a nodular basal cell carcinoma on one arm (which resolved) and an infiltrative BCC on the chest (some focal residual tumor remained).6,14 Topical frankincense or boswellic acid has been given a grade D recommendation for treating skin cancer, however, because of only one level-of-evidence-5 study.6
Antimicrobial activity
In 2012, de Rapper et al. collected samples of three essential oils of frankincense (Boswellia rivae, Boswellia neglecta, and Boswellia papyrifera) and two essential oil samples of myrrh and sweet myrrh from different regions of Ethiopia to study their anti-infective properties alone and in combination. The investigators observed synergistic and additive effects, particularly between B. papyrifera and Commiphora myrrha. While noting the long history of the combined use of frankincense and myrrh essential oils since 1500 BC, the investigators highlighted their study as the first antimicrobial work to verify the effectiveness of this combination, validating the use of this combination to thwart particular pathogens.15
Just 2 years ago, Ljaljević Grbić et al. evaluated the in vitro antimicrobial potential of the liquid and vapor phases of B. carteri and C. myrrha (frankincense and myrrh, respectively) essential oils, finding that frankincense demonstrated marked capacity to act as a natural antimicrobial agent.9
Transdermal delivery
In 2017, Zhu et al. showed that frankincense and myrrh essential oils promoted the permeability of the Chinese herb Chuanxiong and may facilitate drug elimination from the epidermis via dermal capillaries by dint of improved cutaneous blood flow, thereby augmenting transdermal drug delivery.16 The same team also showed that frankincense and myrrh essential oils, by fostering permeation by enhancing drug delivery across the stratum corneum, can also alter the structure of the stratum corneum.17
Conclusion
The use of frankincense in traditional medicine has a long and impressive track record. Recent research provides reason for optimism, and further investigating the possible incorporation of this botanical agent into modern dermatologic therapies appears warranted. Clearly, however, much more research is needed.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.
References
1. Kimmatkar N et al. Phytomedicine. 2003 Jan;10(1):3-7.
2. Ammon HP. Wien Med Wochenschr. 2002;152(15-16):373-8.
3. Efferth T & Oesch F. Semin Cancer Biol. 2020 Feb 4;S1044-579X(20)30034-1.
4. Banno N et al. J Ethnopharmacol. 2006 Sep 19;107(2):249-53.
5. Poeckel D & Werz O. Curr Med Chem. 2006;13(28):3359-69.
6. Li JY, Kampp JT. Dermatol Surg. 2019 Jan;45(1):58-67.
7. Cao B et al. Molecules. 2019 Aug 24;24(17): 3076.
8. Mertens M et al. Flavour Fragr J. 2009;24:279-300.
9. Ljaljević Grbić M et al. J Ethnopharmacol. 2018 Jun 12;219:1-14.
10. Li XJ et al. J Ethnopharmacol. 2016 Feb 17;179:22-6.
11. Han X et al. Biochim Open. 2017 Feb 3;4:31-5.
12. Zhao W et al. Cancer Detect Prev. 2003;27:67-75.
13. Hakkim FL et al. Oncotarget. 2019 May 28;10(37):3472-90.
14. Fung K et al. OA Altern Med 2013;1:14.
15. de Rapper S et al. Lett Appl Microbiol. 2012 Apr;54(4):352-8.
16. Zhu XF et al. Zhongguo Zhong Yao Za Zhi. 2017 Feb;42(4):680-5.
17. Guan YM et al. Zhongguo Zhong Yao Za Zhi. 2017 Sep;42(17):3350-5.
The Boswellia serrata exudate or gum (known in India as “guggulu”) that forms an aromatic resin traditionally used as incense – and known as frankincense (especially when retrieved from Boswellia species found in Eritrea and Somalia but also from the Indian variety) – has been considered for thousands of years to possess therapeutic properties. It is used in Ayurvedic medicine, as well as in traditional medicine in China and the Middle East, particularly for its anti-inflammatory effects to treat chronic conditions.1-8 In fact, such essential oils have been used since 2800 BC to treat various inflammatory conditions, including skin sores and wounds, as well as in perfumes and incense.2,9 In the West, use of frankincense dates back to thousands of years as well, more often found in the form of incense for religious and cultural ceremonies.7 Over the past 2 decades, .3 This column focuses on some of the emerging data on this ancient botanical agent.
Chemical constituents
Terpenoids and essential oils are the primary components of frankincense and are known to impart anti-inflammatory and anticancer activity. The same is true for myrrh, which has been combined with frankincense in traditional Chinese medicine as a single medication for millennia, with the two acting synergistically and considered still to be a potent combination in conferring various biological benefits.7
In 2010, in a systematic review of the anti-inflammatory and anticancer activities of Boswellia species and their chemical ingredients, Efferth and Oesch found that frankincense blocks the production of leukotrienes, cyclooxygenase (COX) 1 and 2, as well as 5-lipoxygenase; and oxidative stress. It also contributes to regulation of immune cells from the innate and acquired immune systems and exerts anticancer activity by influencing signaling transduction responsible for cell cycle arrest, as well as inhibition of proliferation, angiogenesis, invasion, and metastasis. The investigators also reported on clinical trial results that have found efficacy of frankincense and its constituents in ameliorating symptoms of psoriasis and erythematous eczema, among other disorders.3
Anti-inflammatory activity
Li et al. completed a study in 2016 to identify the active ingredients responsible for the anti-inflammatory and analgesic effects of frankincense. They found that alpha-pinene, linalool, and 1-octanol were key contributors. These constituents were noted for suppressing COX-2 overexpression in mice, as well as nociceptive stimulus-induced inflammatory infiltrates.10
Noting the increasing popularity of frankincense essential oil in skin care, despite a paucity of data, in 2017, Han et al. evaluated the biological activities of the essential oil in pre-inflamed human dermal fibroblasts using 17 key protein biomarkers. Frankincense essential oil displayed significant antiproliferative activity and suppressed collagen III, interferon gamma-induced protein 10, and intracellular adhesion molecule 1. The investigators referred to the overall encouraging potential of frankincense essential oil to exert influence over inflammation and tissue remodeling in human skin and called for additional research into its mechanisms of action and active constituents.11
Anticancer activity
The main active ingredient in frankincense, boswellic acid, has been shown to promote apoptosis, suppress matrix metalloproteinase secretion, and hinder migration in metastatic melanoma cell lines in mice.6,12
In 2019, Hakkim et al. demonstrated that frankincense essential oil yielded substantial antimelanoma activity in vitro and in vivo and ameliorated hepatotoxicity caused by acetaminophen.13
There is one case report in the literature on the use of frankincense as a treatment for skin cancer. A 56-year-old man received frankincense oil multiple times a day for 4 months to treat a nodular basal cell carcinoma on one arm (which resolved) and an infiltrative BCC on the chest (some focal residual tumor remained).6,14 Topical frankincense or boswellic acid has been given a grade D recommendation for treating skin cancer, however, because of only one level-of-evidence-5 study.6
Antimicrobial activity
In 2012, de Rapper et al. collected samples of three essential oils of frankincense (Boswellia rivae, Boswellia neglecta, and Boswellia papyrifera) and two essential oil samples of myrrh and sweet myrrh from different regions of Ethiopia to study their anti-infective properties alone and in combination. The investigators observed synergistic and additive effects, particularly between B. papyrifera and Commiphora myrrha. While noting the long history of the combined use of frankincense and myrrh essential oils since 1500 BC, the investigators highlighted their study as the first antimicrobial work to verify the effectiveness of this combination, validating the use of this combination to thwart particular pathogens.15
Just 2 years ago, Ljaljević Grbić et al. evaluated the in vitro antimicrobial potential of the liquid and vapor phases of B. carteri and C. myrrha (frankincense and myrrh, respectively) essential oils, finding that frankincense demonstrated marked capacity to act as a natural antimicrobial agent.9
Transdermal delivery
In 2017, Zhu et al. showed that frankincense and myrrh essential oils promoted the permeability of the Chinese herb Chuanxiong and may facilitate drug elimination from the epidermis via dermal capillaries by dint of improved cutaneous blood flow, thereby augmenting transdermal drug delivery.16 The same team also showed that frankincense and myrrh essential oils, by fostering permeation by enhancing drug delivery across the stratum corneum, can also alter the structure of the stratum corneum.17
Conclusion
The use of frankincense in traditional medicine has a long and impressive track record. Recent research provides reason for optimism, and further investigating the possible incorporation of this botanical agent into modern dermatologic therapies appears warranted. Clearly, however, much more research is needed.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.
References
1. Kimmatkar N et al. Phytomedicine. 2003 Jan;10(1):3-7.
2. Ammon HP. Wien Med Wochenschr. 2002;152(15-16):373-8.
3. Efferth T & Oesch F. Semin Cancer Biol. 2020 Feb 4;S1044-579X(20)30034-1.
4. Banno N et al. J Ethnopharmacol. 2006 Sep 19;107(2):249-53.
5. Poeckel D & Werz O. Curr Med Chem. 2006;13(28):3359-69.
6. Li JY, Kampp JT. Dermatol Surg. 2019 Jan;45(1):58-67.
7. Cao B et al. Molecules. 2019 Aug 24;24(17): 3076.
8. Mertens M et al. Flavour Fragr J. 2009;24:279-300.
9. Ljaljević Grbić M et al. J Ethnopharmacol. 2018 Jun 12;219:1-14.
10. Li XJ et al. J Ethnopharmacol. 2016 Feb 17;179:22-6.
11. Han X et al. Biochim Open. 2017 Feb 3;4:31-5.
12. Zhao W et al. Cancer Detect Prev. 2003;27:67-75.
13. Hakkim FL et al. Oncotarget. 2019 May 28;10(37):3472-90.
14. Fung K et al. OA Altern Med 2013;1:14.
15. de Rapper S et al. Lett Appl Microbiol. 2012 Apr;54(4):352-8.
16. Zhu XF et al. Zhongguo Zhong Yao Za Zhi. 2017 Feb;42(4):680-5.
17. Guan YM et al. Zhongguo Zhong Yao Za Zhi. 2017 Sep;42(17):3350-5.
The Boswellia serrata exudate or gum (known in India as “guggulu”) that forms an aromatic resin traditionally used as incense – and known as frankincense (especially when retrieved from Boswellia species found in Eritrea and Somalia but also from the Indian variety) – has been considered for thousands of years to possess therapeutic properties. It is used in Ayurvedic medicine, as well as in traditional medicine in China and the Middle East, particularly for its anti-inflammatory effects to treat chronic conditions.1-8 In fact, such essential oils have been used since 2800 BC to treat various inflammatory conditions, including skin sores and wounds, as well as in perfumes and incense.2,9 In the West, use of frankincense dates back to thousands of years as well, more often found in the form of incense for religious and cultural ceremonies.7 Over the past 2 decades, .3 This column focuses on some of the emerging data on this ancient botanical agent.
Chemical constituents
Terpenoids and essential oils are the primary components of frankincense and are known to impart anti-inflammatory and anticancer activity. The same is true for myrrh, which has been combined with frankincense in traditional Chinese medicine as a single medication for millennia, with the two acting synergistically and considered still to be a potent combination in conferring various biological benefits.7
In 2010, in a systematic review of the anti-inflammatory and anticancer activities of Boswellia species and their chemical ingredients, Efferth and Oesch found that frankincense blocks the production of leukotrienes, cyclooxygenase (COX) 1 and 2, as well as 5-lipoxygenase; and oxidative stress. It also contributes to regulation of immune cells from the innate and acquired immune systems and exerts anticancer activity by influencing signaling transduction responsible for cell cycle arrest, as well as inhibition of proliferation, angiogenesis, invasion, and metastasis. The investigators also reported on clinical trial results that have found efficacy of frankincense and its constituents in ameliorating symptoms of psoriasis and erythematous eczema, among other disorders.3
Anti-inflammatory activity
Li et al. completed a study in 2016 to identify the active ingredients responsible for the anti-inflammatory and analgesic effects of frankincense. They found that alpha-pinene, linalool, and 1-octanol were key contributors. These constituents were noted for suppressing COX-2 overexpression in mice, as well as nociceptive stimulus-induced inflammatory infiltrates.10
Noting the increasing popularity of frankincense essential oil in skin care, despite a paucity of data, in 2017, Han et al. evaluated the biological activities of the essential oil in pre-inflamed human dermal fibroblasts using 17 key protein biomarkers. Frankincense essential oil displayed significant antiproliferative activity and suppressed collagen III, interferon gamma-induced protein 10, and intracellular adhesion molecule 1. The investigators referred to the overall encouraging potential of frankincense essential oil to exert influence over inflammation and tissue remodeling in human skin and called for additional research into its mechanisms of action and active constituents.11
Anticancer activity
The main active ingredient in frankincense, boswellic acid, has been shown to promote apoptosis, suppress matrix metalloproteinase secretion, and hinder migration in metastatic melanoma cell lines in mice.6,12
In 2019, Hakkim et al. demonstrated that frankincense essential oil yielded substantial antimelanoma activity in vitro and in vivo and ameliorated hepatotoxicity caused by acetaminophen.13
There is one case report in the literature on the use of frankincense as a treatment for skin cancer. A 56-year-old man received frankincense oil multiple times a day for 4 months to treat a nodular basal cell carcinoma on one arm (which resolved) and an infiltrative BCC on the chest (some focal residual tumor remained).6,14 Topical frankincense or boswellic acid has been given a grade D recommendation for treating skin cancer, however, because of only one level-of-evidence-5 study.6
Antimicrobial activity
In 2012, de Rapper et al. collected samples of three essential oils of frankincense (Boswellia rivae, Boswellia neglecta, and Boswellia papyrifera) and two essential oil samples of myrrh and sweet myrrh from different regions of Ethiopia to study their anti-infective properties alone and in combination. The investigators observed synergistic and additive effects, particularly between B. papyrifera and Commiphora myrrha. While noting the long history of the combined use of frankincense and myrrh essential oils since 1500 BC, the investigators highlighted their study as the first antimicrobial work to verify the effectiveness of this combination, validating the use of this combination to thwart particular pathogens.15
Just 2 years ago, Ljaljević Grbić et al. evaluated the in vitro antimicrobial potential of the liquid and vapor phases of B. carteri and C. myrrha (frankincense and myrrh, respectively) essential oils, finding that frankincense demonstrated marked capacity to act as a natural antimicrobial agent.9
Transdermal delivery
In 2017, Zhu et al. showed that frankincense and myrrh essential oils promoted the permeability of the Chinese herb Chuanxiong and may facilitate drug elimination from the epidermis via dermal capillaries by dint of improved cutaneous blood flow, thereby augmenting transdermal drug delivery.16 The same team also showed that frankincense and myrrh essential oils, by fostering permeation by enhancing drug delivery across the stratum corneum, can also alter the structure of the stratum corneum.17
Conclusion
The use of frankincense in traditional medicine has a long and impressive track record. Recent research provides reason for optimism, and further investigating the possible incorporation of this botanical agent into modern dermatologic therapies appears warranted. Clearly, however, much more research is needed.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.
References
1. Kimmatkar N et al. Phytomedicine. 2003 Jan;10(1):3-7.
2. Ammon HP. Wien Med Wochenschr. 2002;152(15-16):373-8.
3. Efferth T & Oesch F. Semin Cancer Biol. 2020 Feb 4;S1044-579X(20)30034-1.
4. Banno N et al. J Ethnopharmacol. 2006 Sep 19;107(2):249-53.
5. Poeckel D & Werz O. Curr Med Chem. 2006;13(28):3359-69.
6. Li JY, Kampp JT. Dermatol Surg. 2019 Jan;45(1):58-67.
7. Cao B et al. Molecules. 2019 Aug 24;24(17): 3076.
8. Mertens M et al. Flavour Fragr J. 2009;24:279-300.
9. Ljaljević Grbić M et al. J Ethnopharmacol. 2018 Jun 12;219:1-14.
10. Li XJ et al. J Ethnopharmacol. 2016 Feb 17;179:22-6.
11. Han X et al. Biochim Open. 2017 Feb 3;4:31-5.
12. Zhao W et al. Cancer Detect Prev. 2003;27:67-75.
13. Hakkim FL et al. Oncotarget. 2019 May 28;10(37):3472-90.
14. Fung K et al. OA Altern Med 2013;1:14.
15. de Rapper S et al. Lett Appl Microbiol. 2012 Apr;54(4):352-8.
16. Zhu XF et al. Zhongguo Zhong Yao Za Zhi. 2017 Feb;42(4):680-5.
17. Guan YM et al. Zhongguo Zhong Yao Za Zhi. 2017 Sep;42(17):3350-5.
Unmasking Our Grief
Since the start of the pandemic, health care systems have requested many in-services for staff on self-care and stress management to help health care workers (HCWs) cope with the heavy toll of COVID-19. The pandemic has set off a global mental health crisis, with unprecedented numbers of individuals meeting criteria for anxiety, depression, and other mental health disorders in response to the intense stressors of living through a pandemic. These calls to assist staff with self-care and burnout prevention have been especially salient for psychologists working in palliative care and geriatrics, where fears of COVID-19 infection and numbers of patient deaths have been high.
Throughout these painful times, we have been grateful for an online community of palliative care psychologists within the US Department of Veterans Affairs (VA) from across the continuum of care and across the country. This community brought together many of us who were both struggling ourselves and striving to support the teams and HCWs around us. We are psychologists who provide home-care services in North Carolina, inpatient hospice and long-term care services in California, and long-term care and outpatient palliative care services in Massachusetts. Through our shared struggles and challenges navigating the pandemic, we realized that our respective teams requested similar services, all focused on staff support.
The psychological impact of COVID-19 on HCWs was clear from the beginning. Early in the pandemic our respective teams requested us to provide staff support and education about coping to our local HCWs. Soon national groups for long-term care staff requested education programs. Through this work, we realized that the emotional needs of HCWs ran much deeper than simple self-care. At the onset of the pandemic, before realizing its chronicity, the trainings we offered focused on stress and coping strategies. We cited several frameworks for staff support and eagerly shared anything that might help us, and our colleagues, survive the immediate anxiety and tumult surrounding us.1-3 In this paper, we briefly discuss the distress affecting the geriatric care workforce, reflect on our efforts to cope as HCWs, and offer recommendations at individual and organization levels to help address our collective grief.
Impact of COVID-19
As the death toll mounted and hospitals were pushed to the brink, we saw the suffering of our fellow HCWs. The lack of personal protective equipment (PPE) and testing supplies led to evolving and increasing anxiety for HCWs about contracting COVID-19, potentially spreading it to one’s social circle or family, fears of becoming sick and dying, and fears of inadvertently spreading the virus to medically-vulnerable patients. Increasing demands on staff required many to work outside their areas of expertise. Clinical practice guidelines changed frequently as information emerged about the virus. Staff members struggled to keep pace with the increasing number of patients, many of whom died despite heroic efforts to save them.
As the medical crisis grew, so too did social uprisings as the general public gained a strengthened awareness of the legacy and ongoing effects of systemic oppression, racism, and social inequities in the United States. Individuals grappled with their own privileges, which often hid such disparities from view. Many HCWs and clinicians of color had to navigate unsolicited questions and discussions about racial injustices while also trying to survive. As psychologists, we strove to support the HCWs around us while also struggling with our own stressors. As the magnitude of the pandemic and ongoing social injustices came into view, we realized that presentations on self-care and burnout prevention did not suffice. We needed discussions on unmasking our grief, acknowledging our traumas, and working toward collective healing.
Geriatric Care Workers
Experiences of grief and trauma hit the geriatric care workforce and especially long-term care facilities particularly hard given the high morbidity and mortality rates of COVID-19.4 The geriatric care workforce itself suffers from institutional vulnerabilities. Individuals are often underpaid, undertrained, and work within a system that continually experiences staffing shortages, high burnout, and consequently high levels of turnover.5,6 Recent immigrants and racial/ethnic minorities disproportionately make up this workforce, who often live in multigenerational households and work in multiple facilities to get by.7,8 Amid the pandemic these HCWs continued to work despite demoralizing negative media coverage of nursing homes.9 Notably, facilities with unionized staff were less likely to need second or third jobs to survive, thus reducing spread across facilities. This along with better access to PPE may have contributed to their lower COVID-19 infection and mortality rates relative to non-unionized staff.10
Similar to long-term care workers, home-care staff had related fears and anxieties, magnified by the need to enter multiple homes. This often overlooked but growing sector of the geriatric care workforce faced the added anxiety of the unknown as they entered multiple homes to provide care to their patients. These staff have little control over who may be in the home when they arrive, the sanitation/PPE practices of the patient/family, and therefore little control over their potential exposure to COVID-19. This also applies to home health aides who, although not providing medical services, are a critical part of home-care services and allow older adults to remain living independently in their home.
Reflection on Grief
As we witnessed the interactive effects of the pandemic and social inequities in geriatrics and palliative care, we frequently sought solace in online communities of psychologists working in similar settings. Over time, our regular community meetings developed a different tone: discussions about caring for others shifted to caring for ourselves. It seemed that in holding others’ pain, many of us neglected to address our own. We needed emotional support. We needed to acknowledge that we were not all okay; that the masks we wear for protection also reveal our vulnerabilities; and that protective equipment in hospitals do not protect us from the hate and bias targeting many of us face everywhere we go.
As we let ourselves be vulnerable with each other, we saw the true face of our pain: it was not stress, it was grief. We were sad, broken, mourning innumerable losses, and grieving, mostly alone. It felt overwhelming. Our minds and hearts often grew numb to find respite from pain. At times we found ourselves seeking haven in our offices, convincing ourselves that paperwork needed to be done when in reality we had no space to hold anyone else’s pain; we could barely contain our own. We could only take so much.
Without space to process, grief festers and eats away at our remaining compassion. How do we hold grace for ourselves, dare to be vulnerable, and allow ourselves to feel, when doing so opens the door to our own grief? How do we allow room for emotional processing when we learned to numb-out in order to function? And as women with diverse intersectional identities, how do we honor our humanity when we live in a society that reflects its indifference? We needed to process our pain in order to heal in the slow and uneven way that grief heals.
Caring During Tough Times
The pain we feel is real and it tears at us over time. Pushing it away disenfranchises ourselves of the opportunity to heal and grow. Our collective grief and trauma demand collective healing and acknowledgment of our individual suffering. We must honor our shared humanity and find commonality amid our differences. Typical self-care (healthy eating, sleep, basic hygiene) may not be enough to mitigate the enormity of these stressors. A glass of wine or a virtual dinner with friends may distract but does not heal our wounds.
Self-care, by definition, centers the self and ignores the larger systemic factors that maintain our struggles. It keeps the focus on the individual and in so doing, risks inducing self-blame should we continue feeling burnout. We must do more. We can advocate that systems acknowledge our grief and suffering as well as our strengths and resiliencies. We can demand that organizations recognize human limits and provide support, rather than promote environments that encourage silent perseverance. And we can deconstruct the cultural narrative that vulnerability is weakness or that we are the “heroes.” Heroism suggests superhuman qualities or extreme courage and often negates the fear and trepidation in its midst.11,12 We can also recognize how intersectional aspects of our identities make navigating the pandemic and systemic racism harder and more dangerous for some than for others.
As noted by President Biden in a speech honoring those lost to COVID-19, “We have to resist becoming numb to the sorrow.”13 The nature of our work (and that of most clinicians) is that it is expected and sometimes necessary to compartmentalize and turn off the emotions so that we can function in a professional manner. But this way of being also serves to hold us back. It does not make space for the very real emotions of trauma and grief that have pervaded HCWs during this pandemic. We must learn a different way of functioning—one where grief is acknowledged and even actively processed while still going about our work. Grief therapist Megan Devine proposes to “tend to pain and grief by bearing witness” and notes that “when we allow the reality of grief to exist, we can focus on helping ourselves—and one another—survive inside pain.”14 She advocates for self-compassion and directs us to “find ways to show our grief to others, in ways that honor the truth of our experience” saying, “we have to be willing to stop diminishing our own pain so that others can be comfortable around us.” But what does this look like among health care teams who are traumatized and grieving?
In our experience, caring for ourselves and our teams in times of prolonged stress, trauma, and grief is essential to maintain functioning over time. We strongly believe that it must occur at both the organizational and individual levels. In the throes of a crisis, teams need support immediately. To offer a timely response, we gathered knowledge of team-based care and collaboration to develop practical strategies that can be implemented swiftly to provide support across the team.15-19
The strategies we developed offer steps for creating and maintaining a supportive, compassionate, and psychologically safe work environment. First, the CARES Strategies for Practical Team Intervention highlights the importance of clear communication, assessing team needs regularly, recognizing the stress that is occurring, engaging staff in discussions, and ensuring psychological safety and comfort (Figure 1). Next, the SHARE approach is laid out to allow for interpersonal support among team members (Figure 2). Showing each other empathy, hoping for better days, acknowledging each other’s pain, reaching out for assistance, and expressing our needs allow HCWs to open up about their grief, stress, and trauma. Of note, we found these sets of strategies interdependent: a team that does not believe the leader/organization CARES is not likely to SHARE. Therefore, we also feel that it is especially important that team leaders work to create or enhance the sense of psychological safety for the team. If team members do not feel safe, they will not disclose their grief and remain stuck in the old mode of suffering in silence.
Conclusions
This pandemic and the collective efforts toward social justice advocacy have revealed our vulnerabilities as well as our strengths. These experiences have forced us to reckon with our past and consider possible futures. It has revealed the inequities in our health care system, including our failure to protect those on the ground who keep our systems running, and prompted us to consider new ways of operating in low-resourced and high-demand environments. These experiences also present us with opportunities to be better and do better as both professionals and people; to reflect on our past and consider what we want different in our lives. As we yearn for better days and brace ourselves for what is to come, we hope that teams and organizations will take advantage of these opportunities for self-reflection and continue unmasking our grief, healing our wounds, and honoring our shared humanity.
1. Blake H, Bermingham F. Psychological wellbeing for health care workers: mitigating the impact of covid-19. Version 2.0. Updated June 18, 2020. Accessed October 12, 2021. https://www.nottingham.ac.uk/toolkits/play_22794
2. Harris R. FACE COVID: how to respond effectively to the corona crisis. Published 2020. Accessed October 12, 2021. http://louisville.edu/counseling/coping-with-covid-19/face-covid-by-dr-russ-harris/view
3. Norcross JC, Phillips CM. Psychologist self-care during the pandemic: now more than ever [published online ahead of print, 2020 May 2]. J Health Serv Psychol. 2020;1-5. doi:10.1007/s42843-020-00010-5
4. Kaiser Family Foundation. State reports of long-term care facility cases and deaths related to COVID-19. 2020. Published April 23, 2020. Accessed October 12, 2021. https://www.kff.org/coronavirus-covid-19/issue-brief/state-reporting-of-cases-and-deaths-due-to-covid-19-in-long-term-care-facilities
5. Sterling MR, Tseng E, Poon A, et al. Experiences of home health care workers in New York City during the coronavirus disease 2019 pandemic: a qualitative analysis. JAMA Intern Med. 2020;180(11):1453-1459. doi:10.1001/jamainternmed.2020.3930
6. Stone R, Wilhelm J, Bishop CE, Bryant NS, Hermer L, Squillace MR. Predictors of intent to leave the job among home health workers: analysis of the National Home Health Aide Survey. Gerontologist. 2017;57(5):890-899. doi:10.1093/geront/gnw075
7. Scales K. It’s time to care: a detailed profile of America’s direct care workforce. PHI. 2020. Published January 21, 2020. Accessed October 12, 2021. https://phinational.org/wp-content/uploads/2020/01/Its-Time-to-Care-2020-PHI.pdf
8. Wolfe R, Harknett K, Schneider D. Inequities at work and the toll of COVID-19. Health Aff Health Policy Brief. Published June 4, 2021. doi: 10.1377/hpb20210428.863621
9. White EM, Wetle TF, Reddy A, Baier RR. Front-line nursing home staff experiences during the COVID-19 pandemic [published correction appears in J Am Med Dir Assoc. 2021 May;22(5):1123]. J Am Med Dir Assoc. 2021;22(1):199-203. doi:10.1016/j.jamda.2020.11.022
10. Dean A, Venkataramani A, Kimmel S. Mortality rates from COVID-19 are lower In unionized nursing homes. Health Aff (Millwood). 2020;39(11):1993-2001.doi:10.1377/hlthaff.2020.01011
11. Cox CL. ‘Healthcare Heroes’: problems with media focus on heroism from healthcare workers during the COVID-19 pandemic. J Med Ethics. 2020;46(8):510-513. doi:10.1136/medethics-2020-106398
12. Stokes-Parish J, Elliott R, Rolls K, Massey D. Angels and heroes: the unintended consequence of the hero narrative. J Nurs Scholarsh. 2020;52(5):462-466. doi:10.1111/jnu.12591
13. Biden J. Remarks by President Biden on the more than 500,000 American lives lost to COVID-19. Published February 22, 2021. Accessed October 12, 2021. https://www.whitehouse.gov/briefing-room/speeches-remarks/2021/02/22/remarks-by-president-biden-on-the-more-than-500000-american-lives-lost-to-covid-19
14. Devine M. It’s Okay That You’re Not Okay: Meeting Grief and Loss in a Culture That Doesn’t Understand. Sounds True; 2017.
15. Center for the Study of Traumatic Stress. Grief leadership during COVID-19. Accessed October 12, 2021. https://www.cstsonline.org/assets/media/documents/CSTS_FS_Grief_Leadership_During_COVID19.pdf
16. Center for the Study of Traumatic Stress. Sustaining the well-being of healthcare personnel during coronavirus and other infectious disease outbreaks. Accessed October 12, 2021. https://www.cstsonline.org/assets/media/documents/CSTS_FS_Sustaining_Well_Being_Health care_Personnel_during.pdf
17. Fessell D, Cherniss C. Coronavirus disease 2019 (COVID-19) and beyond: micropractices for burnout prevention and emotional wellness. J Am Coll Radiol. 2020;17(6):746-748. doi:10.1016/j.jacr.2020.03.013
18. US Department of Veterans Affairs, National Center for PTSD. Managing healthcare workers’ stress associated with the COVID-19 virus outbreak. Updated March 25, 2020, Accessed October 12, 2021. https://www.ptsd.va.gov/covid/COVID_healthcare_workers.asp
19. US Department of Veterans Affairs, Veterans Health Administration, National Center for Organization Development (NCOD). Team Development Guide. 2017. https://vaww.va.gov/NCOD/docs/Team_Development_Guide.docx [Nonpublic source, not verified.]
Since the start of the pandemic, health care systems have requested many in-services for staff on self-care and stress management to help health care workers (HCWs) cope with the heavy toll of COVID-19. The pandemic has set off a global mental health crisis, with unprecedented numbers of individuals meeting criteria for anxiety, depression, and other mental health disorders in response to the intense stressors of living through a pandemic. These calls to assist staff with self-care and burnout prevention have been especially salient for psychologists working in palliative care and geriatrics, where fears of COVID-19 infection and numbers of patient deaths have been high.
Throughout these painful times, we have been grateful for an online community of palliative care psychologists within the US Department of Veterans Affairs (VA) from across the continuum of care and across the country. This community brought together many of us who were both struggling ourselves and striving to support the teams and HCWs around us. We are psychologists who provide home-care services in North Carolina, inpatient hospice and long-term care services in California, and long-term care and outpatient palliative care services in Massachusetts. Through our shared struggles and challenges navigating the pandemic, we realized that our respective teams requested similar services, all focused on staff support.
The psychological impact of COVID-19 on HCWs was clear from the beginning. Early in the pandemic our respective teams requested us to provide staff support and education about coping to our local HCWs. Soon national groups for long-term care staff requested education programs. Through this work, we realized that the emotional needs of HCWs ran much deeper than simple self-care. At the onset of the pandemic, before realizing its chronicity, the trainings we offered focused on stress and coping strategies. We cited several frameworks for staff support and eagerly shared anything that might help us, and our colleagues, survive the immediate anxiety and tumult surrounding us.1-3 In this paper, we briefly discuss the distress affecting the geriatric care workforce, reflect on our efforts to cope as HCWs, and offer recommendations at individual and organization levels to help address our collective grief.
Impact of COVID-19
As the death toll mounted and hospitals were pushed to the brink, we saw the suffering of our fellow HCWs. The lack of personal protective equipment (PPE) and testing supplies led to evolving and increasing anxiety for HCWs about contracting COVID-19, potentially spreading it to one’s social circle or family, fears of becoming sick and dying, and fears of inadvertently spreading the virus to medically-vulnerable patients. Increasing demands on staff required many to work outside their areas of expertise. Clinical practice guidelines changed frequently as information emerged about the virus. Staff members struggled to keep pace with the increasing number of patients, many of whom died despite heroic efforts to save them.
As the medical crisis grew, so too did social uprisings as the general public gained a strengthened awareness of the legacy and ongoing effects of systemic oppression, racism, and social inequities in the United States. Individuals grappled with their own privileges, which often hid such disparities from view. Many HCWs and clinicians of color had to navigate unsolicited questions and discussions about racial injustices while also trying to survive. As psychologists, we strove to support the HCWs around us while also struggling with our own stressors. As the magnitude of the pandemic and ongoing social injustices came into view, we realized that presentations on self-care and burnout prevention did not suffice. We needed discussions on unmasking our grief, acknowledging our traumas, and working toward collective healing.
Geriatric Care Workers
Experiences of grief and trauma hit the geriatric care workforce and especially long-term care facilities particularly hard given the high morbidity and mortality rates of COVID-19.4 The geriatric care workforce itself suffers from institutional vulnerabilities. Individuals are often underpaid, undertrained, and work within a system that continually experiences staffing shortages, high burnout, and consequently high levels of turnover.5,6 Recent immigrants and racial/ethnic minorities disproportionately make up this workforce, who often live in multigenerational households and work in multiple facilities to get by.7,8 Amid the pandemic these HCWs continued to work despite demoralizing negative media coverage of nursing homes.9 Notably, facilities with unionized staff were less likely to need second or third jobs to survive, thus reducing spread across facilities. This along with better access to PPE may have contributed to their lower COVID-19 infection and mortality rates relative to non-unionized staff.10
Similar to long-term care workers, home-care staff had related fears and anxieties, magnified by the need to enter multiple homes. This often overlooked but growing sector of the geriatric care workforce faced the added anxiety of the unknown as they entered multiple homes to provide care to their patients. These staff have little control over who may be in the home when they arrive, the sanitation/PPE practices of the patient/family, and therefore little control over their potential exposure to COVID-19. This also applies to home health aides who, although not providing medical services, are a critical part of home-care services and allow older adults to remain living independently in their home.
Reflection on Grief
As we witnessed the interactive effects of the pandemic and social inequities in geriatrics and palliative care, we frequently sought solace in online communities of psychologists working in similar settings. Over time, our regular community meetings developed a different tone: discussions about caring for others shifted to caring for ourselves. It seemed that in holding others’ pain, many of us neglected to address our own. We needed emotional support. We needed to acknowledge that we were not all okay; that the masks we wear for protection also reveal our vulnerabilities; and that protective equipment in hospitals do not protect us from the hate and bias targeting many of us face everywhere we go.
As we let ourselves be vulnerable with each other, we saw the true face of our pain: it was not stress, it was grief. We were sad, broken, mourning innumerable losses, and grieving, mostly alone. It felt overwhelming. Our minds and hearts often grew numb to find respite from pain. At times we found ourselves seeking haven in our offices, convincing ourselves that paperwork needed to be done when in reality we had no space to hold anyone else’s pain; we could barely contain our own. We could only take so much.
Without space to process, grief festers and eats away at our remaining compassion. How do we hold grace for ourselves, dare to be vulnerable, and allow ourselves to feel, when doing so opens the door to our own grief? How do we allow room for emotional processing when we learned to numb-out in order to function? And as women with diverse intersectional identities, how do we honor our humanity when we live in a society that reflects its indifference? We needed to process our pain in order to heal in the slow and uneven way that grief heals.
Caring During Tough Times
The pain we feel is real and it tears at us over time. Pushing it away disenfranchises ourselves of the opportunity to heal and grow. Our collective grief and trauma demand collective healing and acknowledgment of our individual suffering. We must honor our shared humanity and find commonality amid our differences. Typical self-care (healthy eating, sleep, basic hygiene) may not be enough to mitigate the enormity of these stressors. A glass of wine or a virtual dinner with friends may distract but does not heal our wounds.
Self-care, by definition, centers the self and ignores the larger systemic factors that maintain our struggles. It keeps the focus on the individual and in so doing, risks inducing self-blame should we continue feeling burnout. We must do more. We can advocate that systems acknowledge our grief and suffering as well as our strengths and resiliencies. We can demand that organizations recognize human limits and provide support, rather than promote environments that encourage silent perseverance. And we can deconstruct the cultural narrative that vulnerability is weakness or that we are the “heroes.” Heroism suggests superhuman qualities or extreme courage and often negates the fear and trepidation in its midst.11,12 We can also recognize how intersectional aspects of our identities make navigating the pandemic and systemic racism harder and more dangerous for some than for others.
As noted by President Biden in a speech honoring those lost to COVID-19, “We have to resist becoming numb to the sorrow.”13 The nature of our work (and that of most clinicians) is that it is expected and sometimes necessary to compartmentalize and turn off the emotions so that we can function in a professional manner. But this way of being also serves to hold us back. It does not make space for the very real emotions of trauma and grief that have pervaded HCWs during this pandemic. We must learn a different way of functioning—one where grief is acknowledged and even actively processed while still going about our work. Grief therapist Megan Devine proposes to “tend to pain and grief by bearing witness” and notes that “when we allow the reality of grief to exist, we can focus on helping ourselves—and one another—survive inside pain.”14 She advocates for self-compassion and directs us to “find ways to show our grief to others, in ways that honor the truth of our experience” saying, “we have to be willing to stop diminishing our own pain so that others can be comfortable around us.” But what does this look like among health care teams who are traumatized and grieving?
In our experience, caring for ourselves and our teams in times of prolonged stress, trauma, and grief is essential to maintain functioning over time. We strongly believe that it must occur at both the organizational and individual levels. In the throes of a crisis, teams need support immediately. To offer a timely response, we gathered knowledge of team-based care and collaboration to develop practical strategies that can be implemented swiftly to provide support across the team.15-19
The strategies we developed offer steps for creating and maintaining a supportive, compassionate, and psychologically safe work environment. First, the CARES Strategies for Practical Team Intervention highlights the importance of clear communication, assessing team needs regularly, recognizing the stress that is occurring, engaging staff in discussions, and ensuring psychological safety and comfort (Figure 1). Next, the SHARE approach is laid out to allow for interpersonal support among team members (Figure 2). Showing each other empathy, hoping for better days, acknowledging each other’s pain, reaching out for assistance, and expressing our needs allow HCWs to open up about their grief, stress, and trauma. Of note, we found these sets of strategies interdependent: a team that does not believe the leader/organization CARES is not likely to SHARE. Therefore, we also feel that it is especially important that team leaders work to create or enhance the sense of psychological safety for the team. If team members do not feel safe, they will not disclose their grief and remain stuck in the old mode of suffering in silence.
Conclusions
This pandemic and the collective efforts toward social justice advocacy have revealed our vulnerabilities as well as our strengths. These experiences have forced us to reckon with our past and consider possible futures. It has revealed the inequities in our health care system, including our failure to protect those on the ground who keep our systems running, and prompted us to consider new ways of operating in low-resourced and high-demand environments. These experiences also present us with opportunities to be better and do better as both professionals and people; to reflect on our past and consider what we want different in our lives. As we yearn for better days and brace ourselves for what is to come, we hope that teams and organizations will take advantage of these opportunities for self-reflection and continue unmasking our grief, healing our wounds, and honoring our shared humanity.
Since the start of the pandemic, health care systems have requested many in-services for staff on self-care and stress management to help health care workers (HCWs) cope with the heavy toll of COVID-19. The pandemic has set off a global mental health crisis, with unprecedented numbers of individuals meeting criteria for anxiety, depression, and other mental health disorders in response to the intense stressors of living through a pandemic. These calls to assist staff with self-care and burnout prevention have been especially salient for psychologists working in palliative care and geriatrics, where fears of COVID-19 infection and numbers of patient deaths have been high.
Throughout these painful times, we have been grateful for an online community of palliative care psychologists within the US Department of Veterans Affairs (VA) from across the continuum of care and across the country. This community brought together many of us who were both struggling ourselves and striving to support the teams and HCWs around us. We are psychologists who provide home-care services in North Carolina, inpatient hospice and long-term care services in California, and long-term care and outpatient palliative care services in Massachusetts. Through our shared struggles and challenges navigating the pandemic, we realized that our respective teams requested similar services, all focused on staff support.
The psychological impact of COVID-19 on HCWs was clear from the beginning. Early in the pandemic our respective teams requested us to provide staff support and education about coping to our local HCWs. Soon national groups for long-term care staff requested education programs. Through this work, we realized that the emotional needs of HCWs ran much deeper than simple self-care. At the onset of the pandemic, before realizing its chronicity, the trainings we offered focused on stress and coping strategies. We cited several frameworks for staff support and eagerly shared anything that might help us, and our colleagues, survive the immediate anxiety and tumult surrounding us.1-3 In this paper, we briefly discuss the distress affecting the geriatric care workforce, reflect on our efforts to cope as HCWs, and offer recommendations at individual and organization levels to help address our collective grief.
Impact of COVID-19
As the death toll mounted and hospitals were pushed to the brink, we saw the suffering of our fellow HCWs. The lack of personal protective equipment (PPE) and testing supplies led to evolving and increasing anxiety for HCWs about contracting COVID-19, potentially spreading it to one’s social circle or family, fears of becoming sick and dying, and fears of inadvertently spreading the virus to medically-vulnerable patients. Increasing demands on staff required many to work outside their areas of expertise. Clinical practice guidelines changed frequently as information emerged about the virus. Staff members struggled to keep pace with the increasing number of patients, many of whom died despite heroic efforts to save them.
As the medical crisis grew, so too did social uprisings as the general public gained a strengthened awareness of the legacy and ongoing effects of systemic oppression, racism, and social inequities in the United States. Individuals grappled with their own privileges, which often hid such disparities from view. Many HCWs and clinicians of color had to navigate unsolicited questions and discussions about racial injustices while also trying to survive. As psychologists, we strove to support the HCWs around us while also struggling with our own stressors. As the magnitude of the pandemic and ongoing social injustices came into view, we realized that presentations on self-care and burnout prevention did not suffice. We needed discussions on unmasking our grief, acknowledging our traumas, and working toward collective healing.
Geriatric Care Workers
Experiences of grief and trauma hit the geriatric care workforce and especially long-term care facilities particularly hard given the high morbidity and mortality rates of COVID-19.4 The geriatric care workforce itself suffers from institutional vulnerabilities. Individuals are often underpaid, undertrained, and work within a system that continually experiences staffing shortages, high burnout, and consequently high levels of turnover.5,6 Recent immigrants and racial/ethnic minorities disproportionately make up this workforce, who often live in multigenerational households and work in multiple facilities to get by.7,8 Amid the pandemic these HCWs continued to work despite demoralizing negative media coverage of nursing homes.9 Notably, facilities with unionized staff were less likely to need second or third jobs to survive, thus reducing spread across facilities. This along with better access to PPE may have contributed to their lower COVID-19 infection and mortality rates relative to non-unionized staff.10
Similar to long-term care workers, home-care staff had related fears and anxieties, magnified by the need to enter multiple homes. This often overlooked but growing sector of the geriatric care workforce faced the added anxiety of the unknown as they entered multiple homes to provide care to their patients. These staff have little control over who may be in the home when they arrive, the sanitation/PPE practices of the patient/family, and therefore little control over their potential exposure to COVID-19. This also applies to home health aides who, although not providing medical services, are a critical part of home-care services and allow older adults to remain living independently in their home.
Reflection on Grief
As we witnessed the interactive effects of the pandemic and social inequities in geriatrics and palliative care, we frequently sought solace in online communities of psychologists working in similar settings. Over time, our regular community meetings developed a different tone: discussions about caring for others shifted to caring for ourselves. It seemed that in holding others’ pain, many of us neglected to address our own. We needed emotional support. We needed to acknowledge that we were not all okay; that the masks we wear for protection also reveal our vulnerabilities; and that protective equipment in hospitals do not protect us from the hate and bias targeting many of us face everywhere we go.
As we let ourselves be vulnerable with each other, we saw the true face of our pain: it was not stress, it was grief. We were sad, broken, mourning innumerable losses, and grieving, mostly alone. It felt overwhelming. Our minds and hearts often grew numb to find respite from pain. At times we found ourselves seeking haven in our offices, convincing ourselves that paperwork needed to be done when in reality we had no space to hold anyone else’s pain; we could barely contain our own. We could only take so much.
Without space to process, grief festers and eats away at our remaining compassion. How do we hold grace for ourselves, dare to be vulnerable, and allow ourselves to feel, when doing so opens the door to our own grief? How do we allow room for emotional processing when we learned to numb-out in order to function? And as women with diverse intersectional identities, how do we honor our humanity when we live in a society that reflects its indifference? We needed to process our pain in order to heal in the slow and uneven way that grief heals.
Caring During Tough Times
The pain we feel is real and it tears at us over time. Pushing it away disenfranchises ourselves of the opportunity to heal and grow. Our collective grief and trauma demand collective healing and acknowledgment of our individual suffering. We must honor our shared humanity and find commonality amid our differences. Typical self-care (healthy eating, sleep, basic hygiene) may not be enough to mitigate the enormity of these stressors. A glass of wine or a virtual dinner with friends may distract but does not heal our wounds.
Self-care, by definition, centers the self and ignores the larger systemic factors that maintain our struggles. It keeps the focus on the individual and in so doing, risks inducing self-blame should we continue feeling burnout. We must do more. We can advocate that systems acknowledge our grief and suffering as well as our strengths and resiliencies. We can demand that organizations recognize human limits and provide support, rather than promote environments that encourage silent perseverance. And we can deconstruct the cultural narrative that vulnerability is weakness or that we are the “heroes.” Heroism suggests superhuman qualities or extreme courage and often negates the fear and trepidation in its midst.11,12 We can also recognize how intersectional aspects of our identities make navigating the pandemic and systemic racism harder and more dangerous for some than for others.
As noted by President Biden in a speech honoring those lost to COVID-19, “We have to resist becoming numb to the sorrow.”13 The nature of our work (and that of most clinicians) is that it is expected and sometimes necessary to compartmentalize and turn off the emotions so that we can function in a professional manner. But this way of being also serves to hold us back. It does not make space for the very real emotions of trauma and grief that have pervaded HCWs during this pandemic. We must learn a different way of functioning—one where grief is acknowledged and even actively processed while still going about our work. Grief therapist Megan Devine proposes to “tend to pain and grief by bearing witness” and notes that “when we allow the reality of grief to exist, we can focus on helping ourselves—and one another—survive inside pain.”14 She advocates for self-compassion and directs us to “find ways to show our grief to others, in ways that honor the truth of our experience” saying, “we have to be willing to stop diminishing our own pain so that others can be comfortable around us.” But what does this look like among health care teams who are traumatized and grieving?
In our experience, caring for ourselves and our teams in times of prolonged stress, trauma, and grief is essential to maintain functioning over time. We strongly believe that it must occur at both the organizational and individual levels. In the throes of a crisis, teams need support immediately. To offer a timely response, we gathered knowledge of team-based care and collaboration to develop practical strategies that can be implemented swiftly to provide support across the team.15-19
The strategies we developed offer steps for creating and maintaining a supportive, compassionate, and psychologically safe work environment. First, the CARES Strategies for Practical Team Intervention highlights the importance of clear communication, assessing team needs regularly, recognizing the stress that is occurring, engaging staff in discussions, and ensuring psychological safety and comfort (Figure 1). Next, the SHARE approach is laid out to allow for interpersonal support among team members (Figure 2). Showing each other empathy, hoping for better days, acknowledging each other’s pain, reaching out for assistance, and expressing our needs allow HCWs to open up about their grief, stress, and trauma. Of note, we found these sets of strategies interdependent: a team that does not believe the leader/organization CARES is not likely to SHARE. Therefore, we also feel that it is especially important that team leaders work to create or enhance the sense of psychological safety for the team. If team members do not feel safe, they will not disclose their grief and remain stuck in the old mode of suffering in silence.
Conclusions
This pandemic and the collective efforts toward social justice advocacy have revealed our vulnerabilities as well as our strengths. These experiences have forced us to reckon with our past and consider possible futures. It has revealed the inequities in our health care system, including our failure to protect those on the ground who keep our systems running, and prompted us to consider new ways of operating in low-resourced and high-demand environments. These experiences also present us with opportunities to be better and do better as both professionals and people; to reflect on our past and consider what we want different in our lives. As we yearn for better days and brace ourselves for what is to come, we hope that teams and organizations will take advantage of these opportunities for self-reflection and continue unmasking our grief, healing our wounds, and honoring our shared humanity.
1. Blake H, Bermingham F. Psychological wellbeing for health care workers: mitigating the impact of covid-19. Version 2.0. Updated June 18, 2020. Accessed October 12, 2021. https://www.nottingham.ac.uk/toolkits/play_22794
2. Harris R. FACE COVID: how to respond effectively to the corona crisis. Published 2020. Accessed October 12, 2021. http://louisville.edu/counseling/coping-with-covid-19/face-covid-by-dr-russ-harris/view
3. Norcross JC, Phillips CM. Psychologist self-care during the pandemic: now more than ever [published online ahead of print, 2020 May 2]. J Health Serv Psychol. 2020;1-5. doi:10.1007/s42843-020-00010-5
4. Kaiser Family Foundation. State reports of long-term care facility cases and deaths related to COVID-19. 2020. Published April 23, 2020. Accessed October 12, 2021. https://www.kff.org/coronavirus-covid-19/issue-brief/state-reporting-of-cases-and-deaths-due-to-covid-19-in-long-term-care-facilities
5. Sterling MR, Tseng E, Poon A, et al. Experiences of home health care workers in New York City during the coronavirus disease 2019 pandemic: a qualitative analysis. JAMA Intern Med. 2020;180(11):1453-1459. doi:10.1001/jamainternmed.2020.3930
6. Stone R, Wilhelm J, Bishop CE, Bryant NS, Hermer L, Squillace MR. Predictors of intent to leave the job among home health workers: analysis of the National Home Health Aide Survey. Gerontologist. 2017;57(5):890-899. doi:10.1093/geront/gnw075
7. Scales K. It’s time to care: a detailed profile of America’s direct care workforce. PHI. 2020. Published January 21, 2020. Accessed October 12, 2021. https://phinational.org/wp-content/uploads/2020/01/Its-Time-to-Care-2020-PHI.pdf
8. Wolfe R, Harknett K, Schneider D. Inequities at work and the toll of COVID-19. Health Aff Health Policy Brief. Published June 4, 2021. doi: 10.1377/hpb20210428.863621
9. White EM, Wetle TF, Reddy A, Baier RR. Front-line nursing home staff experiences during the COVID-19 pandemic [published correction appears in J Am Med Dir Assoc. 2021 May;22(5):1123]. J Am Med Dir Assoc. 2021;22(1):199-203. doi:10.1016/j.jamda.2020.11.022
10. Dean A, Venkataramani A, Kimmel S. Mortality rates from COVID-19 are lower In unionized nursing homes. Health Aff (Millwood). 2020;39(11):1993-2001.doi:10.1377/hlthaff.2020.01011
11. Cox CL. ‘Healthcare Heroes’: problems with media focus on heroism from healthcare workers during the COVID-19 pandemic. J Med Ethics. 2020;46(8):510-513. doi:10.1136/medethics-2020-106398
12. Stokes-Parish J, Elliott R, Rolls K, Massey D. Angels and heroes: the unintended consequence of the hero narrative. J Nurs Scholarsh. 2020;52(5):462-466. doi:10.1111/jnu.12591
13. Biden J. Remarks by President Biden on the more than 500,000 American lives lost to COVID-19. Published February 22, 2021. Accessed October 12, 2021. https://www.whitehouse.gov/briefing-room/speeches-remarks/2021/02/22/remarks-by-president-biden-on-the-more-than-500000-american-lives-lost-to-covid-19
14. Devine M. It’s Okay That You’re Not Okay: Meeting Grief and Loss in a Culture That Doesn’t Understand. Sounds True; 2017.
15. Center for the Study of Traumatic Stress. Grief leadership during COVID-19. Accessed October 12, 2021. https://www.cstsonline.org/assets/media/documents/CSTS_FS_Grief_Leadership_During_COVID19.pdf
16. Center for the Study of Traumatic Stress. Sustaining the well-being of healthcare personnel during coronavirus and other infectious disease outbreaks. Accessed October 12, 2021. https://www.cstsonline.org/assets/media/documents/CSTS_FS_Sustaining_Well_Being_Health care_Personnel_during.pdf
17. Fessell D, Cherniss C. Coronavirus disease 2019 (COVID-19) and beyond: micropractices for burnout prevention and emotional wellness. J Am Coll Radiol. 2020;17(6):746-748. doi:10.1016/j.jacr.2020.03.013
18. US Department of Veterans Affairs, National Center for PTSD. Managing healthcare workers’ stress associated with the COVID-19 virus outbreak. Updated March 25, 2020, Accessed October 12, 2021. https://www.ptsd.va.gov/covid/COVID_healthcare_workers.asp
19. US Department of Veterans Affairs, Veterans Health Administration, National Center for Organization Development (NCOD). Team Development Guide. 2017. https://vaww.va.gov/NCOD/docs/Team_Development_Guide.docx [Nonpublic source, not verified.]
1. Blake H, Bermingham F. Psychological wellbeing for health care workers: mitigating the impact of covid-19. Version 2.0. Updated June 18, 2020. Accessed October 12, 2021. https://www.nottingham.ac.uk/toolkits/play_22794
2. Harris R. FACE COVID: how to respond effectively to the corona crisis. Published 2020. Accessed October 12, 2021. http://louisville.edu/counseling/coping-with-covid-19/face-covid-by-dr-russ-harris/view
3. Norcross JC, Phillips CM. Psychologist self-care during the pandemic: now more than ever [published online ahead of print, 2020 May 2]. J Health Serv Psychol. 2020;1-5. doi:10.1007/s42843-020-00010-5
4. Kaiser Family Foundation. State reports of long-term care facility cases and deaths related to COVID-19. 2020. Published April 23, 2020. Accessed October 12, 2021. https://www.kff.org/coronavirus-covid-19/issue-brief/state-reporting-of-cases-and-deaths-due-to-covid-19-in-long-term-care-facilities
5. Sterling MR, Tseng E, Poon A, et al. Experiences of home health care workers in New York City during the coronavirus disease 2019 pandemic: a qualitative analysis. JAMA Intern Med. 2020;180(11):1453-1459. doi:10.1001/jamainternmed.2020.3930
6. Stone R, Wilhelm J, Bishop CE, Bryant NS, Hermer L, Squillace MR. Predictors of intent to leave the job among home health workers: analysis of the National Home Health Aide Survey. Gerontologist. 2017;57(5):890-899. doi:10.1093/geront/gnw075
7. Scales K. It’s time to care: a detailed profile of America’s direct care workforce. PHI. 2020. Published January 21, 2020. Accessed October 12, 2021. https://phinational.org/wp-content/uploads/2020/01/Its-Time-to-Care-2020-PHI.pdf
8. Wolfe R, Harknett K, Schneider D. Inequities at work and the toll of COVID-19. Health Aff Health Policy Brief. Published June 4, 2021. doi: 10.1377/hpb20210428.863621
9. White EM, Wetle TF, Reddy A, Baier RR. Front-line nursing home staff experiences during the COVID-19 pandemic [published correction appears in J Am Med Dir Assoc. 2021 May;22(5):1123]. J Am Med Dir Assoc. 2021;22(1):199-203. doi:10.1016/j.jamda.2020.11.022
10. Dean A, Venkataramani A, Kimmel S. Mortality rates from COVID-19 are lower In unionized nursing homes. Health Aff (Millwood). 2020;39(11):1993-2001.doi:10.1377/hlthaff.2020.01011
11. Cox CL. ‘Healthcare Heroes’: problems with media focus on heroism from healthcare workers during the COVID-19 pandemic. J Med Ethics. 2020;46(8):510-513. doi:10.1136/medethics-2020-106398
12. Stokes-Parish J, Elliott R, Rolls K, Massey D. Angels and heroes: the unintended consequence of the hero narrative. J Nurs Scholarsh. 2020;52(5):462-466. doi:10.1111/jnu.12591
13. Biden J. Remarks by President Biden on the more than 500,000 American lives lost to COVID-19. Published February 22, 2021. Accessed October 12, 2021. https://www.whitehouse.gov/briefing-room/speeches-remarks/2021/02/22/remarks-by-president-biden-on-the-more-than-500000-american-lives-lost-to-covid-19
14. Devine M. It’s Okay That You’re Not Okay: Meeting Grief and Loss in a Culture That Doesn’t Understand. Sounds True; 2017.
15. Center for the Study of Traumatic Stress. Grief leadership during COVID-19. Accessed October 12, 2021. https://www.cstsonline.org/assets/media/documents/CSTS_FS_Grief_Leadership_During_COVID19.pdf
16. Center for the Study of Traumatic Stress. Sustaining the well-being of healthcare personnel during coronavirus and other infectious disease outbreaks. Accessed October 12, 2021. https://www.cstsonline.org/assets/media/documents/CSTS_FS_Sustaining_Well_Being_Health care_Personnel_during.pdf
17. Fessell D, Cherniss C. Coronavirus disease 2019 (COVID-19) and beyond: micropractices for burnout prevention and emotional wellness. J Am Coll Radiol. 2020;17(6):746-748. doi:10.1016/j.jacr.2020.03.013
18. US Department of Veterans Affairs, National Center for PTSD. Managing healthcare workers’ stress associated with the COVID-19 virus outbreak. Updated March 25, 2020, Accessed October 12, 2021. https://www.ptsd.va.gov/covid/COVID_healthcare_workers.asp
19. US Department of Veterans Affairs, Veterans Health Administration, National Center for Organization Development (NCOD). Team Development Guide. 2017. https://vaww.va.gov/NCOD/docs/Team_Development_Guide.docx [Nonpublic source, not verified.]
Update on the Pediatric Dermatology Workforce Shortage
Pediatric dermatology is a relatively young subspecialty. The Society for Pediatric Dermatology (SPD) was established in 1975, followed by the creation of the journal Pediatric Dermatology in 1982 and the American Academy of Pediatrics Section on Dermatology in 1986.1 In 2000, the Accreditation Council for Graduate Medical Education (ACGME) officially recognized pediatric dermatology as a unique subspecialty of the American Board of Dermatology (ABD). During that time, informal fellowship experiences emerged, and formal 1-year training programs approved by the ABD evolved by 2006. A subspecialty certification examination was created and has been administered every other year since 2004.1 Data provided by the SPD indicate that approximately 431 US dermatologists have passed the ABD’s pediatric dermatology board certification examination thus far (unpublished data, September 2021).
In 1986, the first systematic evaluation of the US pediatric dermatology workforce revealed a total of 57 practicing pediatric dermatologists and concluded that job opportunities appeared to be limited at that time.2 Since then, the demand for pediatric dermatology services has continued to grow steadily, and the number of board-certified pediatric dermatologists practicing in the United States has increased to at least 317 per data from a 2020 survey.3 However, given that there are more than 11,000 board-certified dermatologists in the United States, there continues to be a severe shortage of pediatric dermatologists.1
Increased Demand for Pediatric Dermatologists
Approximately 10% to 30% of almost 200 million annual outpatient pediatric primary care visits involve a skin concern. Although many of these problems can be handled by primary care physicians, more than 80% of pediatricians report having difficulty accessing dermatology services for their patients.4 In surveys of pediatricians, pediatric dermatology has the third highest referral rate but has consistently ranked third among the specialties deemed most difficult to access.5-7 In addition, it is not uncommon for the wait time to see a pediatric dermatologist to be 6 weeks or longer.5,8
Recent population data estimate that there are 73 million children living in the United States.9 If there are roughly 317 practicing board-certified pediatric dermatologists, that translates into approximately 4.3 pediatric dermatologists per million children. This number is far smaller than the 4 general dermatologists per 100,000 individuals recommended by Glazer et al10 in 2017. To meet this suggested ratio goal, the workforce of pediatric dermatologists would have to increase to 2920. In addition to this severe workforce shortage, there is an additional problem with geographic maldistribution of pediatric dermatologists. More than 98% of pediatric dermatologists practice in metropolitan areas. At least 8 states and 95% of counties have no pediatric dermatologist, and there are no pediatric dermatologists practicing in rural counties.9 This disparity has considerable implications for barriers to care and lack of access for children living in underserved areas. Suggestions for attracting pediatric dermatologists to practice in these areas have included loan forgiveness programs as well as remote mentorship programs to provide professional support.8,9
Training in Pediatrics
There currently are 38 ABD-approved pediatric dermatology fellowship training programs in the United States. Beginning in 2009, pediatric dermatology fellowship programs have participated in the SF Match program. Data provided by the SPD show that, since 2012, up to 27 programs have participated in the annual Match, offering a total number of positions ranging from 27 to 38; however, only 11 to 21 positions have been filled each year, leaving a large number of post-Match vacancies (unpublished data, September 2021).
Surveys have explored the reasons behind this lack of interest in pediatric dermatology training among dermatology residents. Factors that have been mentioned include lack of exposure and mentorship in medical school and residency, the financial hardship of an additional year of fellowship training, and historically lower salaries for pediatric dermatologists compared to general dermatologists.3,6
A 2004 survey revealed that more than 75% of dermatology department chairs believed it was important to have a pediatric dermatologist on the faculty; however, at that time only 48% of dermatology programs reported having at least 1 full-time pediatric dermatology faculty member.11 By 2008, a follow-up survey showed an increase to 70% of dermatology training programs reporting at least 1 full-time pediatric dermatologist; however, 43% of departments still had at least 1 open position, and 76% of those programs shared that they had been searching for more than 1 year.2 Currently, the Accreditation Data System of the ACGME shows a total of 144 accredited US dermatology training programs. Of those, 117 programs have 1 or more board-certified pediatric dermatology faculty member, and 27 programs still have none (unpublished data, September 2021).
A shortage of pediatric dermatologists in training programs contributes to the lack of exposure and mentorship for medical students and residents during a critical time in professional development. Studies show that up to 91% of pediatric dermatologists decided to pursue training in pediatric dermatology during medical school, pediatrics residency, or dermatology residency. In one survey, 84% of respondents (N=109) cited early mentorship as the most important factor in their decision to pursue pediatric dermatology.6
A lack of pediatric dermatologists also results in suboptimal dermatology training for residents who care for children in primary care specialties, including pediatrics, combined internal medicine and pediatrics, and family practice. Multiple surveys have shown that many pediatricians feel they received inadequate training in dermatology during residency. Up to 38% have cited a need for more pediatric dermatology education (N=755).5,6 In addition, studies show a wide disparity in diagnostic accuracy between dermatologists and pediatricians, with one concluding that more than one-third of referrals to pediatric dermatologists were initially misdiagnosed and/or incorrectly treated.5,7
Recruitment Efforts for Pediatric Dermatologists
There are multiple strategies for recruiting trainees into the pediatric dermatology workforce. First, given the importance of early exposure to the field and role models/mentors, pediatric dermatologists must take advantage of every opportunity to interact with medical students and residents. They can share their genuine enthusiasm and love for the specialty while encouraging and supporting those who show interest. They also should seek opportunities for teaching, lecturing, and advising at every level of training. In addition, they can enhance visibility of the specialty by participating in career forums and/or assuming leadership roles within their departments or institutions.12 Another suggestion is for dermatology training programs to consider giving priority to qualified applicants who express sincere interest in pursuing pediatric dermatology training (including those who have already completed pediatrics residency). Although a 2008 survey revealed that 39% of dermatology residency programs (N=80) favored giving priority to applicants demonstrating interest in pediatric dermatology, others were against it, citing issues such as lack of funding for additional residency training, lack of pediatric dermatology mentors within the program, and an overall mistrust of applicants’ sincerity.2
Final Thoughts
The subspecialty of pediatric dermatology has experienced remarkable growth over the last 40 years; however, demand for pediatric dermatology services has continued to outpace supply, resulting in a persistent and notable workforce shortage. Overall, the current supply of pediatric dermatologists can neither meet the clinical demands of the pediatric population nor fulfill academic needs of existing training programs. We must continue to develop novel strategies for increasing the pool of students and residents who are interested in pursuing careers in pediatric dermatology. Ultimately, we also must create incentives and develop tactics to address the geographic maldistribution that exists within the specialty.
- Prindaville B, Antaya R, Siegfried E. Pediatric dermatology: past, present, and future. Pediatr Dermatol. 2015;32:1-12.
- Craiglow BG, Resneck JS, Lucky AW, et al. Pediatric dermatology workforce shortage: perspectives from academia. J Am Acad Dermatol. 2008;59:986-989.
- Ashrafzadeh S, Peters G, Brandling-Bennett H, et al. The geographic distribution of the US pediatric dermatologist workforce: a national cross-sectional study. Pediatr Dermatol. 2020;37:1098-1105.
- Stephens MR, Murthy AS, McMahon PJ. Wait times, health care touchpoints, and nonattendance in an academic pediatric dermatology clinic. Pediatr Dermatol. 2019;36:893-897.
- Prindaville B, Simon S, Horii K. Dermatology-related outpatient visits by children: implications for workforce and pediatric education. J Am Acad Dermatol. 2016;75:228-229.
- Admani S, Caufield M, Kim S, et al. Understanding the pediatric dermatology workforce shortage: mentoring matters. J Pediatr. 2014;164:372-375.
- Fogel AL, Teng JM. The US pediatric dermatology workforce: an assessment of productivity and practice patterns. Pediatr Dermatol. 2015;32:825-829.
- Prindaville B, Horii K, Siegfried E, et al. Pediatric dermatology workforce in the United States. Pediatr Dermatol. 2019;36:166-168.
- Ugwu-Dike P, Nambudiri V. Access as equity: addressing the distribution of the pediatric dermatology workforce [published online August 2, 2021]. Pediatr Dermatol. doi:10.1111/pde.14665
- Glazer AM, Rigel DS. Analysis of trends in geographic distribution of US dermatology workforce density. JAMA Dermatol. 2017;153:472-473.
- Hester EJ, McNealy KM, Kelloff JN, et al. Demand outstrips supply of US pediatric dermatologists: results from a national survey. J Am Acad Dermatol. 2004;50:431-434.
- Wright TS, Huang JT. Comment on “pediatric dermatology workforce in the United States”. Pediatr Dermatol. 2019;36:177-178.
Pediatric dermatology is a relatively young subspecialty. The Society for Pediatric Dermatology (SPD) was established in 1975, followed by the creation of the journal Pediatric Dermatology in 1982 and the American Academy of Pediatrics Section on Dermatology in 1986.1 In 2000, the Accreditation Council for Graduate Medical Education (ACGME) officially recognized pediatric dermatology as a unique subspecialty of the American Board of Dermatology (ABD). During that time, informal fellowship experiences emerged, and formal 1-year training programs approved by the ABD evolved by 2006. A subspecialty certification examination was created and has been administered every other year since 2004.1 Data provided by the SPD indicate that approximately 431 US dermatologists have passed the ABD’s pediatric dermatology board certification examination thus far (unpublished data, September 2021).
In 1986, the first systematic evaluation of the US pediatric dermatology workforce revealed a total of 57 practicing pediatric dermatologists and concluded that job opportunities appeared to be limited at that time.2 Since then, the demand for pediatric dermatology services has continued to grow steadily, and the number of board-certified pediatric dermatologists practicing in the United States has increased to at least 317 per data from a 2020 survey.3 However, given that there are more than 11,000 board-certified dermatologists in the United States, there continues to be a severe shortage of pediatric dermatologists.1
Increased Demand for Pediatric Dermatologists
Approximately 10% to 30% of almost 200 million annual outpatient pediatric primary care visits involve a skin concern. Although many of these problems can be handled by primary care physicians, more than 80% of pediatricians report having difficulty accessing dermatology services for their patients.4 In surveys of pediatricians, pediatric dermatology has the third highest referral rate but has consistently ranked third among the specialties deemed most difficult to access.5-7 In addition, it is not uncommon for the wait time to see a pediatric dermatologist to be 6 weeks or longer.5,8
Recent population data estimate that there are 73 million children living in the United States.9 If there are roughly 317 practicing board-certified pediatric dermatologists, that translates into approximately 4.3 pediatric dermatologists per million children. This number is far smaller than the 4 general dermatologists per 100,000 individuals recommended by Glazer et al10 in 2017. To meet this suggested ratio goal, the workforce of pediatric dermatologists would have to increase to 2920. In addition to this severe workforce shortage, there is an additional problem with geographic maldistribution of pediatric dermatologists. More than 98% of pediatric dermatologists practice in metropolitan areas. At least 8 states and 95% of counties have no pediatric dermatologist, and there are no pediatric dermatologists practicing in rural counties.9 This disparity has considerable implications for barriers to care and lack of access for children living in underserved areas. Suggestions for attracting pediatric dermatologists to practice in these areas have included loan forgiveness programs as well as remote mentorship programs to provide professional support.8,9
Training in Pediatrics
There currently are 38 ABD-approved pediatric dermatology fellowship training programs in the United States. Beginning in 2009, pediatric dermatology fellowship programs have participated in the SF Match program. Data provided by the SPD show that, since 2012, up to 27 programs have participated in the annual Match, offering a total number of positions ranging from 27 to 38; however, only 11 to 21 positions have been filled each year, leaving a large number of post-Match vacancies (unpublished data, September 2021).
Surveys have explored the reasons behind this lack of interest in pediatric dermatology training among dermatology residents. Factors that have been mentioned include lack of exposure and mentorship in medical school and residency, the financial hardship of an additional year of fellowship training, and historically lower salaries for pediatric dermatologists compared to general dermatologists.3,6
A 2004 survey revealed that more than 75% of dermatology department chairs believed it was important to have a pediatric dermatologist on the faculty; however, at that time only 48% of dermatology programs reported having at least 1 full-time pediatric dermatology faculty member.11 By 2008, a follow-up survey showed an increase to 70% of dermatology training programs reporting at least 1 full-time pediatric dermatologist; however, 43% of departments still had at least 1 open position, and 76% of those programs shared that they had been searching for more than 1 year.2 Currently, the Accreditation Data System of the ACGME shows a total of 144 accredited US dermatology training programs. Of those, 117 programs have 1 or more board-certified pediatric dermatology faculty member, and 27 programs still have none (unpublished data, September 2021).
A shortage of pediatric dermatologists in training programs contributes to the lack of exposure and mentorship for medical students and residents during a critical time in professional development. Studies show that up to 91% of pediatric dermatologists decided to pursue training in pediatric dermatology during medical school, pediatrics residency, or dermatology residency. In one survey, 84% of respondents (N=109) cited early mentorship as the most important factor in their decision to pursue pediatric dermatology.6
A lack of pediatric dermatologists also results in suboptimal dermatology training for residents who care for children in primary care specialties, including pediatrics, combined internal medicine and pediatrics, and family practice. Multiple surveys have shown that many pediatricians feel they received inadequate training in dermatology during residency. Up to 38% have cited a need for more pediatric dermatology education (N=755).5,6 In addition, studies show a wide disparity in diagnostic accuracy between dermatologists and pediatricians, with one concluding that more than one-third of referrals to pediatric dermatologists were initially misdiagnosed and/or incorrectly treated.5,7
Recruitment Efforts for Pediatric Dermatologists
There are multiple strategies for recruiting trainees into the pediatric dermatology workforce. First, given the importance of early exposure to the field and role models/mentors, pediatric dermatologists must take advantage of every opportunity to interact with medical students and residents. They can share their genuine enthusiasm and love for the specialty while encouraging and supporting those who show interest. They also should seek opportunities for teaching, lecturing, and advising at every level of training. In addition, they can enhance visibility of the specialty by participating in career forums and/or assuming leadership roles within their departments or institutions.12 Another suggestion is for dermatology training programs to consider giving priority to qualified applicants who express sincere interest in pursuing pediatric dermatology training (including those who have already completed pediatrics residency). Although a 2008 survey revealed that 39% of dermatology residency programs (N=80) favored giving priority to applicants demonstrating interest in pediatric dermatology, others were against it, citing issues such as lack of funding for additional residency training, lack of pediatric dermatology mentors within the program, and an overall mistrust of applicants’ sincerity.2
Final Thoughts
The subspecialty of pediatric dermatology has experienced remarkable growth over the last 40 years; however, demand for pediatric dermatology services has continued to outpace supply, resulting in a persistent and notable workforce shortage. Overall, the current supply of pediatric dermatologists can neither meet the clinical demands of the pediatric population nor fulfill academic needs of existing training programs. We must continue to develop novel strategies for increasing the pool of students and residents who are interested in pursuing careers in pediatric dermatology. Ultimately, we also must create incentives and develop tactics to address the geographic maldistribution that exists within the specialty.
Pediatric dermatology is a relatively young subspecialty. The Society for Pediatric Dermatology (SPD) was established in 1975, followed by the creation of the journal Pediatric Dermatology in 1982 and the American Academy of Pediatrics Section on Dermatology in 1986.1 In 2000, the Accreditation Council for Graduate Medical Education (ACGME) officially recognized pediatric dermatology as a unique subspecialty of the American Board of Dermatology (ABD). During that time, informal fellowship experiences emerged, and formal 1-year training programs approved by the ABD evolved by 2006. A subspecialty certification examination was created and has been administered every other year since 2004.1 Data provided by the SPD indicate that approximately 431 US dermatologists have passed the ABD’s pediatric dermatology board certification examination thus far (unpublished data, September 2021).
In 1986, the first systematic evaluation of the US pediatric dermatology workforce revealed a total of 57 practicing pediatric dermatologists and concluded that job opportunities appeared to be limited at that time.2 Since then, the demand for pediatric dermatology services has continued to grow steadily, and the number of board-certified pediatric dermatologists practicing in the United States has increased to at least 317 per data from a 2020 survey.3 However, given that there are more than 11,000 board-certified dermatologists in the United States, there continues to be a severe shortage of pediatric dermatologists.1
Increased Demand for Pediatric Dermatologists
Approximately 10% to 30% of almost 200 million annual outpatient pediatric primary care visits involve a skin concern. Although many of these problems can be handled by primary care physicians, more than 80% of pediatricians report having difficulty accessing dermatology services for their patients.4 In surveys of pediatricians, pediatric dermatology has the third highest referral rate but has consistently ranked third among the specialties deemed most difficult to access.5-7 In addition, it is not uncommon for the wait time to see a pediatric dermatologist to be 6 weeks or longer.5,8
Recent population data estimate that there are 73 million children living in the United States.9 If there are roughly 317 practicing board-certified pediatric dermatologists, that translates into approximately 4.3 pediatric dermatologists per million children. This number is far smaller than the 4 general dermatologists per 100,000 individuals recommended by Glazer et al10 in 2017. To meet this suggested ratio goal, the workforce of pediatric dermatologists would have to increase to 2920. In addition to this severe workforce shortage, there is an additional problem with geographic maldistribution of pediatric dermatologists. More than 98% of pediatric dermatologists practice in metropolitan areas. At least 8 states and 95% of counties have no pediatric dermatologist, and there are no pediatric dermatologists practicing in rural counties.9 This disparity has considerable implications for barriers to care and lack of access for children living in underserved areas. Suggestions for attracting pediatric dermatologists to practice in these areas have included loan forgiveness programs as well as remote mentorship programs to provide professional support.8,9
Training in Pediatrics
There currently are 38 ABD-approved pediatric dermatology fellowship training programs in the United States. Beginning in 2009, pediatric dermatology fellowship programs have participated in the SF Match program. Data provided by the SPD show that, since 2012, up to 27 programs have participated in the annual Match, offering a total number of positions ranging from 27 to 38; however, only 11 to 21 positions have been filled each year, leaving a large number of post-Match vacancies (unpublished data, September 2021).
Surveys have explored the reasons behind this lack of interest in pediatric dermatology training among dermatology residents. Factors that have been mentioned include lack of exposure and mentorship in medical school and residency, the financial hardship of an additional year of fellowship training, and historically lower salaries for pediatric dermatologists compared to general dermatologists.3,6
A 2004 survey revealed that more than 75% of dermatology department chairs believed it was important to have a pediatric dermatologist on the faculty; however, at that time only 48% of dermatology programs reported having at least 1 full-time pediatric dermatology faculty member.11 By 2008, a follow-up survey showed an increase to 70% of dermatology training programs reporting at least 1 full-time pediatric dermatologist; however, 43% of departments still had at least 1 open position, and 76% of those programs shared that they had been searching for more than 1 year.2 Currently, the Accreditation Data System of the ACGME shows a total of 144 accredited US dermatology training programs. Of those, 117 programs have 1 or more board-certified pediatric dermatology faculty member, and 27 programs still have none (unpublished data, September 2021).
A shortage of pediatric dermatologists in training programs contributes to the lack of exposure and mentorship for medical students and residents during a critical time in professional development. Studies show that up to 91% of pediatric dermatologists decided to pursue training in pediatric dermatology during medical school, pediatrics residency, or dermatology residency. In one survey, 84% of respondents (N=109) cited early mentorship as the most important factor in their decision to pursue pediatric dermatology.6
A lack of pediatric dermatologists also results in suboptimal dermatology training for residents who care for children in primary care specialties, including pediatrics, combined internal medicine and pediatrics, and family practice. Multiple surveys have shown that many pediatricians feel they received inadequate training in dermatology during residency. Up to 38% have cited a need for more pediatric dermatology education (N=755).5,6 In addition, studies show a wide disparity in diagnostic accuracy between dermatologists and pediatricians, with one concluding that more than one-third of referrals to pediatric dermatologists were initially misdiagnosed and/or incorrectly treated.5,7
Recruitment Efforts for Pediatric Dermatologists
There are multiple strategies for recruiting trainees into the pediatric dermatology workforce. First, given the importance of early exposure to the field and role models/mentors, pediatric dermatologists must take advantage of every opportunity to interact with medical students and residents. They can share their genuine enthusiasm and love for the specialty while encouraging and supporting those who show interest. They also should seek opportunities for teaching, lecturing, and advising at every level of training. In addition, they can enhance visibility of the specialty by participating in career forums and/or assuming leadership roles within their departments or institutions.12 Another suggestion is for dermatology training programs to consider giving priority to qualified applicants who express sincere interest in pursuing pediatric dermatology training (including those who have already completed pediatrics residency). Although a 2008 survey revealed that 39% of dermatology residency programs (N=80) favored giving priority to applicants demonstrating interest in pediatric dermatology, others were against it, citing issues such as lack of funding for additional residency training, lack of pediatric dermatology mentors within the program, and an overall mistrust of applicants’ sincerity.2
Final Thoughts
The subspecialty of pediatric dermatology has experienced remarkable growth over the last 40 years; however, demand for pediatric dermatology services has continued to outpace supply, resulting in a persistent and notable workforce shortage. Overall, the current supply of pediatric dermatologists can neither meet the clinical demands of the pediatric population nor fulfill academic needs of existing training programs. We must continue to develop novel strategies for increasing the pool of students and residents who are interested in pursuing careers in pediatric dermatology. Ultimately, we also must create incentives and develop tactics to address the geographic maldistribution that exists within the specialty.
- Prindaville B, Antaya R, Siegfried E. Pediatric dermatology: past, present, and future. Pediatr Dermatol. 2015;32:1-12.
- Craiglow BG, Resneck JS, Lucky AW, et al. Pediatric dermatology workforce shortage: perspectives from academia. J Am Acad Dermatol. 2008;59:986-989.
- Ashrafzadeh S, Peters G, Brandling-Bennett H, et al. The geographic distribution of the US pediatric dermatologist workforce: a national cross-sectional study. Pediatr Dermatol. 2020;37:1098-1105.
- Stephens MR, Murthy AS, McMahon PJ. Wait times, health care touchpoints, and nonattendance in an academic pediatric dermatology clinic. Pediatr Dermatol. 2019;36:893-897.
- Prindaville B, Simon S, Horii K. Dermatology-related outpatient visits by children: implications for workforce and pediatric education. J Am Acad Dermatol. 2016;75:228-229.
- Admani S, Caufield M, Kim S, et al. Understanding the pediatric dermatology workforce shortage: mentoring matters. J Pediatr. 2014;164:372-375.
- Fogel AL, Teng JM. The US pediatric dermatology workforce: an assessment of productivity and practice patterns. Pediatr Dermatol. 2015;32:825-829.
- Prindaville B, Horii K, Siegfried E, et al. Pediatric dermatology workforce in the United States. Pediatr Dermatol. 2019;36:166-168.
- Ugwu-Dike P, Nambudiri V. Access as equity: addressing the distribution of the pediatric dermatology workforce [published online August 2, 2021]. Pediatr Dermatol. doi:10.1111/pde.14665
- Glazer AM, Rigel DS. Analysis of trends in geographic distribution of US dermatology workforce density. JAMA Dermatol. 2017;153:472-473.
- Hester EJ, McNealy KM, Kelloff JN, et al. Demand outstrips supply of US pediatric dermatologists: results from a national survey. J Am Acad Dermatol. 2004;50:431-434.
- Wright TS, Huang JT. Comment on “pediatric dermatology workforce in the United States”. Pediatr Dermatol. 2019;36:177-178.
- Prindaville B, Antaya R, Siegfried E. Pediatric dermatology: past, present, and future. Pediatr Dermatol. 2015;32:1-12.
- Craiglow BG, Resneck JS, Lucky AW, et al. Pediatric dermatology workforce shortage: perspectives from academia. J Am Acad Dermatol. 2008;59:986-989.
- Ashrafzadeh S, Peters G, Brandling-Bennett H, et al. The geographic distribution of the US pediatric dermatologist workforce: a national cross-sectional study. Pediatr Dermatol. 2020;37:1098-1105.
- Stephens MR, Murthy AS, McMahon PJ. Wait times, health care touchpoints, and nonattendance in an academic pediatric dermatology clinic. Pediatr Dermatol. 2019;36:893-897.
- Prindaville B, Simon S, Horii K. Dermatology-related outpatient visits by children: implications for workforce and pediatric education. J Am Acad Dermatol. 2016;75:228-229.
- Admani S, Caufield M, Kim S, et al. Understanding the pediatric dermatology workforce shortage: mentoring matters. J Pediatr. 2014;164:372-375.
- Fogel AL, Teng JM. The US pediatric dermatology workforce: an assessment of productivity and practice patterns. Pediatr Dermatol. 2015;32:825-829.
- Prindaville B, Horii K, Siegfried E, et al. Pediatric dermatology workforce in the United States. Pediatr Dermatol. 2019;36:166-168.
- Ugwu-Dike P, Nambudiri V. Access as equity: addressing the distribution of the pediatric dermatology workforce [published online August 2, 2021]. Pediatr Dermatol. doi:10.1111/pde.14665
- Glazer AM, Rigel DS. Analysis of trends in geographic distribution of US dermatology workforce density. JAMA Dermatol. 2017;153:472-473.
- Hester EJ, McNealy KM, Kelloff JN, et al. Demand outstrips supply of US pediatric dermatologists: results from a national survey. J Am Acad Dermatol. 2004;50:431-434.
- Wright TS, Huang JT. Comment on “pediatric dermatology workforce in the United States”. Pediatr Dermatol. 2019;36:177-178.
Time to retire race- and ethnicity-based carrier screening
The social reckoning of 2020 has led to many discussions and conversations around equity and disparities. With the COVID-19 pandemic, there has been a particular spotlight on health care disparities and race-based medicine. Racism in medicine is pervasive; little has been done over the years to dismantle and unlearn practices that continue to contribute to existing gaps and disparities. Race and ethnicity are both social constructs that have long been used within medical practice and in dictating the type of care an individual receives. Without a universal definition, race, ethnicity, and ancestry have long been used interchangeably within medicine and society. Appreciating that race and ethnicity-based constructs can have other social implications in health care, with their impact on structural racism beyond health care settings, these constructs may still be part of assessments and key modifiers to understanding health differences. It is imperative that medical providers examine the use of race and ethnicity within the care that they provide.
While racial determinants of health cannot be removed from historical access, utilization, and barriers related to reproductive care, guidelines structured around historical ethnicity and race further restrict universal access to carrier screening and informed reproductive testing decisions.
Carrier screening
The goal of preconception and prenatal carrier screening is to provide individuals and reproductive partners with information to optimize pregnancy outcomes based on personal values and preferences.1 The practice of carrier screening began almost half a century ago with screening for individual conditions seen more frequently in certain populations, such as Tay-Sachs disease in those of Ashkenazi Jewish descent and sickle cell disease in those of African descent. Cystic fibrosis carrier screening was first recommended for individuals of Northern European descent in 2001 before being recommended for pan ethnic screening a decade later. Other individual conditions are also recommended for screening based on race/ethnicity (eg, Canavan disease in the Ashkenazi Jewish population, Tay-Sachs disease in individuals of Cajun or French-Canadian descent).2-4 Practice guidelines from professional societies recommend offering carrier screening for individual conditions based on condition severity, race or ethnicity, prevalence, carrier frequency, detection rates, and residual risk.1 However, this process can be problematic, as the data frequently used in updating guidelines and recommendations come primarily from studies and databases where much of the cohort is White.5,6 Failing to identify genetic associations in diverse populations limits the ability to illuminate new discoveries that inform risk management and treatment, especially for populations that are disproportionately underserved in medicine.7
Need for expanded carrier screening
The evolution of genomics and technology within the realm of carrier screening has enabled the simultaneous screening for many serious Mendelian diseases, known as expanded carrier screening (ECS). A 2016 study illustrated that, in most racial/ethnic categories, the cumulative risk of severe and profound conditions found on ECS panels outside the guideline recommendations are greater than the risk identified by guideline-based panels.8 Additionally, a 2020 study showed that self-reported ethnicity was an imperfect indicator of genetic ancestry, with 9% of those in the cohort having a >50% genetic ancestry from a lineage inconsistent with their self-reported ethnicity.9 Data over the past decade have established the clinical utility,10 clinical validity,11 analytical validity,12 and cost-effectiveness13 of pan-ethnic ECS. In 2021, American College of Medical Genetics and Genomics (ACMG) recommended a panel of pan-ethnic conditions that should be offered to all patients due to smaller ethnicity-based panels failing to provide equitable evaluation of all racial and ethnic groups.14 The guidelines from the American College of Obstetricians and Gynecologists (ACOG) fall short of recommending that ECS be offered to all individuals in lieu of screening based on self-reported ethnicity.3,4
Phasing out ethnicity-based carrier screening
This begs the question: Do race, ethnicity, or ancestry have a role in carrier screening? While each may have had a role at the inception of offering carrier screening due to high costs of technology, recent studies have shown the limitations of using self-reported ethnicity in screening. Guideline-based carrier screenings miss a significant percentage of pregnancies (13% to 94%) affected by serious conditions on expanded carrier screening panels.8 Additionally, 40% of Americans cannot identify the ethnicity of all 4 grandparents.15
Founder mutations due to ancestry patterns are still present; however, stratification of care should only be pursued when the presence or absence of these markers would alter clinical management. While the reproductive risk an individual may receive varies based on their self-reported ethnicity, the clinically indicated follow-up testing is the same: offering carrier screening for the reproductive partner or gamete donor. With increased detection rates via sequencing for most autosomal recessive conditions, if the reproductive partner or gamete donor is not identified as a carrier, no further testing is generally indicated regardless of ancestry. Genotyping platforms should not be used for partner carrier screening as they primarily target common pathogenic variants based on dominant ancestry groups and do not provide the same risk reduction.
Continue to: Variant reporting...
Variant reporting
We have long known that databases and registries in the United States have an increased representation of individuals from European ancestries.5,6 However, there have been limited conversations about how the lack of representation within our databases and registries leads to inequities in guidelines and the care that we provide to patients. As a result, studies have shown higher rates of variants of uncertain significance (VUS) identified during genetic testing in non-White individuals than in Whites.16 When it comes to reporting of variants, carrier screening laboratories follow guidelines set forth by the ACMG, and most laboratories only report likely pathogenic or pathogenic variants.17 It is unknown how the higher rate of VUSs in the non-White population, and lack of data and representation in databases and software used to calculate predicted phenotype, impacts identification of at-risk carrier couples in these underrepresented populations. It is imperative that we increase knowledge and representation of variants across ethnicities to improve sensitivity and specificity across the population and not just for those of European descent.
Moving forward
Being aware of social- and race-based biases in carrier screening is important, but modifying structural systems to increase representation, access, and utility of carrier screening is a critical next step. Organizations like ACOG and ACMG have committed not only to understanding but also to addressing factors that have led to disparities and inequities in health care delivery and access.18,19 Actionable steps include offering a universal carrier screening program to all preconception and prenatal patients that addresses conditions with increased carrier frequency, in any population, defined as severe and moderate phenotype with established natural history.3,4 Educational materials should be provided to detail risks, benefits, and limitations of carrier screening, as well as shared decision making between patient and provider to align the patient’s wishes for the information provided by carrier screening.
A broader number of conditions offered through carrier screening will increase the likelihood of positive carrier results. The increase in carriers identified should be viewed as more accurate reproductive risk assessment in the context of equitable care, rather than justification for panels to be limited to specific ancestries. Simultaneous or tandem reproductive partner or donor testing can be considered to reduce clinical workload and time for results return.
In addition, increased representation of individuals who are from diverse ancestries in promotional and educational resources can reinforce that risk for Mendelian conditions is not specific to single ancestries or for targeted conditions. Future research should be conducted to examine the role of racial disparities related to carrier screening and greater inclusion and recruitment of diverse populations in data sets and research studies.
Learned biases toward race, religion, gender identity, sexual orientation, and economic status in the context of carrier screening should be examined and challenged to increase access for all patients who may benefit from this testing. For example, the use of gendered language within carrier screening guidelines and policies and how such screening is offered to patients should be examined. Guidelines do not specify what to do when someone is adopted, for instance, or does not know their ethnicity. It is important that, as genomic testing becomes more available, individuals and groups are not left behind and existing gaps are not further widened. Assessing for genetic variation that modifies for disease or treatment will be more powerful than stratifying based on race. Carrier screening panels should be comprehensive regardless of ancestry to ensure coverage for global genetic variation and to increase access for all patients to risk assessments that promote informed reproductive decision making.
Health equity requires unlearning certain behaviors
As clinicians we all have a commitment to educate and empower one another to offer care that helps promote health equity. Equitable care requires us to look at the current gaps and figure out what programs and initiatives need to be designed to address those gaps. Carrier screening is one such area in which we can work together to improve the overall care that our patients receive, but it is imperative that we examine our practices and unlearn behaviors that contribute to existing disparities. ●
- Edwards JG, Feldman G, Goldberg J, et al. Expanded carrier screening in reproductive medicine—points to consider: a joint statement of the American College of Medical Genetics and Genomics, American College of Obstetricians and Gynecologists, National Society of Genetic Counselors, Perinatal Quality Foundation, and Society for Maternal-Fetal Medicine. Obstet Gynecol. 2015;125:653-662. doi: 10.1097 /AOG.0000000000000666.
- Grody WW, Thompson BH, Gregg AR, et al. ACMG position statement on prenatal/preconception expanded carrier screening. Genet Med. 2013;15:482-483. doi: 10.1038/gim.2013.47.
- Committee Opinion No. 690. Summary: carrier screening in the age of genomic medicine. Obstet Gynecol. 2017;129: 595-596. doi: 10.1097/AOG.0000000000001947.
- Committee Opinion No. 691. Carrier screening for genetic conditions. Obstet Gynecol. 2017;129:e41-e55. doi: 10.1097 /AOG.0000000000001952.
- Need AC, Goldstein DB. Next generation disparities in human genomics: concerns and remedies. Trends Genet. 2009;25:489-494. doi: 10.1016/j.tig.2009.09.012.
- Popejoy A, Fullerton S. Genomics is failing on diversity. Nature. 2016;538;161-164. doi: 10.1038/538161a.
- Ewing A. Reimagining health equity in genetic testing. Medpage Today. June 17, 2021. https://www.medpagetoday.com /opinion/second-opinions/93173. Accessed October 27, 2021.
- Haque IS, Lazarin GA, Kang HP, et al. Modeled fetal risk of genetic diseases identified by expanded carrier screening. JAMA. 2016;316:734-742. doi: 10.1001/jama.2016.11139.
- Kaseniit KE, Haque IS, Goldberg JD, et al. Genetic ancestry analysis on >93,000 individuals undergoing expanded carrier screening reveals limitations of ethnicity-based medical guidelines. Genet Med. 2020;22:1694-1702. doi: 10 .1038/s41436-020-0869-3.
- Johansen Taber KA, Beauchamp KA, Lazarin GA, et al. Clinical utility of expanded carrier screening: results-guided actionability and outcomes. Genet Med. 2019;21:1041-1048. doi: 10.1038/s41436-018-0321-0.
- Balzotti M, Meng L, Muzzey D, et al. Clinical validity of expanded carrier screening: Evaluating the gene-disease relationship in more than 200 conditions. Hum Mutat. 2020;41:1365-1371. doi: 10.1002/humu.24033.
- Hogan GJ, Vysotskaia VS, Beauchamp KA, et al. Validation of an expanded carrier screen that optimizes sensitivity via full-exon sequencing and panel-wide copy number variant identification. Clin Chem. 2018;64:1063-1073. doi: 10.1373 /clinchem.2018.286823.
- Beauchamp KA, Johansen Taber KA, Muzzey D. Clinical impact and cost-effectiveness of a 176-condition expanded carrier screen. Genet Med. 2019;21:1948-1957. doi: 10.1038/s41436-019-0455-8.
- Gregg AR, Aarabi M, Klugman S, et al. Screening for autosomal recessive and X-linked conditions during pregnancy and preconception: a practice resource of the American College of Medical Genetics and Genomics (ACMG). Genet Med. 2021;23:1793-1806. doi: 10.1038/s41436-021-01203-z.
- Condit C, Templeton A, Bates BR, et al. Attitudinal barriers to delivery of race-targeted pharmacogenomics among informed lay persons. Genet Med. 2003;5:385-392. doi: 10 .1097/01.gim.0000087990.30961.72.
- Caswell-Jin J, Gupta T, Hall E, et al. Racial/ethnic differences in multiple-gene sequencing results for hereditary cancer risk. Genet Med. 2018;20:234-239.
- Richards S, Aziz N, Bale S, et al. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. Genet Med. 2015;17:405-424. doi:10.1038/gim.2015.30.
- Gregg AR. Message from ACMG President: overcoming disparities. Genet Med. 2020;22:1758.
Ms. Dobson is Director of Genetic Counseling and Reproductive Genetic Counselor, Center for Fetal Medicine and Reproductive Genetics, Brigham and Women’s Hospital, Boston, Massachusetts.
Ms. Arjunan is Senior Medical Science Liaison at GRAIL, Menlo Park, California.
Ms. Arjunan reports being a former employee and current shareholder for Myriad Genetics.
Ms. Dobson reports no financial relationships relevant to this article.
Ms. Dobson is Director of Genetic Counseling and Reproductive Genetic Counselor, Center for Fetal Medicine and Reproductive Genetics, Brigham and Women’s Hospital, Boston, Massachusetts.
Ms. Arjunan is Senior Medical Science Liaison at GRAIL, Menlo Park, California.
Ms. Arjunan reports being a former employee and current shareholder for Myriad Genetics.
Ms. Dobson reports no financial relationships relevant to this article.
Ms. Dobson is Director of Genetic Counseling and Reproductive Genetic Counselor, Center for Fetal Medicine and Reproductive Genetics, Brigham and Women’s Hospital, Boston, Massachusetts.
Ms. Arjunan is Senior Medical Science Liaison at GRAIL, Menlo Park, California.
Ms. Arjunan reports being a former employee and current shareholder for Myriad Genetics.
Ms. Dobson reports no financial relationships relevant to this article.
The social reckoning of 2020 has led to many discussions and conversations around equity and disparities. With the COVID-19 pandemic, there has been a particular spotlight on health care disparities and race-based medicine. Racism in medicine is pervasive; little has been done over the years to dismantle and unlearn practices that continue to contribute to existing gaps and disparities. Race and ethnicity are both social constructs that have long been used within medical practice and in dictating the type of care an individual receives. Without a universal definition, race, ethnicity, and ancestry have long been used interchangeably within medicine and society. Appreciating that race and ethnicity-based constructs can have other social implications in health care, with their impact on structural racism beyond health care settings, these constructs may still be part of assessments and key modifiers to understanding health differences. It is imperative that medical providers examine the use of race and ethnicity within the care that they provide.
While racial determinants of health cannot be removed from historical access, utilization, and barriers related to reproductive care, guidelines structured around historical ethnicity and race further restrict universal access to carrier screening and informed reproductive testing decisions.
Carrier screening
The goal of preconception and prenatal carrier screening is to provide individuals and reproductive partners with information to optimize pregnancy outcomes based on personal values and preferences.1 The practice of carrier screening began almost half a century ago with screening for individual conditions seen more frequently in certain populations, such as Tay-Sachs disease in those of Ashkenazi Jewish descent and sickle cell disease in those of African descent. Cystic fibrosis carrier screening was first recommended for individuals of Northern European descent in 2001 before being recommended for pan ethnic screening a decade later. Other individual conditions are also recommended for screening based on race/ethnicity (eg, Canavan disease in the Ashkenazi Jewish population, Tay-Sachs disease in individuals of Cajun or French-Canadian descent).2-4 Practice guidelines from professional societies recommend offering carrier screening for individual conditions based on condition severity, race or ethnicity, prevalence, carrier frequency, detection rates, and residual risk.1 However, this process can be problematic, as the data frequently used in updating guidelines and recommendations come primarily from studies and databases where much of the cohort is White.5,6 Failing to identify genetic associations in diverse populations limits the ability to illuminate new discoveries that inform risk management and treatment, especially for populations that are disproportionately underserved in medicine.7
Need for expanded carrier screening
The evolution of genomics and technology within the realm of carrier screening has enabled the simultaneous screening for many serious Mendelian diseases, known as expanded carrier screening (ECS). A 2016 study illustrated that, in most racial/ethnic categories, the cumulative risk of severe and profound conditions found on ECS panels outside the guideline recommendations are greater than the risk identified by guideline-based panels.8 Additionally, a 2020 study showed that self-reported ethnicity was an imperfect indicator of genetic ancestry, with 9% of those in the cohort having a >50% genetic ancestry from a lineage inconsistent with their self-reported ethnicity.9 Data over the past decade have established the clinical utility,10 clinical validity,11 analytical validity,12 and cost-effectiveness13 of pan-ethnic ECS. In 2021, American College of Medical Genetics and Genomics (ACMG) recommended a panel of pan-ethnic conditions that should be offered to all patients due to smaller ethnicity-based panels failing to provide equitable evaluation of all racial and ethnic groups.14 The guidelines from the American College of Obstetricians and Gynecologists (ACOG) fall short of recommending that ECS be offered to all individuals in lieu of screening based on self-reported ethnicity.3,4
Phasing out ethnicity-based carrier screening
This begs the question: Do race, ethnicity, or ancestry have a role in carrier screening? While each may have had a role at the inception of offering carrier screening due to high costs of technology, recent studies have shown the limitations of using self-reported ethnicity in screening. Guideline-based carrier screenings miss a significant percentage of pregnancies (13% to 94%) affected by serious conditions on expanded carrier screening panels.8 Additionally, 40% of Americans cannot identify the ethnicity of all 4 grandparents.15
Founder mutations due to ancestry patterns are still present; however, stratification of care should only be pursued when the presence or absence of these markers would alter clinical management. While the reproductive risk an individual may receive varies based on their self-reported ethnicity, the clinically indicated follow-up testing is the same: offering carrier screening for the reproductive partner or gamete donor. With increased detection rates via sequencing for most autosomal recessive conditions, if the reproductive partner or gamete donor is not identified as a carrier, no further testing is generally indicated regardless of ancestry. Genotyping platforms should not be used for partner carrier screening as they primarily target common pathogenic variants based on dominant ancestry groups and do not provide the same risk reduction.
Continue to: Variant reporting...
Variant reporting
We have long known that databases and registries in the United States have an increased representation of individuals from European ancestries.5,6 However, there have been limited conversations about how the lack of representation within our databases and registries leads to inequities in guidelines and the care that we provide to patients. As a result, studies have shown higher rates of variants of uncertain significance (VUS) identified during genetic testing in non-White individuals than in Whites.16 When it comes to reporting of variants, carrier screening laboratories follow guidelines set forth by the ACMG, and most laboratories only report likely pathogenic or pathogenic variants.17 It is unknown how the higher rate of VUSs in the non-White population, and lack of data and representation in databases and software used to calculate predicted phenotype, impacts identification of at-risk carrier couples in these underrepresented populations. It is imperative that we increase knowledge and representation of variants across ethnicities to improve sensitivity and specificity across the population and not just for those of European descent.
Moving forward
Being aware of social- and race-based biases in carrier screening is important, but modifying structural systems to increase representation, access, and utility of carrier screening is a critical next step. Organizations like ACOG and ACMG have committed not only to understanding but also to addressing factors that have led to disparities and inequities in health care delivery and access.18,19 Actionable steps include offering a universal carrier screening program to all preconception and prenatal patients that addresses conditions with increased carrier frequency, in any population, defined as severe and moderate phenotype with established natural history.3,4 Educational materials should be provided to detail risks, benefits, and limitations of carrier screening, as well as shared decision making between patient and provider to align the patient’s wishes for the information provided by carrier screening.
A broader number of conditions offered through carrier screening will increase the likelihood of positive carrier results. The increase in carriers identified should be viewed as more accurate reproductive risk assessment in the context of equitable care, rather than justification for panels to be limited to specific ancestries. Simultaneous or tandem reproductive partner or donor testing can be considered to reduce clinical workload and time for results return.
In addition, increased representation of individuals who are from diverse ancestries in promotional and educational resources can reinforce that risk for Mendelian conditions is not specific to single ancestries or for targeted conditions. Future research should be conducted to examine the role of racial disparities related to carrier screening and greater inclusion and recruitment of diverse populations in data sets and research studies.
Learned biases toward race, religion, gender identity, sexual orientation, and economic status in the context of carrier screening should be examined and challenged to increase access for all patients who may benefit from this testing. For example, the use of gendered language within carrier screening guidelines and policies and how such screening is offered to patients should be examined. Guidelines do not specify what to do when someone is adopted, for instance, or does not know their ethnicity. It is important that, as genomic testing becomes more available, individuals and groups are not left behind and existing gaps are not further widened. Assessing for genetic variation that modifies for disease or treatment will be more powerful than stratifying based on race. Carrier screening panels should be comprehensive regardless of ancestry to ensure coverage for global genetic variation and to increase access for all patients to risk assessments that promote informed reproductive decision making.
Health equity requires unlearning certain behaviors
As clinicians we all have a commitment to educate and empower one another to offer care that helps promote health equity. Equitable care requires us to look at the current gaps and figure out what programs and initiatives need to be designed to address those gaps. Carrier screening is one such area in which we can work together to improve the overall care that our patients receive, but it is imperative that we examine our practices and unlearn behaviors that contribute to existing disparities. ●
The social reckoning of 2020 has led to many discussions and conversations around equity and disparities. With the COVID-19 pandemic, there has been a particular spotlight on health care disparities and race-based medicine. Racism in medicine is pervasive; little has been done over the years to dismantle and unlearn practices that continue to contribute to existing gaps and disparities. Race and ethnicity are both social constructs that have long been used within medical practice and in dictating the type of care an individual receives. Without a universal definition, race, ethnicity, and ancestry have long been used interchangeably within medicine and society. Appreciating that race and ethnicity-based constructs can have other social implications in health care, with their impact on structural racism beyond health care settings, these constructs may still be part of assessments and key modifiers to understanding health differences. It is imperative that medical providers examine the use of race and ethnicity within the care that they provide.
While racial determinants of health cannot be removed from historical access, utilization, and barriers related to reproductive care, guidelines structured around historical ethnicity and race further restrict universal access to carrier screening and informed reproductive testing decisions.
Carrier screening
The goal of preconception and prenatal carrier screening is to provide individuals and reproductive partners with information to optimize pregnancy outcomes based on personal values and preferences.1 The practice of carrier screening began almost half a century ago with screening for individual conditions seen more frequently in certain populations, such as Tay-Sachs disease in those of Ashkenazi Jewish descent and sickle cell disease in those of African descent. Cystic fibrosis carrier screening was first recommended for individuals of Northern European descent in 2001 before being recommended for pan ethnic screening a decade later. Other individual conditions are also recommended for screening based on race/ethnicity (eg, Canavan disease in the Ashkenazi Jewish population, Tay-Sachs disease in individuals of Cajun or French-Canadian descent).2-4 Practice guidelines from professional societies recommend offering carrier screening for individual conditions based on condition severity, race or ethnicity, prevalence, carrier frequency, detection rates, and residual risk.1 However, this process can be problematic, as the data frequently used in updating guidelines and recommendations come primarily from studies and databases where much of the cohort is White.5,6 Failing to identify genetic associations in diverse populations limits the ability to illuminate new discoveries that inform risk management and treatment, especially for populations that are disproportionately underserved in medicine.7
Need for expanded carrier screening
The evolution of genomics and technology within the realm of carrier screening has enabled the simultaneous screening for many serious Mendelian diseases, known as expanded carrier screening (ECS). A 2016 study illustrated that, in most racial/ethnic categories, the cumulative risk of severe and profound conditions found on ECS panels outside the guideline recommendations are greater than the risk identified by guideline-based panels.8 Additionally, a 2020 study showed that self-reported ethnicity was an imperfect indicator of genetic ancestry, with 9% of those in the cohort having a >50% genetic ancestry from a lineage inconsistent with their self-reported ethnicity.9 Data over the past decade have established the clinical utility,10 clinical validity,11 analytical validity,12 and cost-effectiveness13 of pan-ethnic ECS. In 2021, American College of Medical Genetics and Genomics (ACMG) recommended a panel of pan-ethnic conditions that should be offered to all patients due to smaller ethnicity-based panels failing to provide equitable evaluation of all racial and ethnic groups.14 The guidelines from the American College of Obstetricians and Gynecologists (ACOG) fall short of recommending that ECS be offered to all individuals in lieu of screening based on self-reported ethnicity.3,4
Phasing out ethnicity-based carrier screening
This begs the question: Do race, ethnicity, or ancestry have a role in carrier screening? While each may have had a role at the inception of offering carrier screening due to high costs of technology, recent studies have shown the limitations of using self-reported ethnicity in screening. Guideline-based carrier screenings miss a significant percentage of pregnancies (13% to 94%) affected by serious conditions on expanded carrier screening panels.8 Additionally, 40% of Americans cannot identify the ethnicity of all 4 grandparents.15
Founder mutations due to ancestry patterns are still present; however, stratification of care should only be pursued when the presence or absence of these markers would alter clinical management. While the reproductive risk an individual may receive varies based on their self-reported ethnicity, the clinically indicated follow-up testing is the same: offering carrier screening for the reproductive partner or gamete donor. With increased detection rates via sequencing for most autosomal recessive conditions, if the reproductive partner or gamete donor is not identified as a carrier, no further testing is generally indicated regardless of ancestry. Genotyping platforms should not be used for partner carrier screening as they primarily target common pathogenic variants based on dominant ancestry groups and do not provide the same risk reduction.
Continue to: Variant reporting...
Variant reporting
We have long known that databases and registries in the United States have an increased representation of individuals from European ancestries.5,6 However, there have been limited conversations about how the lack of representation within our databases and registries leads to inequities in guidelines and the care that we provide to patients. As a result, studies have shown higher rates of variants of uncertain significance (VUS) identified during genetic testing in non-White individuals than in Whites.16 When it comes to reporting of variants, carrier screening laboratories follow guidelines set forth by the ACMG, and most laboratories only report likely pathogenic or pathogenic variants.17 It is unknown how the higher rate of VUSs in the non-White population, and lack of data and representation in databases and software used to calculate predicted phenotype, impacts identification of at-risk carrier couples in these underrepresented populations. It is imperative that we increase knowledge and representation of variants across ethnicities to improve sensitivity and specificity across the population and not just for those of European descent.
Moving forward
Being aware of social- and race-based biases in carrier screening is important, but modifying structural systems to increase representation, access, and utility of carrier screening is a critical next step. Organizations like ACOG and ACMG have committed not only to understanding but also to addressing factors that have led to disparities and inequities in health care delivery and access.18,19 Actionable steps include offering a universal carrier screening program to all preconception and prenatal patients that addresses conditions with increased carrier frequency, in any population, defined as severe and moderate phenotype with established natural history.3,4 Educational materials should be provided to detail risks, benefits, and limitations of carrier screening, as well as shared decision making between patient and provider to align the patient’s wishes for the information provided by carrier screening.
A broader number of conditions offered through carrier screening will increase the likelihood of positive carrier results. The increase in carriers identified should be viewed as more accurate reproductive risk assessment in the context of equitable care, rather than justification for panels to be limited to specific ancestries. Simultaneous or tandem reproductive partner or donor testing can be considered to reduce clinical workload and time for results return.
In addition, increased representation of individuals who are from diverse ancestries in promotional and educational resources can reinforce that risk for Mendelian conditions is not specific to single ancestries or for targeted conditions. Future research should be conducted to examine the role of racial disparities related to carrier screening and greater inclusion and recruitment of diverse populations in data sets and research studies.
Learned biases toward race, religion, gender identity, sexual orientation, and economic status in the context of carrier screening should be examined and challenged to increase access for all patients who may benefit from this testing. For example, the use of gendered language within carrier screening guidelines and policies and how such screening is offered to patients should be examined. Guidelines do not specify what to do when someone is adopted, for instance, or does not know their ethnicity. It is important that, as genomic testing becomes more available, individuals and groups are not left behind and existing gaps are not further widened. Assessing for genetic variation that modifies for disease or treatment will be more powerful than stratifying based on race. Carrier screening panels should be comprehensive regardless of ancestry to ensure coverage for global genetic variation and to increase access for all patients to risk assessments that promote informed reproductive decision making.
Health equity requires unlearning certain behaviors
As clinicians we all have a commitment to educate and empower one another to offer care that helps promote health equity. Equitable care requires us to look at the current gaps and figure out what programs and initiatives need to be designed to address those gaps. Carrier screening is one such area in which we can work together to improve the overall care that our patients receive, but it is imperative that we examine our practices and unlearn behaviors that contribute to existing disparities. ●
- Edwards JG, Feldman G, Goldberg J, et al. Expanded carrier screening in reproductive medicine—points to consider: a joint statement of the American College of Medical Genetics and Genomics, American College of Obstetricians and Gynecologists, National Society of Genetic Counselors, Perinatal Quality Foundation, and Society for Maternal-Fetal Medicine. Obstet Gynecol. 2015;125:653-662. doi: 10.1097 /AOG.0000000000000666.
- Grody WW, Thompson BH, Gregg AR, et al. ACMG position statement on prenatal/preconception expanded carrier screening. Genet Med. 2013;15:482-483. doi: 10.1038/gim.2013.47.
- Committee Opinion No. 690. Summary: carrier screening in the age of genomic medicine. Obstet Gynecol. 2017;129: 595-596. doi: 10.1097/AOG.0000000000001947.
- Committee Opinion No. 691. Carrier screening for genetic conditions. Obstet Gynecol. 2017;129:e41-e55. doi: 10.1097 /AOG.0000000000001952.
- Need AC, Goldstein DB. Next generation disparities in human genomics: concerns and remedies. Trends Genet. 2009;25:489-494. doi: 10.1016/j.tig.2009.09.012.
- Popejoy A, Fullerton S. Genomics is failing on diversity. Nature. 2016;538;161-164. doi: 10.1038/538161a.
- Ewing A. Reimagining health equity in genetic testing. Medpage Today. June 17, 2021. https://www.medpagetoday.com /opinion/second-opinions/93173. Accessed October 27, 2021.
- Haque IS, Lazarin GA, Kang HP, et al. Modeled fetal risk of genetic diseases identified by expanded carrier screening. JAMA. 2016;316:734-742. doi: 10.1001/jama.2016.11139.
- Kaseniit KE, Haque IS, Goldberg JD, et al. Genetic ancestry analysis on >93,000 individuals undergoing expanded carrier screening reveals limitations of ethnicity-based medical guidelines. Genet Med. 2020;22:1694-1702. doi: 10 .1038/s41436-020-0869-3.
- Johansen Taber KA, Beauchamp KA, Lazarin GA, et al. Clinical utility of expanded carrier screening: results-guided actionability and outcomes. Genet Med. 2019;21:1041-1048. doi: 10.1038/s41436-018-0321-0.
- Balzotti M, Meng L, Muzzey D, et al. Clinical validity of expanded carrier screening: Evaluating the gene-disease relationship in more than 200 conditions. Hum Mutat. 2020;41:1365-1371. doi: 10.1002/humu.24033.
- Hogan GJ, Vysotskaia VS, Beauchamp KA, et al. Validation of an expanded carrier screen that optimizes sensitivity via full-exon sequencing and panel-wide copy number variant identification. Clin Chem. 2018;64:1063-1073. doi: 10.1373 /clinchem.2018.286823.
- Beauchamp KA, Johansen Taber KA, Muzzey D. Clinical impact and cost-effectiveness of a 176-condition expanded carrier screen. Genet Med. 2019;21:1948-1957. doi: 10.1038/s41436-019-0455-8.
- Gregg AR, Aarabi M, Klugman S, et al. Screening for autosomal recessive and X-linked conditions during pregnancy and preconception: a practice resource of the American College of Medical Genetics and Genomics (ACMG). Genet Med. 2021;23:1793-1806. doi: 10.1038/s41436-021-01203-z.
- Condit C, Templeton A, Bates BR, et al. Attitudinal barriers to delivery of race-targeted pharmacogenomics among informed lay persons. Genet Med. 2003;5:385-392. doi: 10 .1097/01.gim.0000087990.30961.72.
- Caswell-Jin J, Gupta T, Hall E, et al. Racial/ethnic differences in multiple-gene sequencing results for hereditary cancer risk. Genet Med. 2018;20:234-239.
- Richards S, Aziz N, Bale S, et al. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. Genet Med. 2015;17:405-424. doi:10.1038/gim.2015.30.
- Gregg AR. Message from ACMG President: overcoming disparities. Genet Med. 2020;22:1758.
- Edwards JG, Feldman G, Goldberg J, et al. Expanded carrier screening in reproductive medicine—points to consider: a joint statement of the American College of Medical Genetics and Genomics, American College of Obstetricians and Gynecologists, National Society of Genetic Counselors, Perinatal Quality Foundation, and Society for Maternal-Fetal Medicine. Obstet Gynecol. 2015;125:653-662. doi: 10.1097 /AOG.0000000000000666.
- Grody WW, Thompson BH, Gregg AR, et al. ACMG position statement on prenatal/preconception expanded carrier screening. Genet Med. 2013;15:482-483. doi: 10.1038/gim.2013.47.
- Committee Opinion No. 690. Summary: carrier screening in the age of genomic medicine. Obstet Gynecol. 2017;129: 595-596. doi: 10.1097/AOG.0000000000001947.
- Committee Opinion No. 691. Carrier screening for genetic conditions. Obstet Gynecol. 2017;129:e41-e55. doi: 10.1097 /AOG.0000000000001952.
- Need AC, Goldstein DB. Next generation disparities in human genomics: concerns and remedies. Trends Genet. 2009;25:489-494. doi: 10.1016/j.tig.2009.09.012.
- Popejoy A, Fullerton S. Genomics is failing on diversity. Nature. 2016;538;161-164. doi: 10.1038/538161a.
- Ewing A. Reimagining health equity in genetic testing. Medpage Today. June 17, 2021. https://www.medpagetoday.com /opinion/second-opinions/93173. Accessed October 27, 2021.
- Haque IS, Lazarin GA, Kang HP, et al. Modeled fetal risk of genetic diseases identified by expanded carrier screening. JAMA. 2016;316:734-742. doi: 10.1001/jama.2016.11139.
- Kaseniit KE, Haque IS, Goldberg JD, et al. Genetic ancestry analysis on >93,000 individuals undergoing expanded carrier screening reveals limitations of ethnicity-based medical guidelines. Genet Med. 2020;22:1694-1702. doi: 10 .1038/s41436-020-0869-3.
- Johansen Taber KA, Beauchamp KA, Lazarin GA, et al. Clinical utility of expanded carrier screening: results-guided actionability and outcomes. Genet Med. 2019;21:1041-1048. doi: 10.1038/s41436-018-0321-0.
- Balzotti M, Meng L, Muzzey D, et al. Clinical validity of expanded carrier screening: Evaluating the gene-disease relationship in more than 200 conditions. Hum Mutat. 2020;41:1365-1371. doi: 10.1002/humu.24033.
- Hogan GJ, Vysotskaia VS, Beauchamp KA, et al. Validation of an expanded carrier screen that optimizes sensitivity via full-exon sequencing and panel-wide copy number variant identification. Clin Chem. 2018;64:1063-1073. doi: 10.1373 /clinchem.2018.286823.
- Beauchamp KA, Johansen Taber KA, Muzzey D. Clinical impact and cost-effectiveness of a 176-condition expanded carrier screen. Genet Med. 2019;21:1948-1957. doi: 10.1038/s41436-019-0455-8.
- Gregg AR, Aarabi M, Klugman S, et al. Screening for autosomal recessive and X-linked conditions during pregnancy and preconception: a practice resource of the American College of Medical Genetics and Genomics (ACMG). Genet Med. 2021;23:1793-1806. doi: 10.1038/s41436-021-01203-z.
- Condit C, Templeton A, Bates BR, et al. Attitudinal barriers to delivery of race-targeted pharmacogenomics among informed lay persons. Genet Med. 2003;5:385-392. doi: 10 .1097/01.gim.0000087990.30961.72.
- Caswell-Jin J, Gupta T, Hall E, et al. Racial/ethnic differences in multiple-gene sequencing results for hereditary cancer risk. Genet Med. 2018;20:234-239.
- Richards S, Aziz N, Bale S, et al. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. Genet Med. 2015;17:405-424. doi:10.1038/gim.2015.30.
- Gregg AR. Message from ACMG President: overcoming disparities. Genet Med. 2020;22:1758.
TANS Syndrome: Tanorexia, Anorexia, and Nonmelanoma Skin Cancer
The term tanorexia describes compulsive use of a tanning bed, a disorder often identified in White patients. This compulsion is driven by underlying psychological distress that typically correlates with another psychiatric disorder, such as anxiety, body dysmorphic disorder, or an eating disorder. 1 Severe anorexia combined with excessive indoor tanning led to a notable burden of cutaneous squamous cell carcinomas (SCCs) and keratoacanthomas in one of our patients. We discuss the management and approach to patient care in this difficult situation, which we have coined TANS syndrome (for T anorexia, A norexia, and N onmelanoma s kin cancer).
A Patient With TANS Syndrome
A 35-year-old cachectic woman, who appeared much older than her chronologic age, presented for management of numerous painful bleeding skin lesions. Diffuse, erythematous, tender nodules with central keratotic cores, some several centimeters in diameter, were scattered on the abdomen, chest, and extremities (Figure 1); similar lesions were noted on the neck (Figure 2). Numerous erythematous scaly papules and plaques consistent with actinic keratoses were noted throughout the body.
The patient reported that the cutaneous SCCs presented over the last few years, whereas her eating disorder began in adolescence and persisted despite multiple intensive outpatient and inpatient programs. The patient adamantly refused repeat hospitalization, against repeated suggestions by health care providers and her family. Comorbidities related to her anorexia included severe renal insufficiency, iron deficiency anemia, hypertriglyceridemia, kwashiorkor, and pellagra.
Within the last year, the patient had several biopsies showing SCC, keratoacanthoma type. The largest tumors had been treated by Mohs micrographic surgery, excision, and electrodesiccation or curettage. Adjuvant therapy over the last 2 years consisted of tazarotene cream 0.1%, imiquimod cream 5%, oral nicotinamide 500 mg twice daily, and acitretin 10 to 20 mg daily. Human papillomavirus 9-valent vaccine, recombinant, also had been tried as a chemopreventive and treatment, based on a published report of 2 patients in whom keratinocytic carcinomas decreased after such vaccination.2 The dose of acitretin was kept low because of the patient’s severe renal insufficiency and lack of supporting data for its use in this setting. Despite these modalities, our patient continued to develop new cutaneous SCCs.
We considered starting intralesional methotrexate but deferred this course of action, given the patient’s deteriorating renal function. Our plan was to initiate intralesional 5-fluorouracil; however, the patient was admitted to the hospital and subsequently died due to cardiovascular complications of anorexia.
UV Radiation in the Setting of Immune Compromise
Habitual tanning bed use has been recognized as a psychologic addiction.3,4 After exposure to UV radiation, damaged DNA upregulates pro-opiomelanocortin, which posttranslationally generates β-endorphins to elevate mood.3,5
Tanning beds deliver a higher dose of UVA radiation than UVB radiation and cause darkening of pigmentation by oxidation of preformed melanin and redistribution of melanosomes.3 UVA radiation (320–400 nm) emitted from a tanning bed is 10- to 15-times higher than the radiation emitted by the midday sun and causes DNA damage through generation of reactive oxygen species. UVA penetrates the dermis; its harmful effect on DNA contributes to the pathogenesis of melanoma.
UVB radiation (290–320 nm) is mainly restricted to the epidermis and is largely responsible for erythema of the skin. UVB specifically causes direct damage to DNA by forming pyrimidine dimers, superficially causing sunburn. Excessive exposure to UVB radiation increases the risk for nonmelanoma skin cancer.6
Severe starvation and chronic malnutrition, as seen in anorexia nervosa, also are known to lead to immunosuppression.7 Exposure to UV radiation has been shown to impair the function of antigen-presenting cells, cytokines, and suppressor T cells, and is classified as a Group 1 carcinogen by the World Health Organization.3,8 Combining a compromised immune system in anorexia with DNA damage from frequent indoor tanning provides a dangerous milieu for carcinogenesis.8 Without immune surveillance, as occurs with adequate nutrition, treatment of cutaneous SCC is, at best, challenging.
Primary care physicians, dermatologists, psychiatrists, nutritionists, and public health officials should educate high-risk patients to prevent TANS syndrome.
- Petit A, Karila L, Chalmin F, et al. Phenomenology and psychopathology of excessive indoor tanning. Int J Dermatol. 2014;53:664-672. doi:10.1111/ijd.12336
- Nichols AJ, Allen AH, Shareef S, et al. Association of human papillomavirus vaccine with the development of keratinocyte carcinomas. JAMA Dermatol. 2017;153:571-574. doi:10.1001/jamadermatol.2016.5703
- Madigan LM, Lim HW. Tanning beds: impact on health, and recent regulations. Clin Dermatol. 2016;34:640-648. doi:10.1016/j.clindermatol.2016.05.016
- Schwebel DC. Adolescent tanning, disordered eating, and risk taking. J Dev Behav Pediatr. 2014;35:225-227. doi:10.1097/DBP.0000000000000045
- Friedman B, English JC 3rd, Ferris LK. Indoor tanning, skin cancer and the young female patient: a review of the literature. J Pediatr Adolesc Gynecol. 2015;28:275-283. doi:10.1016/j.jpag.2014.07.015
- Armstrong BK, Kricker A. Epidemiology of UV induced skin cancer. J Photochem Photobiol B. 2001;63:8-18. doi:10.1016/s1011-1344(01)00198-1
- Hanachi M, Bohem V, Bemer P, et al. Negative role of malnutrition in cell-mediated immune response: Pneumocystis jirovecii pneumonia (PCP) in a severely malnourished, HIV-negative patient with anorexia nervosa. Clin Nutr ESPEN. 2018;25:163-165. doi:10.1016/j.clnesp.2018.03.121
- Schwarz T, Beissert S. Milestones in photoimmunology. J Invest Dermatol. 2013;133:E7-E10. doi:10.1038/skinbio.2013.177
The term tanorexia describes compulsive use of a tanning bed, a disorder often identified in White patients. This compulsion is driven by underlying psychological distress that typically correlates with another psychiatric disorder, such as anxiety, body dysmorphic disorder, or an eating disorder. 1 Severe anorexia combined with excessive indoor tanning led to a notable burden of cutaneous squamous cell carcinomas (SCCs) and keratoacanthomas in one of our patients. We discuss the management and approach to patient care in this difficult situation, which we have coined TANS syndrome (for T anorexia, A norexia, and N onmelanoma s kin cancer).
A Patient With TANS Syndrome
A 35-year-old cachectic woman, who appeared much older than her chronologic age, presented for management of numerous painful bleeding skin lesions. Diffuse, erythematous, tender nodules with central keratotic cores, some several centimeters in diameter, were scattered on the abdomen, chest, and extremities (Figure 1); similar lesions were noted on the neck (Figure 2). Numerous erythematous scaly papules and plaques consistent with actinic keratoses were noted throughout the body.
The patient reported that the cutaneous SCCs presented over the last few years, whereas her eating disorder began in adolescence and persisted despite multiple intensive outpatient and inpatient programs. The patient adamantly refused repeat hospitalization, against repeated suggestions by health care providers and her family. Comorbidities related to her anorexia included severe renal insufficiency, iron deficiency anemia, hypertriglyceridemia, kwashiorkor, and pellagra.
Within the last year, the patient had several biopsies showing SCC, keratoacanthoma type. The largest tumors had been treated by Mohs micrographic surgery, excision, and electrodesiccation or curettage. Adjuvant therapy over the last 2 years consisted of tazarotene cream 0.1%, imiquimod cream 5%, oral nicotinamide 500 mg twice daily, and acitretin 10 to 20 mg daily. Human papillomavirus 9-valent vaccine, recombinant, also had been tried as a chemopreventive and treatment, based on a published report of 2 patients in whom keratinocytic carcinomas decreased after such vaccination.2 The dose of acitretin was kept low because of the patient’s severe renal insufficiency and lack of supporting data for its use in this setting. Despite these modalities, our patient continued to develop new cutaneous SCCs.
We considered starting intralesional methotrexate but deferred this course of action, given the patient’s deteriorating renal function. Our plan was to initiate intralesional 5-fluorouracil; however, the patient was admitted to the hospital and subsequently died due to cardiovascular complications of anorexia.
UV Radiation in the Setting of Immune Compromise
Habitual tanning bed use has been recognized as a psychologic addiction.3,4 After exposure to UV radiation, damaged DNA upregulates pro-opiomelanocortin, which posttranslationally generates β-endorphins to elevate mood.3,5
Tanning beds deliver a higher dose of UVA radiation than UVB radiation and cause darkening of pigmentation by oxidation of preformed melanin and redistribution of melanosomes.3 UVA radiation (320–400 nm) emitted from a tanning bed is 10- to 15-times higher than the radiation emitted by the midday sun and causes DNA damage through generation of reactive oxygen species. UVA penetrates the dermis; its harmful effect on DNA contributes to the pathogenesis of melanoma.
UVB radiation (290–320 nm) is mainly restricted to the epidermis and is largely responsible for erythema of the skin. UVB specifically causes direct damage to DNA by forming pyrimidine dimers, superficially causing sunburn. Excessive exposure to UVB radiation increases the risk for nonmelanoma skin cancer.6
Severe starvation and chronic malnutrition, as seen in anorexia nervosa, also are known to lead to immunosuppression.7 Exposure to UV radiation has been shown to impair the function of antigen-presenting cells, cytokines, and suppressor T cells, and is classified as a Group 1 carcinogen by the World Health Organization.3,8 Combining a compromised immune system in anorexia with DNA damage from frequent indoor tanning provides a dangerous milieu for carcinogenesis.8 Without immune surveillance, as occurs with adequate nutrition, treatment of cutaneous SCC is, at best, challenging.
Primary care physicians, dermatologists, psychiatrists, nutritionists, and public health officials should educate high-risk patients to prevent TANS syndrome.
The term tanorexia describes compulsive use of a tanning bed, a disorder often identified in White patients. This compulsion is driven by underlying psychological distress that typically correlates with another psychiatric disorder, such as anxiety, body dysmorphic disorder, or an eating disorder. 1 Severe anorexia combined with excessive indoor tanning led to a notable burden of cutaneous squamous cell carcinomas (SCCs) and keratoacanthomas in one of our patients. We discuss the management and approach to patient care in this difficult situation, which we have coined TANS syndrome (for T anorexia, A norexia, and N onmelanoma s kin cancer).
A Patient With TANS Syndrome
A 35-year-old cachectic woman, who appeared much older than her chronologic age, presented for management of numerous painful bleeding skin lesions. Diffuse, erythematous, tender nodules with central keratotic cores, some several centimeters in diameter, were scattered on the abdomen, chest, and extremities (Figure 1); similar lesions were noted on the neck (Figure 2). Numerous erythematous scaly papules and plaques consistent with actinic keratoses were noted throughout the body.
The patient reported that the cutaneous SCCs presented over the last few years, whereas her eating disorder began in adolescence and persisted despite multiple intensive outpatient and inpatient programs. The patient adamantly refused repeat hospitalization, against repeated suggestions by health care providers and her family. Comorbidities related to her anorexia included severe renal insufficiency, iron deficiency anemia, hypertriglyceridemia, kwashiorkor, and pellagra.
Within the last year, the patient had several biopsies showing SCC, keratoacanthoma type. The largest tumors had been treated by Mohs micrographic surgery, excision, and electrodesiccation or curettage. Adjuvant therapy over the last 2 years consisted of tazarotene cream 0.1%, imiquimod cream 5%, oral nicotinamide 500 mg twice daily, and acitretin 10 to 20 mg daily. Human papillomavirus 9-valent vaccine, recombinant, also had been tried as a chemopreventive and treatment, based on a published report of 2 patients in whom keratinocytic carcinomas decreased after such vaccination.2 The dose of acitretin was kept low because of the patient’s severe renal insufficiency and lack of supporting data for its use in this setting. Despite these modalities, our patient continued to develop new cutaneous SCCs.
We considered starting intralesional methotrexate but deferred this course of action, given the patient’s deteriorating renal function. Our plan was to initiate intralesional 5-fluorouracil; however, the patient was admitted to the hospital and subsequently died due to cardiovascular complications of anorexia.
UV Radiation in the Setting of Immune Compromise
Habitual tanning bed use has been recognized as a psychologic addiction.3,4 After exposure to UV radiation, damaged DNA upregulates pro-opiomelanocortin, which posttranslationally generates β-endorphins to elevate mood.3,5
Tanning beds deliver a higher dose of UVA radiation than UVB radiation and cause darkening of pigmentation by oxidation of preformed melanin and redistribution of melanosomes.3 UVA radiation (320–400 nm) emitted from a tanning bed is 10- to 15-times higher than the radiation emitted by the midday sun and causes DNA damage through generation of reactive oxygen species. UVA penetrates the dermis; its harmful effect on DNA contributes to the pathogenesis of melanoma.
UVB radiation (290–320 nm) is mainly restricted to the epidermis and is largely responsible for erythema of the skin. UVB specifically causes direct damage to DNA by forming pyrimidine dimers, superficially causing sunburn. Excessive exposure to UVB radiation increases the risk for nonmelanoma skin cancer.6
Severe starvation and chronic malnutrition, as seen in anorexia nervosa, also are known to lead to immunosuppression.7 Exposure to UV radiation has been shown to impair the function of antigen-presenting cells, cytokines, and suppressor T cells, and is classified as a Group 1 carcinogen by the World Health Organization.3,8 Combining a compromised immune system in anorexia with DNA damage from frequent indoor tanning provides a dangerous milieu for carcinogenesis.8 Without immune surveillance, as occurs with adequate nutrition, treatment of cutaneous SCC is, at best, challenging.
Primary care physicians, dermatologists, psychiatrists, nutritionists, and public health officials should educate high-risk patients to prevent TANS syndrome.
- Petit A, Karila L, Chalmin F, et al. Phenomenology and psychopathology of excessive indoor tanning. Int J Dermatol. 2014;53:664-672. doi:10.1111/ijd.12336
- Nichols AJ, Allen AH, Shareef S, et al. Association of human papillomavirus vaccine with the development of keratinocyte carcinomas. JAMA Dermatol. 2017;153:571-574. doi:10.1001/jamadermatol.2016.5703
- Madigan LM, Lim HW. Tanning beds: impact on health, and recent regulations. Clin Dermatol. 2016;34:640-648. doi:10.1016/j.clindermatol.2016.05.016
- Schwebel DC. Adolescent tanning, disordered eating, and risk taking. J Dev Behav Pediatr. 2014;35:225-227. doi:10.1097/DBP.0000000000000045
- Friedman B, English JC 3rd, Ferris LK. Indoor tanning, skin cancer and the young female patient: a review of the literature. J Pediatr Adolesc Gynecol. 2015;28:275-283. doi:10.1016/j.jpag.2014.07.015
- Armstrong BK, Kricker A. Epidemiology of UV induced skin cancer. J Photochem Photobiol B. 2001;63:8-18. doi:10.1016/s1011-1344(01)00198-1
- Hanachi M, Bohem V, Bemer P, et al. Negative role of malnutrition in cell-mediated immune response: Pneumocystis jirovecii pneumonia (PCP) in a severely malnourished, HIV-negative patient with anorexia nervosa. Clin Nutr ESPEN. 2018;25:163-165. doi:10.1016/j.clnesp.2018.03.121
- Schwarz T, Beissert S. Milestones in photoimmunology. J Invest Dermatol. 2013;133:E7-E10. doi:10.1038/skinbio.2013.177
- Petit A, Karila L, Chalmin F, et al. Phenomenology and psychopathology of excessive indoor tanning. Int J Dermatol. 2014;53:664-672. doi:10.1111/ijd.12336
- Nichols AJ, Allen AH, Shareef S, et al. Association of human papillomavirus vaccine with the development of keratinocyte carcinomas. JAMA Dermatol. 2017;153:571-574. doi:10.1001/jamadermatol.2016.5703
- Madigan LM, Lim HW. Tanning beds: impact on health, and recent regulations. Clin Dermatol. 2016;34:640-648. doi:10.1016/j.clindermatol.2016.05.016
- Schwebel DC. Adolescent tanning, disordered eating, and risk taking. J Dev Behav Pediatr. 2014;35:225-227. doi:10.1097/DBP.0000000000000045
- Friedman B, English JC 3rd, Ferris LK. Indoor tanning, skin cancer and the young female patient: a review of the literature. J Pediatr Adolesc Gynecol. 2015;28:275-283. doi:10.1016/j.jpag.2014.07.015
- Armstrong BK, Kricker A. Epidemiology of UV induced skin cancer. J Photochem Photobiol B. 2001;63:8-18. doi:10.1016/s1011-1344(01)00198-1
- Hanachi M, Bohem V, Bemer P, et al. Negative role of malnutrition in cell-mediated immune response: Pneumocystis jirovecii pneumonia (PCP) in a severely malnourished, HIV-negative patient with anorexia nervosa. Clin Nutr ESPEN. 2018;25:163-165. doi:10.1016/j.clnesp.2018.03.121
- Schwarz T, Beissert S. Milestones in photoimmunology. J Invest Dermatol. 2013;133:E7-E10. doi:10.1038/skinbio.2013.177
Practice Points
- Primary care physicians, dermatologists, psychiatrists, nutritionists, and public health officials should educate high-risk patients to prevent TANS syndrome.
- Combining a compromised immune system in anorexia with DNA damage from frequent indoor tanning provides a dangerous milieu for carcinogenesis.
- Comorbidities related to TANS syndrome make it challenging to effectively treat cutaneous squamous cell carcinoma.
Q&A: Meeting the challenge of giving COVID vaccines to younger kids
This news organization spoke to several pediatric experts to get answers.
More than 6 million children and adolescents (up to age 18 years) in the United States have been infected with SARS-CoV-2. Children represent about 17% of all cases, and an estimated 0.1%-2% of infected children end up hospitalized, according to Oct. 28 data from the American Academy of Pediatrics.
Physicians and other health care practitioners are gearing up for what could be an influx of patients. “Pediatricians are standing by to talk with families about the vaccine and to administer the vaccine to children as soon as possible,” Lee Savio Beers, MD, FAAP, president of the AAP, said in a statement.
In this Q&A, this news organization asked for additional advice from Sara “Sally” Goza, MD, a pediatrician in Fayetteville, Georgia, and immediate past president of the AAP; Peter Hotez, MD, PhD, dean of the National School of Tropical Medicine at Baylor College of Medicine and codirector of the Texas Children’s Hospital Center for Vaccine Development, both in Houston; and Danielle M. Zerr, MD, professor and chief of the division of pediatric infectious disease at the University of Washington, Seattle, and medical director of infection prevention at Seattle Children’s Hospital.
Q: How are smaller pediatric practices and solo practitioners going to handle the additional vaccinations?
Dr. Goza: It’s a scheduling challenge with this rollout and all the people who want it and want it right now. They’re going to want it this week.
I’ve actually had some children asking their moms: “When can I get it? When can I get it?” It’s been very interesting – they are chomping at the bit.
If I give the vaccine to a patient this week, in 3 weeks the second dose will be right around Thanksgiving. No one in my office is going to want to be here to give the shot on Thanksgiving, and no patient is going to want to come in on Thanksgiving weekend. So I’m trying to delay those parents – saying, let’s do it next week. That way we’re not messing up a holiday.
Children are going to need two doses, and they won’t be fully protected until 2 weeks after their second dose. So they won’t get full protection for Thanksgiving, but they will have full protection for Christmas.
I know there are a lot of pediatricians who have preordered the vaccine. I know in our office they sent us an email ... to let us know our vaccines are being shipped. So I think a lot of pediatricians are going to have the vaccine.
Q: How should pediatricians counsel parents who are fearful or hesitant?
Dr. Hotez: It’s important to emphasize the severity of the 2021 summer Delta epidemic in children. We need to get beyond this false narrative that COVID only produces a mild disease in children. It’s caused thousands of pediatric hospitalizations, not to mention long COVID.
Dr. Zerr: It is key to find out what concerns parents have and then focus on answering their specific questions. It is helpful to emphasize the safety and efficacy of the vaccine and to explain the rigorous processes that the vaccine went through to receive Food and Drug Administration approval.
Q: How should pediatricians counter any misinformation/disinformation out there about the COVID-19 vaccines?
Dr. Goza: The most important thing is not to discount what they are saying. Don’t say: “That’s crazy” or “That’s not true.” Don’t roll your eyes and say: “Really, you’re going to believe all that?”
Instead, have a conversation with them about why we think that is not true, or why we know that’s not true. We really have to have that relationship and ask: “Well, what are your concerns?” And then really counter (any misinformation) with facts, with science, and based on your experience.
Q: Do the data presented to the FDA and the CDC about the safety and effectiveness of the COVID-19 vaccine for 5- to 11-year-olds seem robust to you?
Dr. Zerr: Yes, and data collection will be ongoing.
Dr. Hotez: I’ve only seen what’s publicly available so far, and it seems to support moving forward with emergency use authorization. The only shortfall is the size, roughly 2,200 children, which would not be of sufficient size to detect a rare safety signal.
Q: Do previous controversies around pediatric vaccines (for example, the MMR vaccine and autism) give pediatricians some background and experience so they can address any pushback on the COVID-19 vaccines?
Dr. Goza: Pediatricians have been dealing with vaccine hesitancy for a while now, ever since the MMR and autism controversy started. Even before then, there were certain groups of people who didn’t want vaccines.
We’ve really worked hard at helping teach pediatricians how to deal with the misinformation, how to counter it, and how to help parents understand the vaccines are safe and effective – and that they save lives.
That (experience) will help us in some ways. Unfortunately, there is more misinformation out there – there is almost a concerted effort on misinformation. It’s big.
Pediatricians will do everything we can, but we need help countering it. We need the misinformation to quit getting spread on social media. We can talk one on one with patients and families, but if all they are hearing on social media is the misinformation, it’s really hard.
Q: Are pediatricians, especially solo practitioners or pediatricians at smaller practices, going to face challenges with multidose vials and not wasting vaccine product?
Dr. Goza: I’m at a small practice. We have 3.5 FTEs (full-time equivalents) of MDs and three FTEs of nurse practitioners. So we’re not that big – about six providers.
You know, it is a challenge. We’re not going to buy the super-duper freezer, and we’re not going to be able to store these vaccines for a long period of time.
So when we order, we need smaller amounts. For the 12- to 18-year-olds, [maximum storage] was 45 days. Now for the 5- to 11-year-olds, we’re going to be able to store the vaccine in the refrigerator for 10 weeks, which gives us more leeway there.
We try to do all of vaccinations on 1 day, so we know how many people are coming in, and we are not going to waste too many doses.
Our Department of Public Health in Georgia has said: “We want these vaccines in the arms of kids, and if you have to waste some doses, don’t worry about it.” But it’s a 10-dose vial. It’s going to be hard for me to open it up for one child. I just don’t like wasting anything like this.
Our main goal is to get this vaccine in to the arms of children whose parents want it.
Q: What are some additional sources of information for pediatricians?
Dr. Zerr: There are a lot of great resources on vaccine hesitancy from reputable sources, including these from the CDC and from the National Academies of Sciences, Engineering, and Medicine:
- Building Confidence With OVID-19 Vaccines
- How to Talk With Parents About COVID-19 Vaccination
- Strategies for Building Confidence in the COVID-19 Vaccines
- Communication Strategies for Building Confidence in COVID-19 Vaccines: Addressing Variants and Childhood Vaccinations
A version of this article first appeared on Medscape.com.
This news organization spoke to several pediatric experts to get answers.
More than 6 million children and adolescents (up to age 18 years) in the United States have been infected with SARS-CoV-2. Children represent about 17% of all cases, and an estimated 0.1%-2% of infected children end up hospitalized, according to Oct. 28 data from the American Academy of Pediatrics.
Physicians and other health care practitioners are gearing up for what could be an influx of patients. “Pediatricians are standing by to talk with families about the vaccine and to administer the vaccine to children as soon as possible,” Lee Savio Beers, MD, FAAP, president of the AAP, said in a statement.
In this Q&A, this news organization asked for additional advice from Sara “Sally” Goza, MD, a pediatrician in Fayetteville, Georgia, and immediate past president of the AAP; Peter Hotez, MD, PhD, dean of the National School of Tropical Medicine at Baylor College of Medicine and codirector of the Texas Children’s Hospital Center for Vaccine Development, both in Houston; and Danielle M. Zerr, MD, professor and chief of the division of pediatric infectious disease at the University of Washington, Seattle, and medical director of infection prevention at Seattle Children’s Hospital.
Q: How are smaller pediatric practices and solo practitioners going to handle the additional vaccinations?
Dr. Goza: It’s a scheduling challenge with this rollout and all the people who want it and want it right now. They’re going to want it this week.
I’ve actually had some children asking their moms: “When can I get it? When can I get it?” It’s been very interesting – they are chomping at the bit.
If I give the vaccine to a patient this week, in 3 weeks the second dose will be right around Thanksgiving. No one in my office is going to want to be here to give the shot on Thanksgiving, and no patient is going to want to come in on Thanksgiving weekend. So I’m trying to delay those parents – saying, let’s do it next week. That way we’re not messing up a holiday.
Children are going to need two doses, and they won’t be fully protected until 2 weeks after their second dose. So they won’t get full protection for Thanksgiving, but they will have full protection for Christmas.
I know there are a lot of pediatricians who have preordered the vaccine. I know in our office they sent us an email ... to let us know our vaccines are being shipped. So I think a lot of pediatricians are going to have the vaccine.
Q: How should pediatricians counsel parents who are fearful or hesitant?
Dr. Hotez: It’s important to emphasize the severity of the 2021 summer Delta epidemic in children. We need to get beyond this false narrative that COVID only produces a mild disease in children. It’s caused thousands of pediatric hospitalizations, not to mention long COVID.
Dr. Zerr: It is key to find out what concerns parents have and then focus on answering their specific questions. It is helpful to emphasize the safety and efficacy of the vaccine and to explain the rigorous processes that the vaccine went through to receive Food and Drug Administration approval.
Q: How should pediatricians counter any misinformation/disinformation out there about the COVID-19 vaccines?
Dr. Goza: The most important thing is not to discount what they are saying. Don’t say: “That’s crazy” or “That’s not true.” Don’t roll your eyes and say: “Really, you’re going to believe all that?”
Instead, have a conversation with them about why we think that is not true, or why we know that’s not true. We really have to have that relationship and ask: “Well, what are your concerns?” And then really counter (any misinformation) with facts, with science, and based on your experience.
Q: Do the data presented to the FDA and the CDC about the safety and effectiveness of the COVID-19 vaccine for 5- to 11-year-olds seem robust to you?
Dr. Zerr: Yes, and data collection will be ongoing.
Dr. Hotez: I’ve only seen what’s publicly available so far, and it seems to support moving forward with emergency use authorization. The only shortfall is the size, roughly 2,200 children, which would not be of sufficient size to detect a rare safety signal.
Q: Do previous controversies around pediatric vaccines (for example, the MMR vaccine and autism) give pediatricians some background and experience so they can address any pushback on the COVID-19 vaccines?
Dr. Goza: Pediatricians have been dealing with vaccine hesitancy for a while now, ever since the MMR and autism controversy started. Even before then, there were certain groups of people who didn’t want vaccines.
We’ve really worked hard at helping teach pediatricians how to deal with the misinformation, how to counter it, and how to help parents understand the vaccines are safe and effective – and that they save lives.
That (experience) will help us in some ways. Unfortunately, there is more misinformation out there – there is almost a concerted effort on misinformation. It’s big.
Pediatricians will do everything we can, but we need help countering it. We need the misinformation to quit getting spread on social media. We can talk one on one with patients and families, but if all they are hearing on social media is the misinformation, it’s really hard.
Q: Are pediatricians, especially solo practitioners or pediatricians at smaller practices, going to face challenges with multidose vials and not wasting vaccine product?
Dr. Goza: I’m at a small practice. We have 3.5 FTEs (full-time equivalents) of MDs and three FTEs of nurse practitioners. So we’re not that big – about six providers.
You know, it is a challenge. We’re not going to buy the super-duper freezer, and we’re not going to be able to store these vaccines for a long period of time.
So when we order, we need smaller amounts. For the 12- to 18-year-olds, [maximum storage] was 45 days. Now for the 5- to 11-year-olds, we’re going to be able to store the vaccine in the refrigerator for 10 weeks, which gives us more leeway there.
We try to do all of vaccinations on 1 day, so we know how many people are coming in, and we are not going to waste too many doses.
Our Department of Public Health in Georgia has said: “We want these vaccines in the arms of kids, and if you have to waste some doses, don’t worry about it.” But it’s a 10-dose vial. It’s going to be hard for me to open it up for one child. I just don’t like wasting anything like this.
Our main goal is to get this vaccine in to the arms of children whose parents want it.
Q: What are some additional sources of information for pediatricians?
Dr. Zerr: There are a lot of great resources on vaccine hesitancy from reputable sources, including these from the CDC and from the National Academies of Sciences, Engineering, and Medicine:
- Building Confidence With OVID-19 Vaccines
- How to Talk With Parents About COVID-19 Vaccination
- Strategies for Building Confidence in the COVID-19 Vaccines
- Communication Strategies for Building Confidence in COVID-19 Vaccines: Addressing Variants and Childhood Vaccinations
A version of this article first appeared on Medscape.com.
This news organization spoke to several pediatric experts to get answers.
More than 6 million children and adolescents (up to age 18 years) in the United States have been infected with SARS-CoV-2. Children represent about 17% of all cases, and an estimated 0.1%-2% of infected children end up hospitalized, according to Oct. 28 data from the American Academy of Pediatrics.
Physicians and other health care practitioners are gearing up for what could be an influx of patients. “Pediatricians are standing by to talk with families about the vaccine and to administer the vaccine to children as soon as possible,” Lee Savio Beers, MD, FAAP, president of the AAP, said in a statement.
In this Q&A, this news organization asked for additional advice from Sara “Sally” Goza, MD, a pediatrician in Fayetteville, Georgia, and immediate past president of the AAP; Peter Hotez, MD, PhD, dean of the National School of Tropical Medicine at Baylor College of Medicine and codirector of the Texas Children’s Hospital Center for Vaccine Development, both in Houston; and Danielle M. Zerr, MD, professor and chief of the division of pediatric infectious disease at the University of Washington, Seattle, and medical director of infection prevention at Seattle Children’s Hospital.
Q: How are smaller pediatric practices and solo practitioners going to handle the additional vaccinations?
Dr. Goza: It’s a scheduling challenge with this rollout and all the people who want it and want it right now. They’re going to want it this week.
I’ve actually had some children asking their moms: “When can I get it? When can I get it?” It’s been very interesting – they are chomping at the bit.
If I give the vaccine to a patient this week, in 3 weeks the second dose will be right around Thanksgiving. No one in my office is going to want to be here to give the shot on Thanksgiving, and no patient is going to want to come in on Thanksgiving weekend. So I’m trying to delay those parents – saying, let’s do it next week. That way we’re not messing up a holiday.
Children are going to need two doses, and they won’t be fully protected until 2 weeks after their second dose. So they won’t get full protection for Thanksgiving, but they will have full protection for Christmas.
I know there are a lot of pediatricians who have preordered the vaccine. I know in our office they sent us an email ... to let us know our vaccines are being shipped. So I think a lot of pediatricians are going to have the vaccine.
Q: How should pediatricians counsel parents who are fearful or hesitant?
Dr. Hotez: It’s important to emphasize the severity of the 2021 summer Delta epidemic in children. We need to get beyond this false narrative that COVID only produces a mild disease in children. It’s caused thousands of pediatric hospitalizations, not to mention long COVID.
Dr. Zerr: It is key to find out what concerns parents have and then focus on answering their specific questions. It is helpful to emphasize the safety and efficacy of the vaccine and to explain the rigorous processes that the vaccine went through to receive Food and Drug Administration approval.
Q: How should pediatricians counter any misinformation/disinformation out there about the COVID-19 vaccines?
Dr. Goza: The most important thing is not to discount what they are saying. Don’t say: “That’s crazy” or “That’s not true.” Don’t roll your eyes and say: “Really, you’re going to believe all that?”
Instead, have a conversation with them about why we think that is not true, or why we know that’s not true. We really have to have that relationship and ask: “Well, what are your concerns?” And then really counter (any misinformation) with facts, with science, and based on your experience.
Q: Do the data presented to the FDA and the CDC about the safety and effectiveness of the COVID-19 vaccine for 5- to 11-year-olds seem robust to you?
Dr. Zerr: Yes, and data collection will be ongoing.
Dr. Hotez: I’ve only seen what’s publicly available so far, and it seems to support moving forward with emergency use authorization. The only shortfall is the size, roughly 2,200 children, which would not be of sufficient size to detect a rare safety signal.
Q: Do previous controversies around pediatric vaccines (for example, the MMR vaccine and autism) give pediatricians some background and experience so they can address any pushback on the COVID-19 vaccines?
Dr. Goza: Pediatricians have been dealing with vaccine hesitancy for a while now, ever since the MMR and autism controversy started. Even before then, there were certain groups of people who didn’t want vaccines.
We’ve really worked hard at helping teach pediatricians how to deal with the misinformation, how to counter it, and how to help parents understand the vaccines are safe and effective – and that they save lives.
That (experience) will help us in some ways. Unfortunately, there is more misinformation out there – there is almost a concerted effort on misinformation. It’s big.
Pediatricians will do everything we can, but we need help countering it. We need the misinformation to quit getting spread on social media. We can talk one on one with patients and families, but if all they are hearing on social media is the misinformation, it’s really hard.
Q: Are pediatricians, especially solo practitioners or pediatricians at smaller practices, going to face challenges with multidose vials and not wasting vaccine product?
Dr. Goza: I’m at a small practice. We have 3.5 FTEs (full-time equivalents) of MDs and three FTEs of nurse practitioners. So we’re not that big – about six providers.
You know, it is a challenge. We’re not going to buy the super-duper freezer, and we’re not going to be able to store these vaccines for a long period of time.
So when we order, we need smaller amounts. For the 12- to 18-year-olds, [maximum storage] was 45 days. Now for the 5- to 11-year-olds, we’re going to be able to store the vaccine in the refrigerator for 10 weeks, which gives us more leeway there.
We try to do all of vaccinations on 1 day, so we know how many people are coming in, and we are not going to waste too many doses.
Our Department of Public Health in Georgia has said: “We want these vaccines in the arms of kids, and if you have to waste some doses, don’t worry about it.” But it’s a 10-dose vial. It’s going to be hard for me to open it up for one child. I just don’t like wasting anything like this.
Our main goal is to get this vaccine in to the arms of children whose parents want it.
Q: What are some additional sources of information for pediatricians?
Dr. Zerr: There are a lot of great resources on vaccine hesitancy from reputable sources, including these from the CDC and from the National Academies of Sciences, Engineering, and Medicine:
- Building Confidence With OVID-19 Vaccines
- How to Talk With Parents About COVID-19 Vaccination
- Strategies for Building Confidence in the COVID-19 Vaccines
- Communication Strategies for Building Confidence in COVID-19 Vaccines: Addressing Variants and Childhood Vaccinations
A version of this article first appeared on Medscape.com.