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Defending access to reproductive health care
The 1973 Supreme Court of the United States (SCOTUS) decision in Roe v Wade was a landmark ruling,1 establishing that the United States Constitution provides a fundamental “right to privacy,” protecting pregnant people’s freedom to access all available reproductive health care options. Recognizing that the right to abortion was not absolute, the majority of justices supported a trimester system. In the first trimester, decisions about abortion care are fully controlled by patients and clinicians, and no government could place restrictions on access to abortion. In the second trimester, SCOTUS ruled that states may choose to regulate abortion to protect maternal health. (As an example of such state restrictions, in Massachusetts, for many years, but no longer, the state required that abortions occur in a hospital when the patient was between 18 and 24 weeks’ gestation in order to facilitate comprehensive emergency care for complications.) Beginning in the third trimester, a point at which a fetus could be viable, the Court ruled that a government could prohibit abortion except when an abortion was necessary to protect the life or health of the pregnant person. In 1992, the SCOTUS decision in Planned Parenthood v Casey2 rejected the trimester system, reaffirming the right to an abortion before fetal viability, and adopting a new standard that states may not create an undue burden on a person seeking an abortion b
If, as anticipated, the 2022 SCOTUS decision in Dobbs v Jackson Women’s Health Organization3 overturns the precedents set in Roe v Wade and Planned Parenthood v Casey, decisions on abortion law will be relegated to elected legislators and state courts.4 It is expected that at least 26 state legislatures and governors will enact stringent new restrictions on access to abortion. This cataclysmic reversal of judicial opinion creates a historic challenge to obstetrician-gynecologists and their patients and could threaten access to other vital reproductive services beyond abortion, like contraception. We will be fighting, state by state, for people’s right to access all available reproductive health procedures. This will also significantly affect the ability for providers in women’s reproductive health to obtain appropriate and necessary education and training in a critical skills. If access to safe abortion is restricted, we fear patients may be forced to consider unsafe abortion, raising the specter of a return to the 1960s, when an epidemic of unsafe abortion caused countless injuries and deaths.5,6
How do we best prepare for these challenges?
- We will need to be flexible and continually evolve our clinical practices to be adherent with state and local legislation and regulation.
- To reduce unintended pregnancies, we need to strengthen our efforts to ensure that every patient has ready access to all available contraceptive options with no out-of-pocket cost.
- When a contraceptive is desired, we will focus on educating people about effectiveness, and offering them highly reliable contraception, such as the implant or intrauterine devices.
- We need to ensure timely access to abortion if state-based laws permit abortion before 6 or 7 weeks’ gestation. Providing medication abortion without an in-person visit using a telehealth option would be one option to expand rapid access to early first trimester abortion.
- Clinicians in states with access to abortion services will need to collaborate with colleagues in states with restrictions on abortion services to improve patient access across state borders.
On a national level, advancing our effective advocacy in Congress may lead to national legislation passed and signed by the President. This could supersede most state laws prohibiting access to comprehensive women’s reproductive health and create a unified, national approach to abortion care, allowing for the appropriate training of all obstetrician-gynecologists. We will also need to develop teams in every state capable of advocating for laws that ensure access to all reproductive health care options. The American College of Obstetricians and Gynecologists has leaders trained and tasked with legislative advocacy in every state.7 This network will be a foundation upon which to build additional advocacy efforts.
As women’s health care professionals, our responsibility to our patients, is to work to ensure universal access to safe and effective comprehensive reproductive options, and to ensure that our workforce is prepared to meet the needs of our patients by defending the patient-clinician relationship. Abortion care saves lives of pregnant patients and reduces maternal morbidity.8 Access to safe abortion care as part of comprehensive reproductive services is an important component of health care. ●
- Roe v Wade, 410 U.S. 113 (1973).
- Planned Parenthood v Casey, 505 U.S. 833 (1992).
- Dobbs v Jackson Women’s Health Organization, 19-1392. https://www.supremecourt.gov/search .aspx?filename=/docket/docketfiles/html /public/19-1392.html. Accessed May 18, 2022.
- Gerstein J, Ward A. Supreme Court has voted to overturn abortion rights, draft opinion shows. Politico. May 5, 2022. Updated May 3, 2022.
- Gold RB. Lessons from before Roe: will past be prologue? Guttmacher Institute. March 1, 2003. https://www.guttmacher.org/gpr/2003/03 /lessons-roe-will-past-be-prologue. Accessed May 18, 2022.
- Edelin KC. Broken Justice: A True Story of Race, Sex and Revenge in a Boston Courtroom. Pond View Press; 2007.
- The American College of Obstetricians and Gynecologists. Get involved in your state. ACOG web site. https://www.acog.org/advocacy /get-involved/get-involved-in-your-state. Accessed May 18, 2022.
- Institute of Medicine (US) Committee on Improving Birth Outcomes. Bale JR, Stoll BJ, Lucas AO, eds. Reducing maternal mortality and morbidity. In: Improving Birth Outcomes: Meeting the Challenge in the Developing World. Washington, DC: National Academies Press (US); 2003.
The 1973 Supreme Court of the United States (SCOTUS) decision in Roe v Wade was a landmark ruling,1 establishing that the United States Constitution provides a fundamental “right to privacy,” protecting pregnant people’s freedom to access all available reproductive health care options. Recognizing that the right to abortion was not absolute, the majority of justices supported a trimester system. In the first trimester, decisions about abortion care are fully controlled by patients and clinicians, and no government could place restrictions on access to abortion. In the second trimester, SCOTUS ruled that states may choose to regulate abortion to protect maternal health. (As an example of such state restrictions, in Massachusetts, for many years, but no longer, the state required that abortions occur in a hospital when the patient was between 18 and 24 weeks’ gestation in order to facilitate comprehensive emergency care for complications.) Beginning in the third trimester, a point at which a fetus could be viable, the Court ruled that a government could prohibit abortion except when an abortion was necessary to protect the life or health of the pregnant person. In 1992, the SCOTUS decision in Planned Parenthood v Casey2 rejected the trimester system, reaffirming the right to an abortion before fetal viability, and adopting a new standard that states may not create an undue burden on a person seeking an abortion b
If, as anticipated, the 2022 SCOTUS decision in Dobbs v Jackson Women’s Health Organization3 overturns the precedents set in Roe v Wade and Planned Parenthood v Casey, decisions on abortion law will be relegated to elected legislators and state courts.4 It is expected that at least 26 state legislatures and governors will enact stringent new restrictions on access to abortion. This cataclysmic reversal of judicial opinion creates a historic challenge to obstetrician-gynecologists and their patients and could threaten access to other vital reproductive services beyond abortion, like contraception. We will be fighting, state by state, for people’s right to access all available reproductive health procedures. This will also significantly affect the ability for providers in women’s reproductive health to obtain appropriate and necessary education and training in a critical skills. If access to safe abortion is restricted, we fear patients may be forced to consider unsafe abortion, raising the specter of a return to the 1960s, when an epidemic of unsafe abortion caused countless injuries and deaths.5,6
How do we best prepare for these challenges?
- We will need to be flexible and continually evolve our clinical practices to be adherent with state and local legislation and regulation.
- To reduce unintended pregnancies, we need to strengthen our efforts to ensure that every patient has ready access to all available contraceptive options with no out-of-pocket cost.
- When a contraceptive is desired, we will focus on educating people about effectiveness, and offering them highly reliable contraception, such as the implant or intrauterine devices.
- We need to ensure timely access to abortion if state-based laws permit abortion before 6 or 7 weeks’ gestation. Providing medication abortion without an in-person visit using a telehealth option would be one option to expand rapid access to early first trimester abortion.
- Clinicians in states with access to abortion services will need to collaborate with colleagues in states with restrictions on abortion services to improve patient access across state borders.
On a national level, advancing our effective advocacy in Congress may lead to national legislation passed and signed by the President. This could supersede most state laws prohibiting access to comprehensive women’s reproductive health and create a unified, national approach to abortion care, allowing for the appropriate training of all obstetrician-gynecologists. We will also need to develop teams in every state capable of advocating for laws that ensure access to all reproductive health care options. The American College of Obstetricians and Gynecologists has leaders trained and tasked with legislative advocacy in every state.7 This network will be a foundation upon which to build additional advocacy efforts.
As women’s health care professionals, our responsibility to our patients, is to work to ensure universal access to safe and effective comprehensive reproductive options, and to ensure that our workforce is prepared to meet the needs of our patients by defending the patient-clinician relationship. Abortion care saves lives of pregnant patients and reduces maternal morbidity.8 Access to safe abortion care as part of comprehensive reproductive services is an important component of health care. ●
The 1973 Supreme Court of the United States (SCOTUS) decision in Roe v Wade was a landmark ruling,1 establishing that the United States Constitution provides a fundamental “right to privacy,” protecting pregnant people’s freedom to access all available reproductive health care options. Recognizing that the right to abortion was not absolute, the majority of justices supported a trimester system. In the first trimester, decisions about abortion care are fully controlled by patients and clinicians, and no government could place restrictions on access to abortion. In the second trimester, SCOTUS ruled that states may choose to regulate abortion to protect maternal health. (As an example of such state restrictions, in Massachusetts, for many years, but no longer, the state required that abortions occur in a hospital when the patient was between 18 and 24 weeks’ gestation in order to facilitate comprehensive emergency care for complications.) Beginning in the third trimester, a point at which a fetus could be viable, the Court ruled that a government could prohibit abortion except when an abortion was necessary to protect the life or health of the pregnant person. In 1992, the SCOTUS decision in Planned Parenthood v Casey2 rejected the trimester system, reaffirming the right to an abortion before fetal viability, and adopting a new standard that states may not create an undue burden on a person seeking an abortion b
If, as anticipated, the 2022 SCOTUS decision in Dobbs v Jackson Women’s Health Organization3 overturns the precedents set in Roe v Wade and Planned Parenthood v Casey, decisions on abortion law will be relegated to elected legislators and state courts.4 It is expected that at least 26 state legislatures and governors will enact stringent new restrictions on access to abortion. This cataclysmic reversal of judicial opinion creates a historic challenge to obstetrician-gynecologists and their patients and could threaten access to other vital reproductive services beyond abortion, like contraception. We will be fighting, state by state, for people’s right to access all available reproductive health procedures. This will also significantly affect the ability for providers in women’s reproductive health to obtain appropriate and necessary education and training in a critical skills. If access to safe abortion is restricted, we fear patients may be forced to consider unsafe abortion, raising the specter of a return to the 1960s, when an epidemic of unsafe abortion caused countless injuries and deaths.5,6
How do we best prepare for these challenges?
- We will need to be flexible and continually evolve our clinical practices to be adherent with state and local legislation and regulation.
- To reduce unintended pregnancies, we need to strengthen our efforts to ensure that every patient has ready access to all available contraceptive options with no out-of-pocket cost.
- When a contraceptive is desired, we will focus on educating people about effectiveness, and offering them highly reliable contraception, such as the implant or intrauterine devices.
- We need to ensure timely access to abortion if state-based laws permit abortion before 6 or 7 weeks’ gestation. Providing medication abortion without an in-person visit using a telehealth option would be one option to expand rapid access to early first trimester abortion.
- Clinicians in states with access to abortion services will need to collaborate with colleagues in states with restrictions on abortion services to improve patient access across state borders.
On a national level, advancing our effective advocacy in Congress may lead to national legislation passed and signed by the President. This could supersede most state laws prohibiting access to comprehensive women’s reproductive health and create a unified, national approach to abortion care, allowing for the appropriate training of all obstetrician-gynecologists. We will also need to develop teams in every state capable of advocating for laws that ensure access to all reproductive health care options. The American College of Obstetricians and Gynecologists has leaders trained and tasked with legislative advocacy in every state.7 This network will be a foundation upon which to build additional advocacy efforts.
As women’s health care professionals, our responsibility to our patients, is to work to ensure universal access to safe and effective comprehensive reproductive options, and to ensure that our workforce is prepared to meet the needs of our patients by defending the patient-clinician relationship. Abortion care saves lives of pregnant patients and reduces maternal morbidity.8 Access to safe abortion care as part of comprehensive reproductive services is an important component of health care. ●
- Roe v Wade, 410 U.S. 113 (1973).
- Planned Parenthood v Casey, 505 U.S. 833 (1992).
- Dobbs v Jackson Women’s Health Organization, 19-1392. https://www.supremecourt.gov/search .aspx?filename=/docket/docketfiles/html /public/19-1392.html. Accessed May 18, 2022.
- Gerstein J, Ward A. Supreme Court has voted to overturn abortion rights, draft opinion shows. Politico. May 5, 2022. Updated May 3, 2022.
- Gold RB. Lessons from before Roe: will past be prologue? Guttmacher Institute. March 1, 2003. https://www.guttmacher.org/gpr/2003/03 /lessons-roe-will-past-be-prologue. Accessed May 18, 2022.
- Edelin KC. Broken Justice: A True Story of Race, Sex and Revenge in a Boston Courtroom. Pond View Press; 2007.
- The American College of Obstetricians and Gynecologists. Get involved in your state. ACOG web site. https://www.acog.org/advocacy /get-involved/get-involved-in-your-state. Accessed May 18, 2022.
- Institute of Medicine (US) Committee on Improving Birth Outcomes. Bale JR, Stoll BJ, Lucas AO, eds. Reducing maternal mortality and morbidity. In: Improving Birth Outcomes: Meeting the Challenge in the Developing World. Washington, DC: National Academies Press (US); 2003.
- Roe v Wade, 410 U.S. 113 (1973).
- Planned Parenthood v Casey, 505 U.S. 833 (1992).
- Dobbs v Jackson Women’s Health Organization, 19-1392. https://www.supremecourt.gov/search .aspx?filename=/docket/docketfiles/html /public/19-1392.html. Accessed May 18, 2022.
- Gerstein J, Ward A. Supreme Court has voted to overturn abortion rights, draft opinion shows. Politico. May 5, 2022. Updated May 3, 2022.
- Gold RB. Lessons from before Roe: will past be prologue? Guttmacher Institute. March 1, 2003. https://www.guttmacher.org/gpr/2003/03 /lessons-roe-will-past-be-prologue. Accessed May 18, 2022.
- Edelin KC. Broken Justice: A True Story of Race, Sex and Revenge in a Boston Courtroom. Pond View Press; 2007.
- The American College of Obstetricians and Gynecologists. Get involved in your state. ACOG web site. https://www.acog.org/advocacy /get-involved/get-involved-in-your-state. Accessed May 18, 2022.
- Institute of Medicine (US) Committee on Improving Birth Outcomes. Bale JR, Stoll BJ, Lucas AO, eds. Reducing maternal mortality and morbidity. In: Improving Birth Outcomes: Meeting the Challenge in the Developing World. Washington, DC: National Academies Press (US); 2003.
Is benzophenone safe in skin care? Part 2: Environmental effects
Although it has been . DiNardo and Downs point out that BP-3 has been linked to contact and photocontact allergies in humans and implicated as a potential endocrine disruptor. They add that it can yield deleterious by-products when reacting with chlorine in swimming pools and wastewater treatment plants and can cause additional side effects in humans who ingest fish.1 This column will focus on recent studies, mainly on the role of benzophenones in sunscreen agents that pose considerable risks to waterways and marine life, with concomitant effects on the food chain.
Environmental effects of BPs and legislative responses
Various UV filters, including BP-3, octinoxate, octocrylene, and ethylhexyl salicylate, are thought to pose considerable peril to the marine environment.2,3 In particular, BP-3 has been demonstrated to provoke coral reef bleaching in vitro, leading to ossification and deforming DNA in the larval stage.3,4
According to a 2018 report, BP-3 is believed to be present in approximately two thirds of organic sunscreens used in the United States.3 In addition, several studies have revealed that detectable levels of organic sunscreen ingredients, including BP-3, have been identified in coastal waters around the globe, including Hawaii and the U.S. Virgin Islands.4-8
A surfeit of tourists has been blamed in part, given that an estimated 25% of applied sunscreen is eliminated within 20 minutes of entering the water and thought to release about 4,000-6,000 tons/year into the surrounding coral reefs.9,10 In Hawaii in particular, sewage contamination of the waterways has resulted from wastewater treatment facilities ill-equipped to filter out organic substances such as BP-3 and octinoxate.10,11 In light of such circumstances, the use of sunscreens containing BP-3 and octinoxate have been restricted in Hawaii, particularly in proximity to beaches, since Jan. 1, 2021, because of their apparent environmental impact.10
The exposure of coral to these compounds is believed to result in bleaching because of impaired membrane integrity and photosynthetic pigment loss in the zooxanthellae that coral releases.9,10 Coral and the algae zooxanthellae have a symbiotic relationship, Siller et al. explain, with the coral delivering protection and components essential for photosynthesis and the algae ultimately serving as nutrients for the coral.10 Stress endured by coral is believed to cause algae to detach, rendering coral more vulnerable to disease and less viable overall.10
In 2016, Downs et al. showed that four out of five sampled locations had detectable levels of BP-3 (100 pp trillion) with a fifth tested site measured at 19.2 pp billion.4
In 2019, Sirois acknowledges the problem of coral bleaching around the world but speculates that banning sunscreen ingredients for this purpose will delude people that such a measure will reverse the decline of coral and may lead to the unintended consequence of lower use of sunscreens. Sirois adds that a more comprehensive investigation of the multiple causes of coral reef bleaching is warranted, as are deeper examinations of studies using higher concentrations of sunscreen ingredients in artificial conditions.12
In the same year, Raffa et al. discussed the impending ban in Hawaii of the two sunscreen ingredients (BP-3 and octinoxate) to help preserve coral reefs. In so doing, they detailed the natural and human-induced harm to coral reefs, including pollution, fishing practices, overall impact of global climate change, and alterations in ocean temperature and chemistry. The implication is that sunscreen ingredients, which help prevent sun damage in users, are not the only causes of harm to coral reefs. Nevertheless, they point out that concentration estimates and mechanism studies buttress the argument that sunscreen ingredients contribute to coral bleaching. Still, the ban in Hawaii is thought to be a trend. Opponents of the ban are concerned that human skin cancers will rise in such circumstances. Alternative chemical sunscreens are being investigated, and physical sunscreens have emerged as the go-to recommendation.13
Notably, oxybenzone has been virtually replaced in the European Union with other UV filters with broad-spectrum action, but the majority of such filters have not yet been approved for use in the United States by the Food and Drug Administration.3
Food chain implications
BP-3 and other UV filters have been investigated for their effects on fish and mammals. Schneider and Lim illustrate that BP-3 is among the frequently used organic UV filters (along with 4-methylbenzylidene camphor, octocrylene, and octinoxate [ethylhexyl methoxycinnamate]) found in most water sources in the world, as well as multiple fish species.2 Cod liver in Norway, for instance, was found to contain octocrylene in 80% of cod, with BP-3 identified in 50% of the sample. BP-3 and octinoxate were also found in white fish.2,14 In laboratory studies, BP-3 in particular has been found in high concentrations in rainbow trout and Japanese rice fish (medaka), causing reduced egg production and hatchlings in females and increased vitellogenin protein production in males, suggesting potential feminization.2,15
Schneider and Lim note that standard wastewater treatment approaches cannot address this issue and the presence of such contaminants in fish can pose dangerous ramifications in the food chain. They assert that, despite relatively low concentrations in the fish, bioaccumulation and biomagnification present the potential for chemicals accumulating over time and becoming more deleterious as such ingredients travel up the food chain. As higher-chain organisms absorb higher concentrations of the chemicals not broken down in the lower-chain organisms, though, there have not yet been reports of adverse effects of biomagnification in humans.2
BP-3 has been found by Brausch and Rand to have bioaccumulated in fish at higher levels than the ambient water, however.1,2,16 Schneider and Lim present these issues as relevant to the sun protection discussion, while advocating for dermatologists to continue to counsel wise sun-protective behaviors.2
Conclusion
While calls for additional research are necessary and encouraging, I think human, and likely environmental, health would be better protected by the use of inorganic sunscreens in general and near or in coastal waterways. In light of legislative actions, in particular, it is important for dermatologists to intervene to ensure that patients do not engage in riskier behaviors in the sun in areas facing imminent organic sunscreen bans.
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 [email protected].
References
1. DiNardo JC and Downs CA. J Cosmet Dermatol. 2018 Feb;17(1):15-9.
2. Schneider SL and Lim HW. J Am Acad Dermatol. 2019 Jan;80(1):266-71.
3. Yeager DG and Lim HW. Dermatol Clin. 2019 Apr;37(2):149-57.
4. Downs CA et al. Arch Environ Contam Toxicol 2016 Feb;70(2):265-88.
5. Sánchez Rodríguez A et al. Chemosphere. 2015 Jul;131:85-90.
6. Tovar-Sánchez A et al. PLoS One. 2013 Jun 5;8(6):e65451.
7. Danovaro R and Corinaldesi C. Microb Ecol. 2003 Feb;45(2):109-18.
8. Daughton CG and Ternes TA. Environ Health Perspect. 1999 Dec;107 Suppl 6:907-38.
9. Danovaro R et al. Environ Health Perspect. 2008 Apr;116(4):441-7.
10. Siller A et al. Plast Surg Nur. 2019 Oct/Dec;39(4):157-60.
11. Ramos S et al. Sci Total Environ. 2015 Sep 1;526:278-311.
12. Sirois J. Sci Total Environ. 2019 Jul 15;674:211-2.
13. Raffa RB et al. J Clin Pharm Ther. 2019 Feb;44(1):134-9.
14. Langford KH et al. Environ Int. 2015 Jul;80:1-7.
15. Coronado M et al. Aquat Toxicol. 2008 Nov 21;90(3):182-7.
16. Brausch JM and Rand GM. Chemosphere. 2011 Mar;82(11):1518-32.
Although it has been . DiNardo and Downs point out that BP-3 has been linked to contact and photocontact allergies in humans and implicated as a potential endocrine disruptor. They add that it can yield deleterious by-products when reacting with chlorine in swimming pools and wastewater treatment plants and can cause additional side effects in humans who ingest fish.1 This column will focus on recent studies, mainly on the role of benzophenones in sunscreen agents that pose considerable risks to waterways and marine life, with concomitant effects on the food chain.
Environmental effects of BPs and legislative responses
Various UV filters, including BP-3, octinoxate, octocrylene, and ethylhexyl salicylate, are thought to pose considerable peril to the marine environment.2,3 In particular, BP-3 has been demonstrated to provoke coral reef bleaching in vitro, leading to ossification and deforming DNA in the larval stage.3,4
According to a 2018 report, BP-3 is believed to be present in approximately two thirds of organic sunscreens used in the United States.3 In addition, several studies have revealed that detectable levels of organic sunscreen ingredients, including BP-3, have been identified in coastal waters around the globe, including Hawaii and the U.S. Virgin Islands.4-8
A surfeit of tourists has been blamed in part, given that an estimated 25% of applied sunscreen is eliminated within 20 minutes of entering the water and thought to release about 4,000-6,000 tons/year into the surrounding coral reefs.9,10 In Hawaii in particular, sewage contamination of the waterways has resulted from wastewater treatment facilities ill-equipped to filter out organic substances such as BP-3 and octinoxate.10,11 In light of such circumstances, the use of sunscreens containing BP-3 and octinoxate have been restricted in Hawaii, particularly in proximity to beaches, since Jan. 1, 2021, because of their apparent environmental impact.10
The exposure of coral to these compounds is believed to result in bleaching because of impaired membrane integrity and photosynthetic pigment loss in the zooxanthellae that coral releases.9,10 Coral and the algae zooxanthellae have a symbiotic relationship, Siller et al. explain, with the coral delivering protection and components essential for photosynthesis and the algae ultimately serving as nutrients for the coral.10 Stress endured by coral is believed to cause algae to detach, rendering coral more vulnerable to disease and less viable overall.10
In 2016, Downs et al. showed that four out of five sampled locations had detectable levels of BP-3 (100 pp trillion) with a fifth tested site measured at 19.2 pp billion.4
In 2019, Sirois acknowledges the problem of coral bleaching around the world but speculates that banning sunscreen ingredients for this purpose will delude people that such a measure will reverse the decline of coral and may lead to the unintended consequence of lower use of sunscreens. Sirois adds that a more comprehensive investigation of the multiple causes of coral reef bleaching is warranted, as are deeper examinations of studies using higher concentrations of sunscreen ingredients in artificial conditions.12
In the same year, Raffa et al. discussed the impending ban in Hawaii of the two sunscreen ingredients (BP-3 and octinoxate) to help preserve coral reefs. In so doing, they detailed the natural and human-induced harm to coral reefs, including pollution, fishing practices, overall impact of global climate change, and alterations in ocean temperature and chemistry. The implication is that sunscreen ingredients, which help prevent sun damage in users, are not the only causes of harm to coral reefs. Nevertheless, they point out that concentration estimates and mechanism studies buttress the argument that sunscreen ingredients contribute to coral bleaching. Still, the ban in Hawaii is thought to be a trend. Opponents of the ban are concerned that human skin cancers will rise in such circumstances. Alternative chemical sunscreens are being investigated, and physical sunscreens have emerged as the go-to recommendation.13
Notably, oxybenzone has been virtually replaced in the European Union with other UV filters with broad-spectrum action, but the majority of such filters have not yet been approved for use in the United States by the Food and Drug Administration.3
Food chain implications
BP-3 and other UV filters have been investigated for their effects on fish and mammals. Schneider and Lim illustrate that BP-3 is among the frequently used organic UV filters (along with 4-methylbenzylidene camphor, octocrylene, and octinoxate [ethylhexyl methoxycinnamate]) found in most water sources in the world, as well as multiple fish species.2 Cod liver in Norway, for instance, was found to contain octocrylene in 80% of cod, with BP-3 identified in 50% of the sample. BP-3 and octinoxate were also found in white fish.2,14 In laboratory studies, BP-3 in particular has been found in high concentrations in rainbow trout and Japanese rice fish (medaka), causing reduced egg production and hatchlings in females and increased vitellogenin protein production in males, suggesting potential feminization.2,15
Schneider and Lim note that standard wastewater treatment approaches cannot address this issue and the presence of such contaminants in fish can pose dangerous ramifications in the food chain. They assert that, despite relatively low concentrations in the fish, bioaccumulation and biomagnification present the potential for chemicals accumulating over time and becoming more deleterious as such ingredients travel up the food chain. As higher-chain organisms absorb higher concentrations of the chemicals not broken down in the lower-chain organisms, though, there have not yet been reports of adverse effects of biomagnification in humans.2
BP-3 has been found by Brausch and Rand to have bioaccumulated in fish at higher levels than the ambient water, however.1,2,16 Schneider and Lim present these issues as relevant to the sun protection discussion, while advocating for dermatologists to continue to counsel wise sun-protective behaviors.2
Conclusion
While calls for additional research are necessary and encouraging, I think human, and likely environmental, health would be better protected by the use of inorganic sunscreens in general and near or in coastal waterways. In light of legislative actions, in particular, it is important for dermatologists to intervene to ensure that patients do not engage in riskier behaviors in the sun in areas facing imminent organic sunscreen bans.
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 [email protected].
References
1. DiNardo JC and Downs CA. J Cosmet Dermatol. 2018 Feb;17(1):15-9.
2. Schneider SL and Lim HW. J Am Acad Dermatol. 2019 Jan;80(1):266-71.
3. Yeager DG and Lim HW. Dermatol Clin. 2019 Apr;37(2):149-57.
4. Downs CA et al. Arch Environ Contam Toxicol 2016 Feb;70(2):265-88.
5. Sánchez Rodríguez A et al. Chemosphere. 2015 Jul;131:85-90.
6. Tovar-Sánchez A et al. PLoS One. 2013 Jun 5;8(6):e65451.
7. Danovaro R and Corinaldesi C. Microb Ecol. 2003 Feb;45(2):109-18.
8. Daughton CG and Ternes TA. Environ Health Perspect. 1999 Dec;107 Suppl 6:907-38.
9. Danovaro R et al. Environ Health Perspect. 2008 Apr;116(4):441-7.
10. Siller A et al. Plast Surg Nur. 2019 Oct/Dec;39(4):157-60.
11. Ramos S et al. Sci Total Environ. 2015 Sep 1;526:278-311.
12. Sirois J. Sci Total Environ. 2019 Jul 15;674:211-2.
13. Raffa RB et al. J Clin Pharm Ther. 2019 Feb;44(1):134-9.
14. Langford KH et al. Environ Int. 2015 Jul;80:1-7.
15. Coronado M et al. Aquat Toxicol. 2008 Nov 21;90(3):182-7.
16. Brausch JM and Rand GM. Chemosphere. 2011 Mar;82(11):1518-32.
Although it has been . DiNardo and Downs point out that BP-3 has been linked to contact and photocontact allergies in humans and implicated as a potential endocrine disruptor. They add that it can yield deleterious by-products when reacting with chlorine in swimming pools and wastewater treatment plants and can cause additional side effects in humans who ingest fish.1 This column will focus on recent studies, mainly on the role of benzophenones in sunscreen agents that pose considerable risks to waterways and marine life, with concomitant effects on the food chain.
Environmental effects of BPs and legislative responses
Various UV filters, including BP-3, octinoxate, octocrylene, and ethylhexyl salicylate, are thought to pose considerable peril to the marine environment.2,3 In particular, BP-3 has been demonstrated to provoke coral reef bleaching in vitro, leading to ossification and deforming DNA in the larval stage.3,4
According to a 2018 report, BP-3 is believed to be present in approximately two thirds of organic sunscreens used in the United States.3 In addition, several studies have revealed that detectable levels of organic sunscreen ingredients, including BP-3, have been identified in coastal waters around the globe, including Hawaii and the U.S. Virgin Islands.4-8
A surfeit of tourists has been blamed in part, given that an estimated 25% of applied sunscreen is eliminated within 20 minutes of entering the water and thought to release about 4,000-6,000 tons/year into the surrounding coral reefs.9,10 In Hawaii in particular, sewage contamination of the waterways has resulted from wastewater treatment facilities ill-equipped to filter out organic substances such as BP-3 and octinoxate.10,11 In light of such circumstances, the use of sunscreens containing BP-3 and octinoxate have been restricted in Hawaii, particularly in proximity to beaches, since Jan. 1, 2021, because of their apparent environmental impact.10
The exposure of coral to these compounds is believed to result in bleaching because of impaired membrane integrity and photosynthetic pigment loss in the zooxanthellae that coral releases.9,10 Coral and the algae zooxanthellae have a symbiotic relationship, Siller et al. explain, with the coral delivering protection and components essential for photosynthesis and the algae ultimately serving as nutrients for the coral.10 Stress endured by coral is believed to cause algae to detach, rendering coral more vulnerable to disease and less viable overall.10
In 2016, Downs et al. showed that four out of five sampled locations had detectable levels of BP-3 (100 pp trillion) with a fifth tested site measured at 19.2 pp billion.4
In 2019, Sirois acknowledges the problem of coral bleaching around the world but speculates that banning sunscreen ingredients for this purpose will delude people that such a measure will reverse the decline of coral and may lead to the unintended consequence of lower use of sunscreens. Sirois adds that a more comprehensive investigation of the multiple causes of coral reef bleaching is warranted, as are deeper examinations of studies using higher concentrations of sunscreen ingredients in artificial conditions.12
In the same year, Raffa et al. discussed the impending ban in Hawaii of the two sunscreen ingredients (BP-3 and octinoxate) to help preserve coral reefs. In so doing, they detailed the natural and human-induced harm to coral reefs, including pollution, fishing practices, overall impact of global climate change, and alterations in ocean temperature and chemistry. The implication is that sunscreen ingredients, which help prevent sun damage in users, are not the only causes of harm to coral reefs. Nevertheless, they point out that concentration estimates and mechanism studies buttress the argument that sunscreen ingredients contribute to coral bleaching. Still, the ban in Hawaii is thought to be a trend. Opponents of the ban are concerned that human skin cancers will rise in such circumstances. Alternative chemical sunscreens are being investigated, and physical sunscreens have emerged as the go-to recommendation.13
Notably, oxybenzone has been virtually replaced in the European Union with other UV filters with broad-spectrum action, but the majority of such filters have not yet been approved for use in the United States by the Food and Drug Administration.3
Food chain implications
BP-3 and other UV filters have been investigated for their effects on fish and mammals. Schneider and Lim illustrate that BP-3 is among the frequently used organic UV filters (along with 4-methylbenzylidene camphor, octocrylene, and octinoxate [ethylhexyl methoxycinnamate]) found in most water sources in the world, as well as multiple fish species.2 Cod liver in Norway, for instance, was found to contain octocrylene in 80% of cod, with BP-3 identified in 50% of the sample. BP-3 and octinoxate were also found in white fish.2,14 In laboratory studies, BP-3 in particular has been found in high concentrations in rainbow trout and Japanese rice fish (medaka), causing reduced egg production and hatchlings in females and increased vitellogenin protein production in males, suggesting potential feminization.2,15
Schneider and Lim note that standard wastewater treatment approaches cannot address this issue and the presence of such contaminants in fish can pose dangerous ramifications in the food chain. They assert that, despite relatively low concentrations in the fish, bioaccumulation and biomagnification present the potential for chemicals accumulating over time and becoming more deleterious as such ingredients travel up the food chain. As higher-chain organisms absorb higher concentrations of the chemicals not broken down in the lower-chain organisms, though, there have not yet been reports of adverse effects of biomagnification in humans.2
BP-3 has been found by Brausch and Rand to have bioaccumulated in fish at higher levels than the ambient water, however.1,2,16 Schneider and Lim present these issues as relevant to the sun protection discussion, while advocating for dermatologists to continue to counsel wise sun-protective behaviors.2
Conclusion
While calls for additional research are necessary and encouraging, I think human, and likely environmental, health would be better protected by the use of inorganic sunscreens in general and near or in coastal waterways. In light of legislative actions, in particular, it is important for dermatologists to intervene to ensure that patients do not engage in riskier behaviors in the sun in areas facing imminent organic sunscreen bans.
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 [email protected].
References
1. DiNardo JC and Downs CA. J Cosmet Dermatol. 2018 Feb;17(1):15-9.
2. Schneider SL and Lim HW. J Am Acad Dermatol. 2019 Jan;80(1):266-71.
3. Yeager DG and Lim HW. Dermatol Clin. 2019 Apr;37(2):149-57.
4. Downs CA et al. Arch Environ Contam Toxicol 2016 Feb;70(2):265-88.
5. Sánchez Rodríguez A et al. Chemosphere. 2015 Jul;131:85-90.
6. Tovar-Sánchez A et al. PLoS One. 2013 Jun 5;8(6):e65451.
7. Danovaro R and Corinaldesi C. Microb Ecol. 2003 Feb;45(2):109-18.
8. Daughton CG and Ternes TA. Environ Health Perspect. 1999 Dec;107 Suppl 6:907-38.
9. Danovaro R et al. Environ Health Perspect. 2008 Apr;116(4):441-7.
10. Siller A et al. Plast Surg Nur. 2019 Oct/Dec;39(4):157-60.
11. Ramos S et al. Sci Total Environ. 2015 Sep 1;526:278-311.
12. Sirois J. Sci Total Environ. 2019 Jul 15;674:211-2.
13. Raffa RB et al. J Clin Pharm Ther. 2019 Feb;44(1):134-9.
14. Langford KH et al. Environ Int. 2015 Jul;80:1-7.
15. Coronado M et al. Aquat Toxicol. 2008 Nov 21;90(3):182-7.
16. Brausch JM and Rand GM. Chemosphere. 2011 Mar;82(11):1518-32.
Going Beyond Hydroquinone: Alternative Skin Lightening Agents
Disorders of hyperpigmentation—melasma, postinflammatory hyperpigmentation, lichen planus pigmentosus, erythema dyschromicum perstans, and pigmented contact dermatitis, among others—are common and challenging to treat. Although they can affect individuals of all skin types, they most commonly are seen in skin of color; in fact, dyspigmentation is one of the most common chief concerns for which individuals of color see a dermatologist.1,2
For many years, hydroquinone (HQ) was one of the main options available for use as a lightening agent. Although effective, it has the risk of causing irritant dermatitis, potentially leading to further dyspigmentation, in addition to the risk of ochronosis with long-term use. It remains an important and useful treatment for pigmentary disorders, but there are numerous other lightening agents that also can be considered in the treatment of disorders of hyperpigmentation.
Herein, we provide recommendations for traditional and newer non-HQ lightening agents that can be considered when treating disorders of hyperpigmentation.
Traditional Non-HQ Lightening Agents
Retinoids—Retinoids are topical vitamin A derivatives that have been used safely and effectively for decades in the treatment of pigmentary disorders. Retinoids have multiple mechanisms of action in improving pigmentation. In addition to impeding tyrosinase induction, they inhibit pigment transfer to keratinocytes and lead to accelerated pigment loss due to epidermal shedding.3 Over-the-counter formulations include retinol, retinaldehyde, and adapalene. Prescription formulations include tretinoin and tazarotene in different strengths and vehicle formulations.4
Glycolic Acid—Glycolic acid is derived from sugarcane and is considered an α-hydroxy acid that leads to rapid desquamation of pigmented keratinocytes.5 Glycolic acid can not only be used in chemical peels but also in topical creams. It is the most common α-hydroxy acid peel and is sometimes paired with HQ and other topical lightening agents for increased penetration. Glycolic acid peels are available in concentrations of 20% to 70% and can be used at various depths. When used incorrectly, it can cause redness, burning, and even skin discoloration; however, when used at the proper concentrations and depth according to Fitzpatrick skin type, there typically are no notable adverse effects, and clinical results are favorable.
Kojic Acid—Kojic acid is a natural metabolite derived from fungi and is widely used in Asian countries. It works by inhibiting the catecholase activity of tyrosinase6 and typically is available in concentrations of 1% to 4%. A study suggested that a concentration of 1% or less typically is safe to use for prolonged periods without adverse effects. Although not more effective than HQ as a monotherapy, kojic acid has been shown to haveimproved efficacy when used in combination with other lightening agents.7
Azelaic Acid—Azelaic acid works by inhibiting tyrosinase, mitochondrial oxidoreductase activation, and DNA synthesis. It preferentially targets heavily pigmented melanocytes and possesses anti-inflammatory and antibacterial properties.8 A 20% concentration of azelaic acid was compared to HQ 4% for the treatment of melasma, and results revealed that the liposomal form of azelaic acid was considerably more tolerable than HQ 4% and also more effective.9
Licorice Extracts—Licorice extracts have been safely used in several cosmeceutical skin lightening products.10 The main active compounds in licorice root are glabridin and liquiritin, which work to disperse melanin. These compounds often are used topically at concentrations of 10% to 40%. A study by Amer and Metwalli11 found that topical liquiritin produced a reduction of pigmentary intensity, with 80% of patients showing an excellent response, which was described as no difference between the previously pigmented area and the normal skin surrounding it.
Aloesin—Aloesin is a low-molecular-weight glycoprotein found in aloe vera plants. Its mechanism of action includes competitive inhibition of the dihydroxyphenylalanine oxidation site, resulting in the inhibition of tyrosinase.12 It often is combined with arbutin for an enhanced lightening effect.
Niacinamide—Niacinamide is a form of vitamin B3 that works by suppressing the transfer of melanosomes to keratinocytes.13 In addition to its skin lightening effects, it also is photoprotective and antimicrobial, and its tolerability and safety have led to its inclusion in many cosmeceutical and prescription products.14
Ascorbic Acid—Ascorbic acid affects the monopherase activity of tyrosinase, thus reducing the synthesis of melanin. It also serves as an antioxidant in the skin by preventing the production of free radicals that can induce melanogenesis.15 Although it tends to be well tolerated with a low adverse effect profile, its relative instability and varying permeability can present a challenge. It is less effective as a monotherapy, so it often is combined with other lightening ingredients for greater efficacy.
Corticosteroids—Topical corticosteroids are anti-inflammatory and impact melanogenesis, though the mechanism of action of the latter has not been fully elucidated.16,17 Low- to mid-potency topical steroids often are used in conjunction with skin lightening products to diminish irritation and decrease inflammation.18 However, prolonged use of corticosteroids can lead to cutaneous adverse effects such as striae, hypopigmentation, and acne, as well as systemic side effects if there is sufficient absorption over time.
Soybean Extracts—Soybean extracts contain serine protease inhibitors that reduce the transfer of melanosomes into keratinocytes by inhibiting the PAR-2 (protease-activated receptor 2) pathway.19,20
Ellagic Acid—Ellagic acid is found in common plants such as eucalyptus and strawberry as well as green tea.21 It works as an antioxidant and decreases melanogenesis through inhibition of tyrosinase activity.
Paper Mulberry—Paper mulberry extract comes from the roots of the Broussonetia papyrifera tree and functions by inhibiting tyrosinase activity. It is widely used in South Africa and Europe.22
Resveratrol—Resveratrol is an ingredient extracted from Morus alba L and functions as an antimelanogentic agent by directly inhibiting tyrosinase as well as transcriptional and posttranscriptional processing of tyrosinase.23 It also holds antiproliferative, anti-inflammatory, and antioxidant properties and has widely been used for antiaging and skin lightening purposes.24
Newer Non-HQ Lightening Agents
Silymarin—Silymarin (also known as milk thistle [Silybum marianum]), is a polyphenolic flavonoid that possesses anticarcinogenic, antioxidant, and anti-inflammatory properties. It prevents melanin production in a dose-dependent manner by inhibiting levodopa (L-dopa) oxidation activity of tyrosinase and also reduces the expression of tyrosinase protein.25 In combination with vitamins C and E and hexylresorcinol, silymarin has been found to reduce the effects of photodamage, brighten skin, improve evenness and lines, as well as improve global facial appearance.26
Malassezin—Malassezin is an indole produced by Malessezia furfur yeast and has recently been investigated for melanogenesis suppression. Grimes et al27 assessed the efficacy of topical malassezin in 7 patients with facial hyperpigmentation applied twice daily for 14 weeks. Punch biopsies were taken at weeks 0, 8, 14, and 22. Biopsies from weeks 8 and 14 demonstrated reduced epidermal melanin compared to baseline in all participants; however, at 22 weeks, biopsies showed no difference in melanin content compared to baseline, indicating a temporary process induced by the malassezin.27 More clinical studies are needed to investigate this further.
N-acetyl-glucosamine—N-acetyl-glucosamine is an aminosaccharide that inhibits the glycosylation of tyrosinase as well as its function in melanogenesis.28 It is synthesized and included in topical products for wound healing, rhytides, moisturization, and pigmentation disorders.
Topical Tranexamic Acid—Tranexamic acid traditionally has been used orally for the treatment of menorrhagia but also has been found to be beneficial as a therapy for hyperpigmentation and erythema. Tranexamic acid interferes with plasmin activity, thus indirectly inhibiting melanogenesis while also inhibiting angiogenesis by targeting vascular endothelial growth factor (VEGF) receptors.29 It also leads to an increase in the levels of β-endorphin and μ-opioid receptors as well as the expression of estrogen receptor β on the surface of mast cells.30 Its oral benefit led to the development of topical formulations, typically in 2% to 5% concentrations. It has proven particularly beneficial in the treatment of melasma due to its effects on improving pigmentation, erythema, and skin barrier function.31 Topical tranexamic acid has a relatively high safety profile, with minor side effects such as transient skin irritation and erythema being reported.32
Cysteamine—Cysteamine inhibits tyrosinase, peroxidase, and chelating copper ions necessary for melanogenesis. It has proven to be effective in treating melasma and chronic severe postinflammatory hyperpigmentation when used in a 5% cream formulation.33,34 Lima et al35 were the first to compare the effects of topical cysteamine to HQ in the treatment of facial melasma. They found that the mean reduction in modified Melasma Area and Severity Index score was 24% for cysteamine and 41% for HQ after 60 days. There were no severe adverse effects with either treatment group.35
Final Thoughts
Hydroquinone remains the gold standard for treatment of hyperpigmentation; however, its side-effect profile and risk of ochronosis with long-term use has ushered in various other safe and effective skin lightening agents that can be used as monotherapies or in combination with other lightening agents. Many of these products also can be used effectively with procedural treatments such as chemical peels, lasers, and microneedling for enhanced absorption and efficacy. As newer agents are developed, additional well-designed studies will be needed to determine their safety and efficacy in different skin types as well as their role in the treatment of pigmentary disorders.
- Woolery-Lloyd H, Kammer JN. Treatment of hyperpigmentation. Semin Cutan Med Surg. 2011;30:171-175. doi:10.1016/j.sder.2011.06.004
- Desai SR. Hyperpigmentation therapy: a review. J Clin Aesthet Dermatol. 2014;7:13-17.
- Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol. 1975;111:40-48.
- Kligman AM, Grove GL, Hirose R, et al. Topical tretinoin for photoaged skin. J Am Acad Dermatol. 1986;15(4 pt 2):836-859. doi:10.1016/s0190-9622(86)70242-9
- Sharad J. Glycolic acid peel therapy—a current review. Clin Cosmet Investig Dermatol. 2013;6:281-288. doi:10.2147/CCID.S34029
- Nautiyal A, Wairkar S. Management of hyperpigmentation: current treatments and emerging therapies. Pigment Cell Melanoma Res. 2021;34:1000-1014. doi:10.1111/pcmr.12986
- Saeedi M, Eslamifar M, Khezri K. Kojic acid applications in cosmetic and pharmaceutical preparations. Biomed Pharmacother. 2019;110:582-593. doi:10.1016/j.biopha.2018.12.006
- Schulte BC, Wu W, Rosen T. Azelaic acid: evidence-based update on mechanism of action and clinical application. J Drugs Dermatol. 2015;14:964-968.
- Akl EM. Liposomal azelaic acid 20% cream vs hydroquinone 4% cream as adjuvant to oral tranexamic acid in melasma: a comparative study [published online April 7, 2021]. J Dermatol Treat. doi:10.1080/09546634.2021.1905765
- Holloway VL. Ethnic cosmetic products. Dermatol Clin. 2003;21:743-749. doi:10.1016/s0733-8635(03)00089-5
- Amer M, Metwalli M. Topical liquiritin improves melasma. Int J Dermatol. 2000;39:299-301. doi:10.1046/j.1365-4362.2000.00943.x
- Jones K, Hughes J, Hong M, et al. Modulation of melanogenesis by aloesin: a competitive inhibitor of tyrosinase. Pigment Cell Res. 2002;15:335-340. doi:10.1034/j.1600-0749.2002.02014.x
- Hakozaki T, Minwalla L, Zhuang J, et al. The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer. Br J Dermatol. 2002;147:20-31. doi:10.1046/j.1365-2133.2002.04834.x
- Wohlrab J, Kreft D. Niacinamide—mechanisms of action and its topical use in dermatology. Skin Pharmacol Physiol. 2014;27:311-315. doi:10.1159/000359974
- Fitzpatrick RE, Rostan EF. Double-blind, half-face study comparing topical vitamin C and vehicle for rejuvenation of photodamage. Dermatol Surg. 2002;28:231-236. doi:10.1046/j.1524-4725.2002.01129.x
- Mehta AB, Nadkarni NJ, Patil SP, et al. Topical corticosteroids in dermatology. Indian J Dermatol Venereol Leprol. 2016;82:371-378. doi:10.4103/0378-6323.178903
- Petit L, Piérard GE. Skin-lightening products revisited. Int J Cosmet Sci. 2003;25:169-181. doi:10.1046/j.1467-2494.2003.00182.x
- Kanwar AJ, Dhar S, Kaur S. Treatment of melasma with potent topical corticosteroids. Dermatol Basel Switz. 1994;188:170. doi:10.1159/000247129
- Paine C, Sharlow E, Liebel F, et al. An alternative approach to depigmentation by soybean extracts via inhibition of the PAR-2 pathway. J Invest Dermatol. 2001;116:587-595. doi:10.1046/j.1523-1747.2001.01291.x
- Seiberg M, Paine C, Sharlow E, et al. Inhibition of melanosome transfer results in skin lightening. J Invest Dermatol. 2000;115:162-167. doi:10.1046/j.1523-1747.2000.00035.x
- Shimogaki H, Tanaka Y, Tamai H, et al. In vitro and in vivo evaluation of ellagic acid on melanogenesis inhibition. Int J Cosmet Sci. 2000;22:291-303. doi:10.1046/j.1467-2494.2000.00023.x
- Rendon MI, Gaviria JI. Review of skin-lightening agents. Dermatol Surg. 2005;31(7 pt 2):886-889; discussion 889. doi:10.1111/j.1524-4725.2005.31736
- Na JI, Shin JW, Choi HR, et al. Resveratrol as a multifunctional topical hypopigmenting agent [published online February 22, 2019]. Int J Mol Sci. 2019;20:956. doi:10.3390/ijms20040956
- Ratz-Łyko A, Arct J. Resveratrol as an active ingredient for cosmetic and dermatological applications: a review. J Cosmet Laser Ther. 2019;21:84-90. doi:10.1080/14764172.2018.1469767
- Choo SJ, Ryoo IJ, Kim YH, et al. Silymarin inhibits melanin synthesis in melanocyte cells. J Pharm Pharmacol. 2009;61:663-667. doi:10.1211/jpp/61.05.0016
- Draelos ZD, Diaz I, Cohen A, et al. A novel skin brightening topical technology. J Cosmet Dermatol. 2020;19:3280-3285. doi:10.1111/jocd.13741
- Grimes P, Bhawan J, Howell M, et al. Histopathological changes induced by malassezin: a novel natural microbiome indole for treatment of facial hyperpigmentation. J Drugs Dermatol. 2022;21:141-145. doi:10.36849/jdd.6596
- Bissett DL. Glucosamine: an ingredient with skin and other benefits. J Cosmet Dermatol. 2006;5:309-315. doi:10.1111/j.1473-2165.2006.00277.x
- Zhu JW, Ni YJ, Tong XY, et al. Tranexamic acid inhibits angiogenesis and melanogenesis in vitro by targeting VEGF receptors. Int J Med Sci. 2020;17:903-911. doi:10.7150/ijms.44188
- Hiramoto K, Yamate Y, Sugiyama D, et al. Tranexamic acid inhibits the plasma and non-irradiated skin markers of photoaging induced by long-term UVA eye irradiation in female mice. Biomed Pharmacother. 2018;107:54-58. doi:10.1016/j.biopha.2018.07.146
- da Silva Souza ID, Lampe L, Winn D. New topical tranexamic acid derivative for the improvement of hyperpigmentation and inflammation in the sun-damaged skin. J Cosmet Dermatol. 2021;20:561-565. doi:10.1111/jocd.13545
- Kim HJ, Moon SH, Cho SH, et al. Efficacy and safety of tranexamic acid in melasma: a meta-analysis and systematic review. Acta Derm Venereol. 2017;97:776-781. doi:10.2340/00015555-2668
- Mathe N, Balogun M, Yoo J. A case report on the use of topical cysteamine 5% cream in the management of refractory postinflammatory hyperpigmentation (PIH) resistant to triple combination cream (hydroquinone, topical corticosteroids, and retinoids). J Cosmet Dermatol. 2021;20:204-206. doi:10.1111/jocd.13755
- Mansouri P, Farshi S, Hashemi Z, et al. Evaluation of the efficacy of cysteamine 5% cream in the treatment of epidermal melasma: a randomized double-blind placebo-controlled trial. Br J Dermatol. 2015;173:209-217. doi:10.1111/bjd.13424
- Lima PB, Dias JAF, Cassiano D, et al. A comparative study of topical 5% cysteamine versus 4% hydroquinone in the treatment of facial melasma in women. Int J Dermatol. 2020;59:1531-1536. doi:10.1111/ijd.15146
Disorders of hyperpigmentation—melasma, postinflammatory hyperpigmentation, lichen planus pigmentosus, erythema dyschromicum perstans, and pigmented contact dermatitis, among others—are common and challenging to treat. Although they can affect individuals of all skin types, they most commonly are seen in skin of color; in fact, dyspigmentation is one of the most common chief concerns for which individuals of color see a dermatologist.1,2
For many years, hydroquinone (HQ) was one of the main options available for use as a lightening agent. Although effective, it has the risk of causing irritant dermatitis, potentially leading to further dyspigmentation, in addition to the risk of ochronosis with long-term use. It remains an important and useful treatment for pigmentary disorders, but there are numerous other lightening agents that also can be considered in the treatment of disorders of hyperpigmentation.
Herein, we provide recommendations for traditional and newer non-HQ lightening agents that can be considered when treating disorders of hyperpigmentation.
Traditional Non-HQ Lightening Agents
Retinoids—Retinoids are topical vitamin A derivatives that have been used safely and effectively for decades in the treatment of pigmentary disorders. Retinoids have multiple mechanisms of action in improving pigmentation. In addition to impeding tyrosinase induction, they inhibit pigment transfer to keratinocytes and lead to accelerated pigment loss due to epidermal shedding.3 Over-the-counter formulations include retinol, retinaldehyde, and adapalene. Prescription formulations include tretinoin and tazarotene in different strengths and vehicle formulations.4
Glycolic Acid—Glycolic acid is derived from sugarcane and is considered an α-hydroxy acid that leads to rapid desquamation of pigmented keratinocytes.5 Glycolic acid can not only be used in chemical peels but also in topical creams. It is the most common α-hydroxy acid peel and is sometimes paired with HQ and other topical lightening agents for increased penetration. Glycolic acid peels are available in concentrations of 20% to 70% and can be used at various depths. When used incorrectly, it can cause redness, burning, and even skin discoloration; however, when used at the proper concentrations and depth according to Fitzpatrick skin type, there typically are no notable adverse effects, and clinical results are favorable.
Kojic Acid—Kojic acid is a natural metabolite derived from fungi and is widely used in Asian countries. It works by inhibiting the catecholase activity of tyrosinase6 and typically is available in concentrations of 1% to 4%. A study suggested that a concentration of 1% or less typically is safe to use for prolonged periods without adverse effects. Although not more effective than HQ as a monotherapy, kojic acid has been shown to haveimproved efficacy when used in combination with other lightening agents.7
Azelaic Acid—Azelaic acid works by inhibiting tyrosinase, mitochondrial oxidoreductase activation, and DNA synthesis. It preferentially targets heavily pigmented melanocytes and possesses anti-inflammatory and antibacterial properties.8 A 20% concentration of azelaic acid was compared to HQ 4% for the treatment of melasma, and results revealed that the liposomal form of azelaic acid was considerably more tolerable than HQ 4% and also more effective.9
Licorice Extracts—Licorice extracts have been safely used in several cosmeceutical skin lightening products.10 The main active compounds in licorice root are glabridin and liquiritin, which work to disperse melanin. These compounds often are used topically at concentrations of 10% to 40%. A study by Amer and Metwalli11 found that topical liquiritin produced a reduction of pigmentary intensity, with 80% of patients showing an excellent response, which was described as no difference between the previously pigmented area and the normal skin surrounding it.
Aloesin—Aloesin is a low-molecular-weight glycoprotein found in aloe vera plants. Its mechanism of action includes competitive inhibition of the dihydroxyphenylalanine oxidation site, resulting in the inhibition of tyrosinase.12 It often is combined with arbutin for an enhanced lightening effect.
Niacinamide—Niacinamide is a form of vitamin B3 that works by suppressing the transfer of melanosomes to keratinocytes.13 In addition to its skin lightening effects, it also is photoprotective and antimicrobial, and its tolerability and safety have led to its inclusion in many cosmeceutical and prescription products.14
Ascorbic Acid—Ascorbic acid affects the monopherase activity of tyrosinase, thus reducing the synthesis of melanin. It also serves as an antioxidant in the skin by preventing the production of free radicals that can induce melanogenesis.15 Although it tends to be well tolerated with a low adverse effect profile, its relative instability and varying permeability can present a challenge. It is less effective as a monotherapy, so it often is combined with other lightening ingredients for greater efficacy.
Corticosteroids—Topical corticosteroids are anti-inflammatory and impact melanogenesis, though the mechanism of action of the latter has not been fully elucidated.16,17 Low- to mid-potency topical steroids often are used in conjunction with skin lightening products to diminish irritation and decrease inflammation.18 However, prolonged use of corticosteroids can lead to cutaneous adverse effects such as striae, hypopigmentation, and acne, as well as systemic side effects if there is sufficient absorption over time.
Soybean Extracts—Soybean extracts contain serine protease inhibitors that reduce the transfer of melanosomes into keratinocytes by inhibiting the PAR-2 (protease-activated receptor 2) pathway.19,20
Ellagic Acid—Ellagic acid is found in common plants such as eucalyptus and strawberry as well as green tea.21 It works as an antioxidant and decreases melanogenesis through inhibition of tyrosinase activity.
Paper Mulberry—Paper mulberry extract comes from the roots of the Broussonetia papyrifera tree and functions by inhibiting tyrosinase activity. It is widely used in South Africa and Europe.22
Resveratrol—Resveratrol is an ingredient extracted from Morus alba L and functions as an antimelanogentic agent by directly inhibiting tyrosinase as well as transcriptional and posttranscriptional processing of tyrosinase.23 It also holds antiproliferative, anti-inflammatory, and antioxidant properties and has widely been used for antiaging and skin lightening purposes.24
Newer Non-HQ Lightening Agents
Silymarin—Silymarin (also known as milk thistle [Silybum marianum]), is a polyphenolic flavonoid that possesses anticarcinogenic, antioxidant, and anti-inflammatory properties. It prevents melanin production in a dose-dependent manner by inhibiting levodopa (L-dopa) oxidation activity of tyrosinase and also reduces the expression of tyrosinase protein.25 In combination with vitamins C and E and hexylresorcinol, silymarin has been found to reduce the effects of photodamage, brighten skin, improve evenness and lines, as well as improve global facial appearance.26
Malassezin—Malassezin is an indole produced by Malessezia furfur yeast and has recently been investigated for melanogenesis suppression. Grimes et al27 assessed the efficacy of topical malassezin in 7 patients with facial hyperpigmentation applied twice daily for 14 weeks. Punch biopsies were taken at weeks 0, 8, 14, and 22. Biopsies from weeks 8 and 14 demonstrated reduced epidermal melanin compared to baseline in all participants; however, at 22 weeks, biopsies showed no difference in melanin content compared to baseline, indicating a temporary process induced by the malassezin.27 More clinical studies are needed to investigate this further.
N-acetyl-glucosamine—N-acetyl-glucosamine is an aminosaccharide that inhibits the glycosylation of tyrosinase as well as its function in melanogenesis.28 It is synthesized and included in topical products for wound healing, rhytides, moisturization, and pigmentation disorders.
Topical Tranexamic Acid—Tranexamic acid traditionally has been used orally for the treatment of menorrhagia but also has been found to be beneficial as a therapy for hyperpigmentation and erythema. Tranexamic acid interferes with plasmin activity, thus indirectly inhibiting melanogenesis while also inhibiting angiogenesis by targeting vascular endothelial growth factor (VEGF) receptors.29 It also leads to an increase in the levels of β-endorphin and μ-opioid receptors as well as the expression of estrogen receptor β on the surface of mast cells.30 Its oral benefit led to the development of topical formulations, typically in 2% to 5% concentrations. It has proven particularly beneficial in the treatment of melasma due to its effects on improving pigmentation, erythema, and skin barrier function.31 Topical tranexamic acid has a relatively high safety profile, with minor side effects such as transient skin irritation and erythema being reported.32
Cysteamine—Cysteamine inhibits tyrosinase, peroxidase, and chelating copper ions necessary for melanogenesis. It has proven to be effective in treating melasma and chronic severe postinflammatory hyperpigmentation when used in a 5% cream formulation.33,34 Lima et al35 were the first to compare the effects of topical cysteamine to HQ in the treatment of facial melasma. They found that the mean reduction in modified Melasma Area and Severity Index score was 24% for cysteamine and 41% for HQ after 60 days. There were no severe adverse effects with either treatment group.35
Final Thoughts
Hydroquinone remains the gold standard for treatment of hyperpigmentation; however, its side-effect profile and risk of ochronosis with long-term use has ushered in various other safe and effective skin lightening agents that can be used as monotherapies or in combination with other lightening agents. Many of these products also can be used effectively with procedural treatments such as chemical peels, lasers, and microneedling for enhanced absorption and efficacy. As newer agents are developed, additional well-designed studies will be needed to determine their safety and efficacy in different skin types as well as their role in the treatment of pigmentary disorders.
Disorders of hyperpigmentation—melasma, postinflammatory hyperpigmentation, lichen planus pigmentosus, erythema dyschromicum perstans, and pigmented contact dermatitis, among others—are common and challenging to treat. Although they can affect individuals of all skin types, they most commonly are seen in skin of color; in fact, dyspigmentation is one of the most common chief concerns for which individuals of color see a dermatologist.1,2
For many years, hydroquinone (HQ) was one of the main options available for use as a lightening agent. Although effective, it has the risk of causing irritant dermatitis, potentially leading to further dyspigmentation, in addition to the risk of ochronosis with long-term use. It remains an important and useful treatment for pigmentary disorders, but there are numerous other lightening agents that also can be considered in the treatment of disorders of hyperpigmentation.
Herein, we provide recommendations for traditional and newer non-HQ lightening agents that can be considered when treating disorders of hyperpigmentation.
Traditional Non-HQ Lightening Agents
Retinoids—Retinoids are topical vitamin A derivatives that have been used safely and effectively for decades in the treatment of pigmentary disorders. Retinoids have multiple mechanisms of action in improving pigmentation. In addition to impeding tyrosinase induction, they inhibit pigment transfer to keratinocytes and lead to accelerated pigment loss due to epidermal shedding.3 Over-the-counter formulations include retinol, retinaldehyde, and adapalene. Prescription formulations include tretinoin and tazarotene in different strengths and vehicle formulations.4
Glycolic Acid—Glycolic acid is derived from sugarcane and is considered an α-hydroxy acid that leads to rapid desquamation of pigmented keratinocytes.5 Glycolic acid can not only be used in chemical peels but also in topical creams. It is the most common α-hydroxy acid peel and is sometimes paired with HQ and other topical lightening agents for increased penetration. Glycolic acid peels are available in concentrations of 20% to 70% and can be used at various depths. When used incorrectly, it can cause redness, burning, and even skin discoloration; however, when used at the proper concentrations and depth according to Fitzpatrick skin type, there typically are no notable adverse effects, and clinical results are favorable.
Kojic Acid—Kojic acid is a natural metabolite derived from fungi and is widely used in Asian countries. It works by inhibiting the catecholase activity of tyrosinase6 and typically is available in concentrations of 1% to 4%. A study suggested that a concentration of 1% or less typically is safe to use for prolonged periods without adverse effects. Although not more effective than HQ as a monotherapy, kojic acid has been shown to haveimproved efficacy when used in combination with other lightening agents.7
Azelaic Acid—Azelaic acid works by inhibiting tyrosinase, mitochondrial oxidoreductase activation, and DNA synthesis. It preferentially targets heavily pigmented melanocytes and possesses anti-inflammatory and antibacterial properties.8 A 20% concentration of azelaic acid was compared to HQ 4% for the treatment of melasma, and results revealed that the liposomal form of azelaic acid was considerably more tolerable than HQ 4% and also more effective.9
Licorice Extracts—Licorice extracts have been safely used in several cosmeceutical skin lightening products.10 The main active compounds in licorice root are glabridin and liquiritin, which work to disperse melanin. These compounds often are used topically at concentrations of 10% to 40%. A study by Amer and Metwalli11 found that topical liquiritin produced a reduction of pigmentary intensity, with 80% of patients showing an excellent response, which was described as no difference between the previously pigmented area and the normal skin surrounding it.
Aloesin—Aloesin is a low-molecular-weight glycoprotein found in aloe vera plants. Its mechanism of action includes competitive inhibition of the dihydroxyphenylalanine oxidation site, resulting in the inhibition of tyrosinase.12 It often is combined with arbutin for an enhanced lightening effect.
Niacinamide—Niacinamide is a form of vitamin B3 that works by suppressing the transfer of melanosomes to keratinocytes.13 In addition to its skin lightening effects, it also is photoprotective and antimicrobial, and its tolerability and safety have led to its inclusion in many cosmeceutical and prescription products.14
Ascorbic Acid—Ascorbic acid affects the monopherase activity of tyrosinase, thus reducing the synthesis of melanin. It also serves as an antioxidant in the skin by preventing the production of free radicals that can induce melanogenesis.15 Although it tends to be well tolerated with a low adverse effect profile, its relative instability and varying permeability can present a challenge. It is less effective as a monotherapy, so it often is combined with other lightening ingredients for greater efficacy.
Corticosteroids—Topical corticosteroids are anti-inflammatory and impact melanogenesis, though the mechanism of action of the latter has not been fully elucidated.16,17 Low- to mid-potency topical steroids often are used in conjunction with skin lightening products to diminish irritation and decrease inflammation.18 However, prolonged use of corticosteroids can lead to cutaneous adverse effects such as striae, hypopigmentation, and acne, as well as systemic side effects if there is sufficient absorption over time.
Soybean Extracts—Soybean extracts contain serine protease inhibitors that reduce the transfer of melanosomes into keratinocytes by inhibiting the PAR-2 (protease-activated receptor 2) pathway.19,20
Ellagic Acid—Ellagic acid is found in common plants such as eucalyptus and strawberry as well as green tea.21 It works as an antioxidant and decreases melanogenesis through inhibition of tyrosinase activity.
Paper Mulberry—Paper mulberry extract comes from the roots of the Broussonetia papyrifera tree and functions by inhibiting tyrosinase activity. It is widely used in South Africa and Europe.22
Resveratrol—Resveratrol is an ingredient extracted from Morus alba L and functions as an antimelanogentic agent by directly inhibiting tyrosinase as well as transcriptional and posttranscriptional processing of tyrosinase.23 It also holds antiproliferative, anti-inflammatory, and antioxidant properties and has widely been used for antiaging and skin lightening purposes.24
Newer Non-HQ Lightening Agents
Silymarin—Silymarin (also known as milk thistle [Silybum marianum]), is a polyphenolic flavonoid that possesses anticarcinogenic, antioxidant, and anti-inflammatory properties. It prevents melanin production in a dose-dependent manner by inhibiting levodopa (L-dopa) oxidation activity of tyrosinase and also reduces the expression of tyrosinase protein.25 In combination with vitamins C and E and hexylresorcinol, silymarin has been found to reduce the effects of photodamage, brighten skin, improve evenness and lines, as well as improve global facial appearance.26
Malassezin—Malassezin is an indole produced by Malessezia furfur yeast and has recently been investigated for melanogenesis suppression. Grimes et al27 assessed the efficacy of topical malassezin in 7 patients with facial hyperpigmentation applied twice daily for 14 weeks. Punch biopsies were taken at weeks 0, 8, 14, and 22. Biopsies from weeks 8 and 14 demonstrated reduced epidermal melanin compared to baseline in all participants; however, at 22 weeks, biopsies showed no difference in melanin content compared to baseline, indicating a temporary process induced by the malassezin.27 More clinical studies are needed to investigate this further.
N-acetyl-glucosamine—N-acetyl-glucosamine is an aminosaccharide that inhibits the glycosylation of tyrosinase as well as its function in melanogenesis.28 It is synthesized and included in topical products for wound healing, rhytides, moisturization, and pigmentation disorders.
Topical Tranexamic Acid—Tranexamic acid traditionally has been used orally for the treatment of menorrhagia but also has been found to be beneficial as a therapy for hyperpigmentation and erythema. Tranexamic acid interferes with plasmin activity, thus indirectly inhibiting melanogenesis while also inhibiting angiogenesis by targeting vascular endothelial growth factor (VEGF) receptors.29 It also leads to an increase in the levels of β-endorphin and μ-opioid receptors as well as the expression of estrogen receptor β on the surface of mast cells.30 Its oral benefit led to the development of topical formulations, typically in 2% to 5% concentrations. It has proven particularly beneficial in the treatment of melasma due to its effects on improving pigmentation, erythema, and skin barrier function.31 Topical tranexamic acid has a relatively high safety profile, with minor side effects such as transient skin irritation and erythema being reported.32
Cysteamine—Cysteamine inhibits tyrosinase, peroxidase, and chelating copper ions necessary for melanogenesis. It has proven to be effective in treating melasma and chronic severe postinflammatory hyperpigmentation when used in a 5% cream formulation.33,34 Lima et al35 were the first to compare the effects of topical cysteamine to HQ in the treatment of facial melasma. They found that the mean reduction in modified Melasma Area and Severity Index score was 24% for cysteamine and 41% for HQ after 60 days. There were no severe adverse effects with either treatment group.35
Final Thoughts
Hydroquinone remains the gold standard for treatment of hyperpigmentation; however, its side-effect profile and risk of ochronosis with long-term use has ushered in various other safe and effective skin lightening agents that can be used as monotherapies or in combination with other lightening agents. Many of these products also can be used effectively with procedural treatments such as chemical peels, lasers, and microneedling for enhanced absorption and efficacy. As newer agents are developed, additional well-designed studies will be needed to determine their safety and efficacy in different skin types as well as their role in the treatment of pigmentary disorders.
- Woolery-Lloyd H, Kammer JN. Treatment of hyperpigmentation. Semin Cutan Med Surg. 2011;30:171-175. doi:10.1016/j.sder.2011.06.004
- Desai SR. Hyperpigmentation therapy: a review. J Clin Aesthet Dermatol. 2014;7:13-17.
- Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol. 1975;111:40-48.
- Kligman AM, Grove GL, Hirose R, et al. Topical tretinoin for photoaged skin. J Am Acad Dermatol. 1986;15(4 pt 2):836-859. doi:10.1016/s0190-9622(86)70242-9
- Sharad J. Glycolic acid peel therapy—a current review. Clin Cosmet Investig Dermatol. 2013;6:281-288. doi:10.2147/CCID.S34029
- Nautiyal A, Wairkar S. Management of hyperpigmentation: current treatments and emerging therapies. Pigment Cell Melanoma Res. 2021;34:1000-1014. doi:10.1111/pcmr.12986
- Saeedi M, Eslamifar M, Khezri K. Kojic acid applications in cosmetic and pharmaceutical preparations. Biomed Pharmacother. 2019;110:582-593. doi:10.1016/j.biopha.2018.12.006
- Schulte BC, Wu W, Rosen T. Azelaic acid: evidence-based update on mechanism of action and clinical application. J Drugs Dermatol. 2015;14:964-968.
- Akl EM. Liposomal azelaic acid 20% cream vs hydroquinone 4% cream as adjuvant to oral tranexamic acid in melasma: a comparative study [published online April 7, 2021]. J Dermatol Treat. doi:10.1080/09546634.2021.1905765
- Holloway VL. Ethnic cosmetic products. Dermatol Clin. 2003;21:743-749. doi:10.1016/s0733-8635(03)00089-5
- Amer M, Metwalli M. Topical liquiritin improves melasma. Int J Dermatol. 2000;39:299-301. doi:10.1046/j.1365-4362.2000.00943.x
- Jones K, Hughes J, Hong M, et al. Modulation of melanogenesis by aloesin: a competitive inhibitor of tyrosinase. Pigment Cell Res. 2002;15:335-340. doi:10.1034/j.1600-0749.2002.02014.x
- Hakozaki T, Minwalla L, Zhuang J, et al. The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer. Br J Dermatol. 2002;147:20-31. doi:10.1046/j.1365-2133.2002.04834.x
- Wohlrab J, Kreft D. Niacinamide—mechanisms of action and its topical use in dermatology. Skin Pharmacol Physiol. 2014;27:311-315. doi:10.1159/000359974
- Fitzpatrick RE, Rostan EF. Double-blind, half-face study comparing topical vitamin C and vehicle for rejuvenation of photodamage. Dermatol Surg. 2002;28:231-236. doi:10.1046/j.1524-4725.2002.01129.x
- Mehta AB, Nadkarni NJ, Patil SP, et al. Topical corticosteroids in dermatology. Indian J Dermatol Venereol Leprol. 2016;82:371-378. doi:10.4103/0378-6323.178903
- Petit L, Piérard GE. Skin-lightening products revisited. Int J Cosmet Sci. 2003;25:169-181. doi:10.1046/j.1467-2494.2003.00182.x
- Kanwar AJ, Dhar S, Kaur S. Treatment of melasma with potent topical corticosteroids. Dermatol Basel Switz. 1994;188:170. doi:10.1159/000247129
- Paine C, Sharlow E, Liebel F, et al. An alternative approach to depigmentation by soybean extracts via inhibition of the PAR-2 pathway. J Invest Dermatol. 2001;116:587-595. doi:10.1046/j.1523-1747.2001.01291.x
- Seiberg M, Paine C, Sharlow E, et al. Inhibition of melanosome transfer results in skin lightening. J Invest Dermatol. 2000;115:162-167. doi:10.1046/j.1523-1747.2000.00035.x
- Shimogaki H, Tanaka Y, Tamai H, et al. In vitro and in vivo evaluation of ellagic acid on melanogenesis inhibition. Int J Cosmet Sci. 2000;22:291-303. doi:10.1046/j.1467-2494.2000.00023.x
- Rendon MI, Gaviria JI. Review of skin-lightening agents. Dermatol Surg. 2005;31(7 pt 2):886-889; discussion 889. doi:10.1111/j.1524-4725.2005.31736
- Na JI, Shin JW, Choi HR, et al. Resveratrol as a multifunctional topical hypopigmenting agent [published online February 22, 2019]. Int J Mol Sci. 2019;20:956. doi:10.3390/ijms20040956
- Ratz-Łyko A, Arct J. Resveratrol as an active ingredient for cosmetic and dermatological applications: a review. J Cosmet Laser Ther. 2019;21:84-90. doi:10.1080/14764172.2018.1469767
- Choo SJ, Ryoo IJ, Kim YH, et al. Silymarin inhibits melanin synthesis in melanocyte cells. J Pharm Pharmacol. 2009;61:663-667. doi:10.1211/jpp/61.05.0016
- Draelos ZD, Diaz I, Cohen A, et al. A novel skin brightening topical technology. J Cosmet Dermatol. 2020;19:3280-3285. doi:10.1111/jocd.13741
- Grimes P, Bhawan J, Howell M, et al. Histopathological changes induced by malassezin: a novel natural microbiome indole for treatment of facial hyperpigmentation. J Drugs Dermatol. 2022;21:141-145. doi:10.36849/jdd.6596
- Bissett DL. Glucosamine: an ingredient with skin and other benefits. J Cosmet Dermatol. 2006;5:309-315. doi:10.1111/j.1473-2165.2006.00277.x
- Zhu JW, Ni YJ, Tong XY, et al. Tranexamic acid inhibits angiogenesis and melanogenesis in vitro by targeting VEGF receptors. Int J Med Sci. 2020;17:903-911. doi:10.7150/ijms.44188
- Hiramoto K, Yamate Y, Sugiyama D, et al. Tranexamic acid inhibits the plasma and non-irradiated skin markers of photoaging induced by long-term UVA eye irradiation in female mice. Biomed Pharmacother. 2018;107:54-58. doi:10.1016/j.biopha.2018.07.146
- da Silva Souza ID, Lampe L, Winn D. New topical tranexamic acid derivative for the improvement of hyperpigmentation and inflammation in the sun-damaged skin. J Cosmet Dermatol. 2021;20:561-565. doi:10.1111/jocd.13545
- Kim HJ, Moon SH, Cho SH, et al. Efficacy and safety of tranexamic acid in melasma: a meta-analysis and systematic review. Acta Derm Venereol. 2017;97:776-781. doi:10.2340/00015555-2668
- Mathe N, Balogun M, Yoo J. A case report on the use of topical cysteamine 5% cream in the management of refractory postinflammatory hyperpigmentation (PIH) resistant to triple combination cream (hydroquinone, topical corticosteroids, and retinoids). J Cosmet Dermatol. 2021;20:204-206. doi:10.1111/jocd.13755
- Mansouri P, Farshi S, Hashemi Z, et al. Evaluation of the efficacy of cysteamine 5% cream in the treatment of epidermal melasma: a randomized double-blind placebo-controlled trial. Br J Dermatol. 2015;173:209-217. doi:10.1111/bjd.13424
- Lima PB, Dias JAF, Cassiano D, et al. A comparative study of topical 5% cysteamine versus 4% hydroquinone in the treatment of facial melasma in women. Int J Dermatol. 2020;59:1531-1536. doi:10.1111/ijd.15146
- Woolery-Lloyd H, Kammer JN. Treatment of hyperpigmentation. Semin Cutan Med Surg. 2011;30:171-175. doi:10.1016/j.sder.2011.06.004
- Desai SR. Hyperpigmentation therapy: a review. J Clin Aesthet Dermatol. 2014;7:13-17.
- Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol. 1975;111:40-48.
- Kligman AM, Grove GL, Hirose R, et al. Topical tretinoin for photoaged skin. J Am Acad Dermatol. 1986;15(4 pt 2):836-859. doi:10.1016/s0190-9622(86)70242-9
- Sharad J. Glycolic acid peel therapy—a current review. Clin Cosmet Investig Dermatol. 2013;6:281-288. doi:10.2147/CCID.S34029
- Nautiyal A, Wairkar S. Management of hyperpigmentation: current treatments and emerging therapies. Pigment Cell Melanoma Res. 2021;34:1000-1014. doi:10.1111/pcmr.12986
- Saeedi M, Eslamifar M, Khezri K. Kojic acid applications in cosmetic and pharmaceutical preparations. Biomed Pharmacother. 2019;110:582-593. doi:10.1016/j.biopha.2018.12.006
- Schulte BC, Wu W, Rosen T. Azelaic acid: evidence-based update on mechanism of action and clinical application. J Drugs Dermatol. 2015;14:964-968.
- Akl EM. Liposomal azelaic acid 20% cream vs hydroquinone 4% cream as adjuvant to oral tranexamic acid in melasma: a comparative study [published online April 7, 2021]. J Dermatol Treat. doi:10.1080/09546634.2021.1905765
- Holloway VL. Ethnic cosmetic products. Dermatol Clin. 2003;21:743-749. doi:10.1016/s0733-8635(03)00089-5
- Amer M, Metwalli M. Topical liquiritin improves melasma. Int J Dermatol. 2000;39:299-301. doi:10.1046/j.1365-4362.2000.00943.x
- Jones K, Hughes J, Hong M, et al. Modulation of melanogenesis by aloesin: a competitive inhibitor of tyrosinase. Pigment Cell Res. 2002;15:335-340. doi:10.1034/j.1600-0749.2002.02014.x
- Hakozaki T, Minwalla L, Zhuang J, et al. The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer. Br J Dermatol. 2002;147:20-31. doi:10.1046/j.1365-2133.2002.04834.x
- Wohlrab J, Kreft D. Niacinamide—mechanisms of action and its topical use in dermatology. Skin Pharmacol Physiol. 2014;27:311-315. doi:10.1159/000359974
- Fitzpatrick RE, Rostan EF. Double-blind, half-face study comparing topical vitamin C and vehicle for rejuvenation of photodamage. Dermatol Surg. 2002;28:231-236. doi:10.1046/j.1524-4725.2002.01129.x
- Mehta AB, Nadkarni NJ, Patil SP, et al. Topical corticosteroids in dermatology. Indian J Dermatol Venereol Leprol. 2016;82:371-378. doi:10.4103/0378-6323.178903
- Petit L, Piérard GE. Skin-lightening products revisited. Int J Cosmet Sci. 2003;25:169-181. doi:10.1046/j.1467-2494.2003.00182.x
- Kanwar AJ, Dhar S, Kaur S. Treatment of melasma with potent topical corticosteroids. Dermatol Basel Switz. 1994;188:170. doi:10.1159/000247129
- Paine C, Sharlow E, Liebel F, et al. An alternative approach to depigmentation by soybean extracts via inhibition of the PAR-2 pathway. J Invest Dermatol. 2001;116:587-595. doi:10.1046/j.1523-1747.2001.01291.x
- Seiberg M, Paine C, Sharlow E, et al. Inhibition of melanosome transfer results in skin lightening. J Invest Dermatol. 2000;115:162-167. doi:10.1046/j.1523-1747.2000.00035.x
- Shimogaki H, Tanaka Y, Tamai H, et al. In vitro and in vivo evaluation of ellagic acid on melanogenesis inhibition. Int J Cosmet Sci. 2000;22:291-303. doi:10.1046/j.1467-2494.2000.00023.x
- Rendon MI, Gaviria JI. Review of skin-lightening agents. Dermatol Surg. 2005;31(7 pt 2):886-889; discussion 889. doi:10.1111/j.1524-4725.2005.31736
- Na JI, Shin JW, Choi HR, et al. Resveratrol as a multifunctional topical hypopigmenting agent [published online February 22, 2019]. Int J Mol Sci. 2019;20:956. doi:10.3390/ijms20040956
- Ratz-Łyko A, Arct J. Resveratrol as an active ingredient for cosmetic and dermatological applications: a review. J Cosmet Laser Ther. 2019;21:84-90. doi:10.1080/14764172.2018.1469767
- Choo SJ, Ryoo IJ, Kim YH, et al. Silymarin inhibits melanin synthesis in melanocyte cells. J Pharm Pharmacol. 2009;61:663-667. doi:10.1211/jpp/61.05.0016
- Draelos ZD, Diaz I, Cohen A, et al. A novel skin brightening topical technology. J Cosmet Dermatol. 2020;19:3280-3285. doi:10.1111/jocd.13741
- Grimes P, Bhawan J, Howell M, et al. Histopathological changes induced by malassezin: a novel natural microbiome indole for treatment of facial hyperpigmentation. J Drugs Dermatol. 2022;21:141-145. doi:10.36849/jdd.6596
- Bissett DL. Glucosamine: an ingredient with skin and other benefits. J Cosmet Dermatol. 2006;5:309-315. doi:10.1111/j.1473-2165.2006.00277.x
- Zhu JW, Ni YJ, Tong XY, et al. Tranexamic acid inhibits angiogenesis and melanogenesis in vitro by targeting VEGF receptors. Int J Med Sci. 2020;17:903-911. doi:10.7150/ijms.44188
- Hiramoto K, Yamate Y, Sugiyama D, et al. Tranexamic acid inhibits the plasma and non-irradiated skin markers of photoaging induced by long-term UVA eye irradiation in female mice. Biomed Pharmacother. 2018;107:54-58. doi:10.1016/j.biopha.2018.07.146
- da Silva Souza ID, Lampe L, Winn D. New topical tranexamic acid derivative for the improvement of hyperpigmentation and inflammation in the sun-damaged skin. J Cosmet Dermatol. 2021;20:561-565. doi:10.1111/jocd.13545
- Kim HJ, Moon SH, Cho SH, et al. Efficacy and safety of tranexamic acid in melasma: a meta-analysis and systematic review. Acta Derm Venereol. 2017;97:776-781. doi:10.2340/00015555-2668
- Mathe N, Balogun M, Yoo J. A case report on the use of topical cysteamine 5% cream in the management of refractory postinflammatory hyperpigmentation (PIH) resistant to triple combination cream (hydroquinone, topical corticosteroids, and retinoids). J Cosmet Dermatol. 2021;20:204-206. doi:10.1111/jocd.13755
- Mansouri P, Farshi S, Hashemi Z, et al. Evaluation of the efficacy of cysteamine 5% cream in the treatment of epidermal melasma: a randomized double-blind placebo-controlled trial. Br J Dermatol. 2015;173:209-217. doi:10.1111/bjd.13424
- Lima PB, Dias JAF, Cassiano D, et al. A comparative study of topical 5% cysteamine versus 4% hydroquinone in the treatment of facial melasma in women. Int J Dermatol. 2020;59:1531-1536. doi:10.1111/ijd.15146
The power of napping
As a physician who has had a career-long obsession with the underappreciated value of sleep, a recent study published in the journal Child Development caught my eye. The findings presented by a group of Australian-based psychologists and educators suggest a positive association between napping and learning by preschool children. While the study itself relied on a very small sample and may not prove to be repeatable, the authors included in their introduction an excellent discussion of a large collection of recent studies supporting the educational benefit of sleep in general and napping in particular.
Although sleep seems to finally be receiving some of the attention it deserves, I am still concerned that as a profession we are failing to give it the appropriate weight at our health maintenance visits. This is particularly true of napping. Understandably, napping doesn’t feel urgent to parents in those turbulent first 4 or 5 months of night wakings and erratic settling. However, as a child approaches the 6-month milestone, napping is a topic ripe for well-considered anticipatory guidance.
When the recurrent cycles of awake-eat-sleep begin to develop into a somewhat predictable pattern and solid food is introduced, it’s time to suggest to parents a strategy that will encourage a napping pattern that will hopefully habituate into toddlerhood and beyond.
It can begin simply as a matter of defining the feeding in the middle of the day as lunch and then programming the period immediately following that meal as a siesta – a segment of the day completely reserved for rest. Many warm-weather countries have been using this strategy for centuries. Try to go to the pharmacy to pick up a prescription at 2 o’clock in the afternoon in rural Spain. It just ain’t gonna happen.
Most adults and children I know seem to be sleepy during this midday postprandial period. It makes more than a little sense to harness this natural drowsiness into creating a napping habit. However, the challenge for many young families is controlling their schedule to create a period of time when nothing else is going on in the child’s environment, leaving sleep as the only option. For some parents this requires the discipline to pause their own lives long enough so that the children realize that they aren’t missing out on something fun. This means no TV, no phone conversations, no visitors. Obviously, it also means not scheduling any appointments during this siesta period. Skilled day care providers have been doing this for years. But the message hasn’t seeped into the general population and sadly I occasionally see mothers with toddlers in the grocery store at 1 in the afternoon.
Once the nap/siesta is firmly welded to lunch, this gives the parent the ability to make minor adjustments that reflect the child’s stamina. If the child seems to be tiring/getting grumpy, serve up lunch a bit early and the restorative nap follows. As the child gets older and his or her stamina improves he or she may not be sleepy but the siesta remains as a quiet time. Some days it may be a nap, some days just a rest for an hour. By counseling parents to define the period after lunch as a siesta you will be helping them avoid that dreaded transition period called “giving up the nap.”
You may already be including this strategy in your anticipatory guidance. It may help to add to your advice the accumulating evidence that napping may play an important role in the child’s development and education.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
As a physician who has had a career-long obsession with the underappreciated value of sleep, a recent study published in the journal Child Development caught my eye. The findings presented by a group of Australian-based psychologists and educators suggest a positive association between napping and learning by preschool children. While the study itself relied on a very small sample and may not prove to be repeatable, the authors included in their introduction an excellent discussion of a large collection of recent studies supporting the educational benefit of sleep in general and napping in particular.
Although sleep seems to finally be receiving some of the attention it deserves, I am still concerned that as a profession we are failing to give it the appropriate weight at our health maintenance visits. This is particularly true of napping. Understandably, napping doesn’t feel urgent to parents in those turbulent first 4 or 5 months of night wakings and erratic settling. However, as a child approaches the 6-month milestone, napping is a topic ripe for well-considered anticipatory guidance.
When the recurrent cycles of awake-eat-sleep begin to develop into a somewhat predictable pattern and solid food is introduced, it’s time to suggest to parents a strategy that will encourage a napping pattern that will hopefully habituate into toddlerhood and beyond.
It can begin simply as a matter of defining the feeding in the middle of the day as lunch and then programming the period immediately following that meal as a siesta – a segment of the day completely reserved for rest. Many warm-weather countries have been using this strategy for centuries. Try to go to the pharmacy to pick up a prescription at 2 o’clock in the afternoon in rural Spain. It just ain’t gonna happen.
Most adults and children I know seem to be sleepy during this midday postprandial period. It makes more than a little sense to harness this natural drowsiness into creating a napping habit. However, the challenge for many young families is controlling their schedule to create a period of time when nothing else is going on in the child’s environment, leaving sleep as the only option. For some parents this requires the discipline to pause their own lives long enough so that the children realize that they aren’t missing out on something fun. This means no TV, no phone conversations, no visitors. Obviously, it also means not scheduling any appointments during this siesta period. Skilled day care providers have been doing this for years. But the message hasn’t seeped into the general population and sadly I occasionally see mothers with toddlers in the grocery store at 1 in the afternoon.
Once the nap/siesta is firmly welded to lunch, this gives the parent the ability to make minor adjustments that reflect the child’s stamina. If the child seems to be tiring/getting grumpy, serve up lunch a bit early and the restorative nap follows. As the child gets older and his or her stamina improves he or she may not be sleepy but the siesta remains as a quiet time. Some days it may be a nap, some days just a rest for an hour. By counseling parents to define the period after lunch as a siesta you will be helping them avoid that dreaded transition period called “giving up the nap.”
You may already be including this strategy in your anticipatory guidance. It may help to add to your advice the accumulating evidence that napping may play an important role in the child’s development and education.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
As a physician who has had a career-long obsession with the underappreciated value of sleep, a recent study published in the journal Child Development caught my eye. The findings presented by a group of Australian-based psychologists and educators suggest a positive association between napping and learning by preschool children. While the study itself relied on a very small sample and may not prove to be repeatable, the authors included in their introduction an excellent discussion of a large collection of recent studies supporting the educational benefit of sleep in general and napping in particular.
Although sleep seems to finally be receiving some of the attention it deserves, I am still concerned that as a profession we are failing to give it the appropriate weight at our health maintenance visits. This is particularly true of napping. Understandably, napping doesn’t feel urgent to parents in those turbulent first 4 or 5 months of night wakings and erratic settling. However, as a child approaches the 6-month milestone, napping is a topic ripe for well-considered anticipatory guidance.
When the recurrent cycles of awake-eat-sleep begin to develop into a somewhat predictable pattern and solid food is introduced, it’s time to suggest to parents a strategy that will encourage a napping pattern that will hopefully habituate into toddlerhood and beyond.
It can begin simply as a matter of defining the feeding in the middle of the day as lunch and then programming the period immediately following that meal as a siesta – a segment of the day completely reserved for rest. Many warm-weather countries have been using this strategy for centuries. Try to go to the pharmacy to pick up a prescription at 2 o’clock in the afternoon in rural Spain. It just ain’t gonna happen.
Most adults and children I know seem to be sleepy during this midday postprandial period. It makes more than a little sense to harness this natural drowsiness into creating a napping habit. However, the challenge for many young families is controlling their schedule to create a period of time when nothing else is going on in the child’s environment, leaving sleep as the only option. For some parents this requires the discipline to pause their own lives long enough so that the children realize that they aren’t missing out on something fun. This means no TV, no phone conversations, no visitors. Obviously, it also means not scheduling any appointments during this siesta period. Skilled day care providers have been doing this for years. But the message hasn’t seeped into the general population and sadly I occasionally see mothers with toddlers in the grocery store at 1 in the afternoon.
Once the nap/siesta is firmly welded to lunch, this gives the parent the ability to make minor adjustments that reflect the child’s stamina. If the child seems to be tiring/getting grumpy, serve up lunch a bit early and the restorative nap follows. As the child gets older and his or her stamina improves he or she may not be sleepy but the siesta remains as a quiet time. Some days it may be a nap, some days just a rest for an hour. By counseling parents to define the period after lunch as a siesta you will be helping them avoid that dreaded transition period called “giving up the nap.”
You may already be including this strategy in your anticipatory guidance. It may help to add to your advice the accumulating evidence that napping may play an important role in the child’s development and education.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Childhood cardiovascular risks and longevity
Now hot off the press from the “always-guessed-it-was-true-but-now-you-know-it” department comes a multinational study that looked at childhood cardiovascular risk factors and longevity.
Using data collected from individuals in Finland, Australia, and the United States the International Childhood Cardiovascular Cohorts Consortium Outcomes Study investigators sought links between subjects’ body mass index, systolic blood pressure, total cholesterol, blood triglyceride level, and smoking in childhood with cardiovascular disease and outcomes as they aged into adulthood.
The children were initially enrolled in the 1970s and 1980s. The adult evaluations were done in 2015-2019 when the subjects’ average age was 46. Of the 40,000 individuals who originally entered the study, 800 were found to have cardiovascular events of which over 300 had resulted in death. I found these numbers a bit surprising given the relatively young age at which the follow-up data were collected.
What was less surprising is that people with higher than normal values for all five risk factors as children had nearly three times the risk of cardiovascular disease as adults. Researchers found that smoking at a young age was biggest risk factor with body mass index, systolic blood pressure, blood triglycerides, and cholesterol following in descending order. They also found that adults who were obese as children had triple the risk of cardiovascular disease as adults. High blood pressure in childhood doubled the risk.
It will be interesting to see if and how these trends change as the study population ages. It could be that the effect of these childhood risk factors is blunted as the those segments at the highest risk die off and/or risk- associated behaviors adopted in adulthood become more prominent. But, it feels more likely that the childhood risk factors will remain as major contributors.
Is this just another ho-hum-told-you-so study or does it have some special relevance for us as pediatricians? At a minimum these findings should inspire us to stick with our calling to commit ourselves to the health of children. A healthy adult population is clearly our legacy.
Of course the two individual risk factors in childhood that appear to be the most potent in adulthood, obesity and smoking, are also the most frustrating for pediatricians to address. However, the study suggests that we should rejoice in those few successes when we achieve them. Childhood obesity has been a tough nut to crack. On the other hand, the societal change that has made great strides in adult smoking over the last half century should encourage us that our work with the pediatric population will eventually bring rewards.
Smoking and obesity can include components of both patient and parental behavior. Monitoring cholesterol, triglycerides, and blood pressure hinges on our behavior as providers. Although there have been recent recommendations that we be more attentive, we don’t have a strong history when it comes to detecting and addressing high blood pressure in children. This study should serve as an another reminder to take blood pressure more seriously.
I was surprised and somewhat disappointed that I first learned about the results of this study in an email newsletter from the medical school I attended. I would have hoped that a paper like this from a well known peer-reviewed journal with a clear message about the relationship of childhood health and longevity should have been picked up quickly by the lay press. Again, this leaves it to us to promote the message that the health of children is important in and of itself but plays a critical role in the health of adults.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Now hot off the press from the “always-guessed-it-was-true-but-now-you-know-it” department comes a multinational study that looked at childhood cardiovascular risk factors and longevity.
Using data collected from individuals in Finland, Australia, and the United States the International Childhood Cardiovascular Cohorts Consortium Outcomes Study investigators sought links between subjects’ body mass index, systolic blood pressure, total cholesterol, blood triglyceride level, and smoking in childhood with cardiovascular disease and outcomes as they aged into adulthood.
The children were initially enrolled in the 1970s and 1980s. The adult evaluations were done in 2015-2019 when the subjects’ average age was 46. Of the 40,000 individuals who originally entered the study, 800 were found to have cardiovascular events of which over 300 had resulted in death. I found these numbers a bit surprising given the relatively young age at which the follow-up data were collected.
What was less surprising is that people with higher than normal values for all five risk factors as children had nearly three times the risk of cardiovascular disease as adults. Researchers found that smoking at a young age was biggest risk factor with body mass index, systolic blood pressure, blood triglycerides, and cholesterol following in descending order. They also found that adults who were obese as children had triple the risk of cardiovascular disease as adults. High blood pressure in childhood doubled the risk.
It will be interesting to see if and how these trends change as the study population ages. It could be that the effect of these childhood risk factors is blunted as the those segments at the highest risk die off and/or risk- associated behaviors adopted in adulthood become more prominent. But, it feels more likely that the childhood risk factors will remain as major contributors.
Is this just another ho-hum-told-you-so study or does it have some special relevance for us as pediatricians? At a minimum these findings should inspire us to stick with our calling to commit ourselves to the health of children. A healthy adult population is clearly our legacy.
Of course the two individual risk factors in childhood that appear to be the most potent in adulthood, obesity and smoking, are also the most frustrating for pediatricians to address. However, the study suggests that we should rejoice in those few successes when we achieve them. Childhood obesity has been a tough nut to crack. On the other hand, the societal change that has made great strides in adult smoking over the last half century should encourage us that our work with the pediatric population will eventually bring rewards.
Smoking and obesity can include components of both patient and parental behavior. Monitoring cholesterol, triglycerides, and blood pressure hinges on our behavior as providers. Although there have been recent recommendations that we be more attentive, we don’t have a strong history when it comes to detecting and addressing high blood pressure in children. This study should serve as an another reminder to take blood pressure more seriously.
I was surprised and somewhat disappointed that I first learned about the results of this study in an email newsletter from the medical school I attended. I would have hoped that a paper like this from a well known peer-reviewed journal with a clear message about the relationship of childhood health and longevity should have been picked up quickly by the lay press. Again, this leaves it to us to promote the message that the health of children is important in and of itself but plays a critical role in the health of adults.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Now hot off the press from the “always-guessed-it-was-true-but-now-you-know-it” department comes a multinational study that looked at childhood cardiovascular risk factors and longevity.
Using data collected from individuals in Finland, Australia, and the United States the International Childhood Cardiovascular Cohorts Consortium Outcomes Study investigators sought links between subjects’ body mass index, systolic blood pressure, total cholesterol, blood triglyceride level, and smoking in childhood with cardiovascular disease and outcomes as they aged into adulthood.
The children were initially enrolled in the 1970s and 1980s. The adult evaluations were done in 2015-2019 when the subjects’ average age was 46. Of the 40,000 individuals who originally entered the study, 800 were found to have cardiovascular events of which over 300 had resulted in death. I found these numbers a bit surprising given the relatively young age at which the follow-up data were collected.
What was less surprising is that people with higher than normal values for all five risk factors as children had nearly three times the risk of cardiovascular disease as adults. Researchers found that smoking at a young age was biggest risk factor with body mass index, systolic blood pressure, blood triglycerides, and cholesterol following in descending order. They also found that adults who were obese as children had triple the risk of cardiovascular disease as adults. High blood pressure in childhood doubled the risk.
It will be interesting to see if and how these trends change as the study population ages. It could be that the effect of these childhood risk factors is blunted as the those segments at the highest risk die off and/or risk- associated behaviors adopted in adulthood become more prominent. But, it feels more likely that the childhood risk factors will remain as major contributors.
Is this just another ho-hum-told-you-so study or does it have some special relevance for us as pediatricians? At a minimum these findings should inspire us to stick with our calling to commit ourselves to the health of children. A healthy adult population is clearly our legacy.
Of course the two individual risk factors in childhood that appear to be the most potent in adulthood, obesity and smoking, are also the most frustrating for pediatricians to address. However, the study suggests that we should rejoice in those few successes when we achieve them. Childhood obesity has been a tough nut to crack. On the other hand, the societal change that has made great strides in adult smoking over the last half century should encourage us that our work with the pediatric population will eventually bring rewards.
Smoking and obesity can include components of both patient and parental behavior. Monitoring cholesterol, triglycerides, and blood pressure hinges on our behavior as providers. Although there have been recent recommendations that we be more attentive, we don’t have a strong history when it comes to detecting and addressing high blood pressure in children. This study should serve as an another reminder to take blood pressure more seriously.
I was surprised and somewhat disappointed that I first learned about the results of this study in an email newsletter from the medical school I attended. I would have hoped that a paper like this from a well known peer-reviewed journal with a clear message about the relationship of childhood health and longevity should have been picked up quickly by the lay press. Again, this leaves it to us to promote the message that the health of children is important in and of itself but plays a critical role in the health of adults.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
The mental health of health care professionals takes center stage
Mental illness has been waiting in the wings for years; ignored, ridiculed, minimized, and stigmatized. Those who succumbed to it tried to lend testimonials, but to no avail. Those who were spared its effects remained in disbelief. So, it stayed on the sidelines, growing in intensity and breadth, yet stifled by the masses, until 2 years ago.
In March 2020, when COVID-19 became a pandemic, the importance of mental health finally became undeniable. As the pandemic’s effects progressed and wreaked havoc on our nation, our mental illness rates simultaneously surged. This surge paralleled that of the COVID-19 pandemic’s and in fact, contributed to a secondary crisis, allowing mental health to finally be addressed and gain center stage status.
But “mental health” is not easily defined, as it takes on many forms and is expressed in a variety of ways and via a myriad of symptoms. It does not discriminate by gender, race, age, socioeconomic status, educational level, profession, religion, or geography. At times, mental health status is consistent but at other times it can fluctuate in intensity, duration, and expression. It can be difficult to manage, yet there are various treatment modalities that can be implemented to lessen the impact of mental illness. Stressful events seem to potentiate its manifestation and yet, there are times it seems to appear spontaneously, much as an uninvited guest.
Mental health has a strong synergistic relationship with physical health, as they are very interdependent and allow us to function at our best only when they are both operating optimally. It should come as no surprise then, that the COVID-19 pandemic contributed to the exponential surge of mental illnesses. Capitalizing on its nondiscriminatory nature, mental illness impacted a large segment of the population – both those suffering from COVID-19 as well as those treating them.
As the nation starts to heal from the immediate and lingering physical and emotional consequences of the COVID-19 pandemic, President Biden has chosen to address and try to meet the needs of the health care heroes, the healers. The signing of H.R. 1667, the Dr. Lorna Breen Health Care Provider Protection Act into law on March 18, 2022, showed dedication to the health care community that has given tirelessly to our nation during the COVID-19 pandemic, and is itself recuperating from that effort.
Taking a top-down approach is essential to assuring the health of the nation. If our healers are not healthy, physically and mentally, they will not be able treat those whom they are dedicated to helping. Openly discussing and acknowledging the mental health problems of health care workers as a community makes it okay to not be okay. It normalizes the need for health care workers to prioritize their own mental health. It can also start to ease the fear of professional backlash or repercussions for practicing self-care.
I, for one, am very grateful for the prioritizing and promoting of the importance of mental health and wellness amongst health care workers. This helps to reduce the stigma of mental illness, helps us understand its impact, and allows us to formulate strategies and solutions to address its effects. The time has come.
Dr. Jarkon is a psychiatrist and director of the Center for Behavioral Health at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y.
Mental illness has been waiting in the wings for years; ignored, ridiculed, minimized, and stigmatized. Those who succumbed to it tried to lend testimonials, but to no avail. Those who were spared its effects remained in disbelief. So, it stayed on the sidelines, growing in intensity and breadth, yet stifled by the masses, until 2 years ago.
In March 2020, when COVID-19 became a pandemic, the importance of mental health finally became undeniable. As the pandemic’s effects progressed and wreaked havoc on our nation, our mental illness rates simultaneously surged. This surge paralleled that of the COVID-19 pandemic’s and in fact, contributed to a secondary crisis, allowing mental health to finally be addressed and gain center stage status.
But “mental health” is not easily defined, as it takes on many forms and is expressed in a variety of ways and via a myriad of symptoms. It does not discriminate by gender, race, age, socioeconomic status, educational level, profession, religion, or geography. At times, mental health status is consistent but at other times it can fluctuate in intensity, duration, and expression. It can be difficult to manage, yet there are various treatment modalities that can be implemented to lessen the impact of mental illness. Stressful events seem to potentiate its manifestation and yet, there are times it seems to appear spontaneously, much as an uninvited guest.
Mental health has a strong synergistic relationship with physical health, as they are very interdependent and allow us to function at our best only when they are both operating optimally. It should come as no surprise then, that the COVID-19 pandemic contributed to the exponential surge of mental illnesses. Capitalizing on its nondiscriminatory nature, mental illness impacted a large segment of the population – both those suffering from COVID-19 as well as those treating them.
As the nation starts to heal from the immediate and lingering physical and emotional consequences of the COVID-19 pandemic, President Biden has chosen to address and try to meet the needs of the health care heroes, the healers. The signing of H.R. 1667, the Dr. Lorna Breen Health Care Provider Protection Act into law on March 18, 2022, showed dedication to the health care community that has given tirelessly to our nation during the COVID-19 pandemic, and is itself recuperating from that effort.
Taking a top-down approach is essential to assuring the health of the nation. If our healers are not healthy, physically and mentally, they will not be able treat those whom they are dedicated to helping. Openly discussing and acknowledging the mental health problems of health care workers as a community makes it okay to not be okay. It normalizes the need for health care workers to prioritize their own mental health. It can also start to ease the fear of professional backlash or repercussions for practicing self-care.
I, for one, am very grateful for the prioritizing and promoting of the importance of mental health and wellness amongst health care workers. This helps to reduce the stigma of mental illness, helps us understand its impact, and allows us to formulate strategies and solutions to address its effects. The time has come.
Dr. Jarkon is a psychiatrist and director of the Center for Behavioral Health at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y.
Mental illness has been waiting in the wings for years; ignored, ridiculed, minimized, and stigmatized. Those who succumbed to it tried to lend testimonials, but to no avail. Those who were spared its effects remained in disbelief. So, it stayed on the sidelines, growing in intensity and breadth, yet stifled by the masses, until 2 years ago.
In March 2020, when COVID-19 became a pandemic, the importance of mental health finally became undeniable. As the pandemic’s effects progressed and wreaked havoc on our nation, our mental illness rates simultaneously surged. This surge paralleled that of the COVID-19 pandemic’s and in fact, contributed to a secondary crisis, allowing mental health to finally be addressed and gain center stage status.
But “mental health” is not easily defined, as it takes on many forms and is expressed in a variety of ways and via a myriad of symptoms. It does not discriminate by gender, race, age, socioeconomic status, educational level, profession, religion, or geography. At times, mental health status is consistent but at other times it can fluctuate in intensity, duration, and expression. It can be difficult to manage, yet there are various treatment modalities that can be implemented to lessen the impact of mental illness. Stressful events seem to potentiate its manifestation and yet, there are times it seems to appear spontaneously, much as an uninvited guest.
Mental health has a strong synergistic relationship with physical health, as they are very interdependent and allow us to function at our best only when they are both operating optimally. It should come as no surprise then, that the COVID-19 pandemic contributed to the exponential surge of mental illnesses. Capitalizing on its nondiscriminatory nature, mental illness impacted a large segment of the population – both those suffering from COVID-19 as well as those treating them.
As the nation starts to heal from the immediate and lingering physical and emotional consequences of the COVID-19 pandemic, President Biden has chosen to address and try to meet the needs of the health care heroes, the healers. The signing of H.R. 1667, the Dr. Lorna Breen Health Care Provider Protection Act into law on March 18, 2022, showed dedication to the health care community that has given tirelessly to our nation during the COVID-19 pandemic, and is itself recuperating from that effort.
Taking a top-down approach is essential to assuring the health of the nation. If our healers are not healthy, physically and mentally, they will not be able treat those whom they are dedicated to helping. Openly discussing and acknowledging the mental health problems of health care workers as a community makes it okay to not be okay. It normalizes the need for health care workers to prioritize their own mental health. It can also start to ease the fear of professional backlash or repercussions for practicing self-care.
I, for one, am very grateful for the prioritizing and promoting of the importance of mental health and wellness amongst health care workers. This helps to reduce the stigma of mental illness, helps us understand its impact, and allows us to formulate strategies and solutions to address its effects. The time has come.
Dr. Jarkon is a psychiatrist and director of the Center for Behavioral Health at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y.
Are teenagers tone deaf?
I suspect that you have heard or read about the recent study in the Journal of Neuroscience that claims to have discovered evidence that as children become teenagers, their brains begin to tune out their mother’s voices. The story appeared in at least 10 Internet news sources including the American Academy of Pediatrics’ daily briefing.
Based on functional MRI studies by a group at Stanford (Calif.) University, the researchers found that while in general, teenagers became more attentive to all voices as they reached puberty, novel voices were favored over the maternal voices that had flooded their environment as younger children. Of course none of this comes as a surprise to anyone who has parented a teenager or spent any time trying to communicate with adolescents. Although we all must be a bit careful not to put too much stock in functional MRI studies, these findings do suggest a physiologic basis for the peer pressure that becomes one of the hallmarks of adolescence. I wouldn’t be surprised if some clever entrepreneur has already begun using MRI to search for just the right tonal qualities that will make the perfect Internet influencer.
But, will these MRI studies help parents who have already thrown up their arms and admitted defeat mumbling, “He’s stopped listening to me?” The more observant parents already realized long ago that their words were often the least effective tools in their tool kit when it comes to modifying behavior.
Just listen in any neighborhood playground or grocery store to how often you hear a parent trying to get a toddler or young child to correct a misbehavior using threats or promises that you and everyone else within earshot knows will never be followed by any consequence. How often do you see a parent modeling behaviors that they expect their children to avoid?
Some more “enlightened” parents will avoid threats and instead attempt to engage in a dialogue with their misbehaving child hoping that a rational discussion with a sleep-deprived toddler in full tantrum mode can convince the youngster to self-correct.
I’m sure you learned and may have even used the playground retort “sticks and stones may break my bones but words will never hurt me.” Of course more untrue words were never spoken. Words can hurt and they can scar. But words and threats can also be hollow and will fall on ears deafened by months and years during which there were no consequences. It is certainly nice to know that there is some physiologic correlation to what we all suspected. The good news is that teenagers are still listening to us, although they are increasingly more interested in what their peers and the rest of the world has to say.
What the study fails to point out is that while teenagers may still be listening to us their behavior is molded not so much by what we say but how we as parents and adults behave. Have we parented in a way in which our words are followed up with appropriate consequences? And, more importantly, have we modeled behavior that matches our words? We need to help parents realize that words can be important but parenting by example is the gold standard.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
I suspect that you have heard or read about the recent study in the Journal of Neuroscience that claims to have discovered evidence that as children become teenagers, their brains begin to tune out their mother’s voices. The story appeared in at least 10 Internet news sources including the American Academy of Pediatrics’ daily briefing.
Based on functional MRI studies by a group at Stanford (Calif.) University, the researchers found that while in general, teenagers became more attentive to all voices as they reached puberty, novel voices were favored over the maternal voices that had flooded their environment as younger children. Of course none of this comes as a surprise to anyone who has parented a teenager or spent any time trying to communicate with adolescents. Although we all must be a bit careful not to put too much stock in functional MRI studies, these findings do suggest a physiologic basis for the peer pressure that becomes one of the hallmarks of adolescence. I wouldn’t be surprised if some clever entrepreneur has already begun using MRI to search for just the right tonal qualities that will make the perfect Internet influencer.
But, will these MRI studies help parents who have already thrown up their arms and admitted defeat mumbling, “He’s stopped listening to me?” The more observant parents already realized long ago that their words were often the least effective tools in their tool kit when it comes to modifying behavior.
Just listen in any neighborhood playground or grocery store to how often you hear a parent trying to get a toddler or young child to correct a misbehavior using threats or promises that you and everyone else within earshot knows will never be followed by any consequence. How often do you see a parent modeling behaviors that they expect their children to avoid?
Some more “enlightened” parents will avoid threats and instead attempt to engage in a dialogue with their misbehaving child hoping that a rational discussion with a sleep-deprived toddler in full tantrum mode can convince the youngster to self-correct.
I’m sure you learned and may have even used the playground retort “sticks and stones may break my bones but words will never hurt me.” Of course more untrue words were never spoken. Words can hurt and they can scar. But words and threats can also be hollow and will fall on ears deafened by months and years during which there were no consequences. It is certainly nice to know that there is some physiologic correlation to what we all suspected. The good news is that teenagers are still listening to us, although they are increasingly more interested in what their peers and the rest of the world has to say.
What the study fails to point out is that while teenagers may still be listening to us their behavior is molded not so much by what we say but how we as parents and adults behave. Have we parented in a way in which our words are followed up with appropriate consequences? And, more importantly, have we modeled behavior that matches our words? We need to help parents realize that words can be important but parenting by example is the gold standard.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
I suspect that you have heard or read about the recent study in the Journal of Neuroscience that claims to have discovered evidence that as children become teenagers, their brains begin to tune out their mother’s voices. The story appeared in at least 10 Internet news sources including the American Academy of Pediatrics’ daily briefing.
Based on functional MRI studies by a group at Stanford (Calif.) University, the researchers found that while in general, teenagers became more attentive to all voices as they reached puberty, novel voices were favored over the maternal voices that had flooded their environment as younger children. Of course none of this comes as a surprise to anyone who has parented a teenager or spent any time trying to communicate with adolescents. Although we all must be a bit careful not to put too much stock in functional MRI studies, these findings do suggest a physiologic basis for the peer pressure that becomes one of the hallmarks of adolescence. I wouldn’t be surprised if some clever entrepreneur has already begun using MRI to search for just the right tonal qualities that will make the perfect Internet influencer.
But, will these MRI studies help parents who have already thrown up their arms and admitted defeat mumbling, “He’s stopped listening to me?” The more observant parents already realized long ago that their words were often the least effective tools in their tool kit when it comes to modifying behavior.
Just listen in any neighborhood playground or grocery store to how often you hear a parent trying to get a toddler or young child to correct a misbehavior using threats or promises that you and everyone else within earshot knows will never be followed by any consequence. How often do you see a parent modeling behaviors that they expect their children to avoid?
Some more “enlightened” parents will avoid threats and instead attempt to engage in a dialogue with their misbehaving child hoping that a rational discussion with a sleep-deprived toddler in full tantrum mode can convince the youngster to self-correct.
I’m sure you learned and may have even used the playground retort “sticks and stones may break my bones but words will never hurt me.” Of course more untrue words were never spoken. Words can hurt and they can scar. But words and threats can also be hollow and will fall on ears deafened by months and years during which there were no consequences. It is certainly nice to know that there is some physiologic correlation to what we all suspected. The good news is that teenagers are still listening to us, although they are increasingly more interested in what their peers and the rest of the world has to say.
What the study fails to point out is that while teenagers may still be listening to us their behavior is molded not so much by what we say but how we as parents and adults behave. Have we parented in a way in which our words are followed up with appropriate consequences? And, more importantly, have we modeled behavior that matches our words? We need to help parents realize that words can be important but parenting by example is the gold standard.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Informal human-milk donation: How to counsel patients
I have become obsessed with the reality that the unprecedented national shortage of formula is keeping some families from adequately feeding their infants and young children. I am deeply concerned, both as a family medicine physician and a new mother, about the heartbreaking stories that I’ve heard from parents of all socioeconomic backgrounds. New mothers, unable to breastfeed for a multitude of reasons, find themselves standing in front of empty store shelves, in tears.
In recent months, many health care providers have had patients disclose that they are diluting ready-to-feed formula or mixing powdered formula with more water than instructed to make it go further. Some parents are giving cow’s milk to their children at too young an age because they can’t find formula. Others are foregoing milk altogether and feeding their children beverages such as juice or soda. All of these practices can threaten a child’s life, growth, and development.
When breastfeeding isn’t possible
We all know that human milk is the optimal, most nutritionally complete food source for newborn babies and infants. It can improve dental health and neurodevelopmental outcomes, as well as reduce the risk for asthma, eczema, diabetes, and obesity. An added benefit during the COVID-19 pandemic has been providing newborn infants with a boost of immunity before they are able to be vaccinated against SARS-CoV-2 infection.
But lactation and breastfeeding aren’t possible for everyone. Earlier this year, when my daughter was born more than a month prematurely, I worried that I would be unable to breastfeed her. The complications of prematurity can interfere with establishing lactation, and my daughter spent some time in the neonatal intensive care unit (NICU), requiring frequent feedings to treat hypoglycemia. She also lacked the muscle strength or coordination to latch on to the breast, so she was fed my colostrum and donor breast milk by bottle.
Not knowing when my mature milk would come in, my family scoured the retail stores for formula while I was still recovering from delivery. My daughter needed a specific type of high-calorie formula for premature infants. Eventually, my mother found one can of this powdered formula. The hospital also sent us home with 16 oz of ready-to-feed samples and enough donor breastmilk to last 24 hours at home. We considered ourselves lucky. The fear and anxiety about being able to feed my baby still stands out in my mind.
Pumping and sharing
Over the next few months, out of necessity, I became an “exclusively pumping” mother. My daughter, unable to latch, drank my pumped milk from a bottle. My body started to produce more milk than she needed in a day. In an effort to pay it forward and to put my extra milk to use, I became a human-milk donor. I underwent rigorous screening, including testing for infectious diseases such as HIV and hepatitis C. I was approved to donate to our local hospital’s milk bank, helping other families in the NICU feed their babies. Through informal connections on the internet, I also provide expressed milk to another mother in the community who is unable to lactate. To date, I’ve donated more than 1,500 oz of human milk (and counting).
The practice of human-milk donation dates back millennia with wet-nursing, when children were breastfed by someone other than their biological mothers: relatives, friends, or even strangers. The first milk bank in the United States opened in Boston in the early 20th century. In 1980, the World Health Organization and the United Nations Children’s Fund released a joint statement supporting the use of human-donor milk as the first alternative if the biological mother is unable to breastfeed. Donor milk is a safe option for families who cannot provide their own human milk to their children.
Human-milk banks
More than 30 nonprofit milk banks now operate in the United States. Because their mission is primarily to meet the needs of sick and hospitalized children rather than the general public, these milk banks are an impractical solution to the national formula shortage. Although families with healthy children can purchase donor milk with a prescription, supplies are scarce, and insurance doesn’t cover the cost.
Milk provided by formal human-milk banks is considered safe. Certain infections such as HIV and hepatitis can be transmitted through human milk. However, milk banks screen their donors and safely pasteurize and store donated breastmilk, following standard protocols. The risk of contracting an illness from banked donor milk is very low. The American Academy of Pediatrics recommends accepting donor milk only from a milk bank.
Informal human-milk donation
An increasingly popular alternative to formal human-milk banks is informal human-milk sharing. But many people, including health care professionals, hold misconceptions about how informal milk donation works. Today’s informal milk donation looks very different from age-old wet-nursing: Moms in support groups, often via social media, are requesting pumped milk from one another. (Note that this definition of “informal human-milk donation” does not include selling or purchasing human milk.)
Although the safety of sharing pumped human milk this way cannot be guaranteed, a harm-reduction approach is warranted, especially in view of the current formula scarcity.
I believe that medical professionals have a responsibility to raise awareness and dispel myths about donor breast milk. Many physicians acknowledge that informal milk sharing is common but rarely recommend it to patients. Whether they are donors or recipients, families who choose to participate need to be educated about how to go about the process as safely as possible.
Patients who are considering accepting informally donated human milk should ask key questions of the donor to gauge the risk of pathogens or other harmful substances being passed to their babies:
- What medications do you take?
- What supplements do you take?
- What recreational drugs do you take?
- Any recent travel?
- Any tattoos and if so, how recent?
- How much alcohol do you drink and how often?
- Have you been diagnosed with any infections?
- Any recent illness?
- How do you pump your breast milk?
- How do you store your breast milk?
- When was the available milk pumped?
We can help families by offering our medical expertise, allowing them to make an informed decision about whether to accept donated human milk. Clinicians can encourage patients and their families to use resources like the Infant Risk Center, which provides evidence-based information about medication safety and breast milk.
If your lactating patient is considering donating milk through informal channels to a family in need, encourage them to be open and honest about their medical history and lifestyle habits. If they cannot be transparent, they should not donate. A mutual level of respect and honesty can ensure the safety of those they hope to help. It is also important to counsel prospective milk donors to notify their milk recipients of any new illnesses, substance use, medications, travel, tattoos, or changes to their medical history.
Finally, encourage lactating patients who are able to do so to donate their extra milk to local nonprofit milk banks to increase the availability of screened, pasteurized breast milk in the community.
As a physician and mother, I hope that U.S. families will be less vulnerable to future formula shortages. Human milk is an ideal food source, but not everyone can lactate. Though not perfect, human milk donated outside of formal milk banks offers a safer alternative to diluting formula or feeding other unsuitable beverages to infants and children. As health care professionals, we need to counsel our patients about how to engage in this practice safely.
Dr. Mieses Malchuk is assistant professor in the department of family medicine at the University of North Carolina at Chapel Hill and a board-certified family physician and attending physician at UNC Health in Chapel Hill. She has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
I have become obsessed with the reality that the unprecedented national shortage of formula is keeping some families from adequately feeding their infants and young children. I am deeply concerned, both as a family medicine physician and a new mother, about the heartbreaking stories that I’ve heard from parents of all socioeconomic backgrounds. New mothers, unable to breastfeed for a multitude of reasons, find themselves standing in front of empty store shelves, in tears.
In recent months, many health care providers have had patients disclose that they are diluting ready-to-feed formula or mixing powdered formula with more water than instructed to make it go further. Some parents are giving cow’s milk to their children at too young an age because they can’t find formula. Others are foregoing milk altogether and feeding their children beverages such as juice or soda. All of these practices can threaten a child’s life, growth, and development.
When breastfeeding isn’t possible
We all know that human milk is the optimal, most nutritionally complete food source for newborn babies and infants. It can improve dental health and neurodevelopmental outcomes, as well as reduce the risk for asthma, eczema, diabetes, and obesity. An added benefit during the COVID-19 pandemic has been providing newborn infants with a boost of immunity before they are able to be vaccinated against SARS-CoV-2 infection.
But lactation and breastfeeding aren’t possible for everyone. Earlier this year, when my daughter was born more than a month prematurely, I worried that I would be unable to breastfeed her. The complications of prematurity can interfere with establishing lactation, and my daughter spent some time in the neonatal intensive care unit (NICU), requiring frequent feedings to treat hypoglycemia. She also lacked the muscle strength or coordination to latch on to the breast, so she was fed my colostrum and donor breast milk by bottle.
Not knowing when my mature milk would come in, my family scoured the retail stores for formula while I was still recovering from delivery. My daughter needed a specific type of high-calorie formula for premature infants. Eventually, my mother found one can of this powdered formula. The hospital also sent us home with 16 oz of ready-to-feed samples and enough donor breastmilk to last 24 hours at home. We considered ourselves lucky. The fear and anxiety about being able to feed my baby still stands out in my mind.
Pumping and sharing
Over the next few months, out of necessity, I became an “exclusively pumping” mother. My daughter, unable to latch, drank my pumped milk from a bottle. My body started to produce more milk than she needed in a day. In an effort to pay it forward and to put my extra milk to use, I became a human-milk donor. I underwent rigorous screening, including testing for infectious diseases such as HIV and hepatitis C. I was approved to donate to our local hospital’s milk bank, helping other families in the NICU feed their babies. Through informal connections on the internet, I also provide expressed milk to another mother in the community who is unable to lactate. To date, I’ve donated more than 1,500 oz of human milk (and counting).
The practice of human-milk donation dates back millennia with wet-nursing, when children were breastfed by someone other than their biological mothers: relatives, friends, or even strangers. The first milk bank in the United States opened in Boston in the early 20th century. In 1980, the World Health Organization and the United Nations Children’s Fund released a joint statement supporting the use of human-donor milk as the first alternative if the biological mother is unable to breastfeed. Donor milk is a safe option for families who cannot provide their own human milk to their children.
Human-milk banks
More than 30 nonprofit milk banks now operate in the United States. Because their mission is primarily to meet the needs of sick and hospitalized children rather than the general public, these milk banks are an impractical solution to the national formula shortage. Although families with healthy children can purchase donor milk with a prescription, supplies are scarce, and insurance doesn’t cover the cost.
Milk provided by formal human-milk banks is considered safe. Certain infections such as HIV and hepatitis can be transmitted through human milk. However, milk banks screen their donors and safely pasteurize and store donated breastmilk, following standard protocols. The risk of contracting an illness from banked donor milk is very low. The American Academy of Pediatrics recommends accepting donor milk only from a milk bank.
Informal human-milk donation
An increasingly popular alternative to formal human-milk banks is informal human-milk sharing. But many people, including health care professionals, hold misconceptions about how informal milk donation works. Today’s informal milk donation looks very different from age-old wet-nursing: Moms in support groups, often via social media, are requesting pumped milk from one another. (Note that this definition of “informal human-milk donation” does not include selling or purchasing human milk.)
Although the safety of sharing pumped human milk this way cannot be guaranteed, a harm-reduction approach is warranted, especially in view of the current formula scarcity.
I believe that medical professionals have a responsibility to raise awareness and dispel myths about donor breast milk. Many physicians acknowledge that informal milk sharing is common but rarely recommend it to patients. Whether they are donors or recipients, families who choose to participate need to be educated about how to go about the process as safely as possible.
Patients who are considering accepting informally donated human milk should ask key questions of the donor to gauge the risk of pathogens or other harmful substances being passed to their babies:
- What medications do you take?
- What supplements do you take?
- What recreational drugs do you take?
- Any recent travel?
- Any tattoos and if so, how recent?
- How much alcohol do you drink and how often?
- Have you been diagnosed with any infections?
- Any recent illness?
- How do you pump your breast milk?
- How do you store your breast milk?
- When was the available milk pumped?
We can help families by offering our medical expertise, allowing them to make an informed decision about whether to accept donated human milk. Clinicians can encourage patients and their families to use resources like the Infant Risk Center, which provides evidence-based information about medication safety and breast milk.
If your lactating patient is considering donating milk through informal channels to a family in need, encourage them to be open and honest about their medical history and lifestyle habits. If they cannot be transparent, they should not donate. A mutual level of respect and honesty can ensure the safety of those they hope to help. It is also important to counsel prospective milk donors to notify their milk recipients of any new illnesses, substance use, medications, travel, tattoos, or changes to their medical history.
Finally, encourage lactating patients who are able to do so to donate their extra milk to local nonprofit milk banks to increase the availability of screened, pasteurized breast milk in the community.
As a physician and mother, I hope that U.S. families will be less vulnerable to future formula shortages. Human milk is an ideal food source, but not everyone can lactate. Though not perfect, human milk donated outside of formal milk banks offers a safer alternative to diluting formula or feeding other unsuitable beverages to infants and children. As health care professionals, we need to counsel our patients about how to engage in this practice safely.
Dr. Mieses Malchuk is assistant professor in the department of family medicine at the University of North Carolina at Chapel Hill and a board-certified family physician and attending physician at UNC Health in Chapel Hill. She has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
I have become obsessed with the reality that the unprecedented national shortage of formula is keeping some families from adequately feeding their infants and young children. I am deeply concerned, both as a family medicine physician and a new mother, about the heartbreaking stories that I’ve heard from parents of all socioeconomic backgrounds. New mothers, unable to breastfeed for a multitude of reasons, find themselves standing in front of empty store shelves, in tears.
In recent months, many health care providers have had patients disclose that they are diluting ready-to-feed formula or mixing powdered formula with more water than instructed to make it go further. Some parents are giving cow’s milk to their children at too young an age because they can’t find formula. Others are foregoing milk altogether and feeding their children beverages such as juice or soda. All of these practices can threaten a child’s life, growth, and development.
When breastfeeding isn’t possible
We all know that human milk is the optimal, most nutritionally complete food source for newborn babies and infants. It can improve dental health and neurodevelopmental outcomes, as well as reduce the risk for asthma, eczema, diabetes, and obesity. An added benefit during the COVID-19 pandemic has been providing newborn infants with a boost of immunity before they are able to be vaccinated against SARS-CoV-2 infection.
But lactation and breastfeeding aren’t possible for everyone. Earlier this year, when my daughter was born more than a month prematurely, I worried that I would be unable to breastfeed her. The complications of prematurity can interfere with establishing lactation, and my daughter spent some time in the neonatal intensive care unit (NICU), requiring frequent feedings to treat hypoglycemia. She also lacked the muscle strength or coordination to latch on to the breast, so she was fed my colostrum and donor breast milk by bottle.
Not knowing when my mature milk would come in, my family scoured the retail stores for formula while I was still recovering from delivery. My daughter needed a specific type of high-calorie formula for premature infants. Eventually, my mother found one can of this powdered formula. The hospital also sent us home with 16 oz of ready-to-feed samples and enough donor breastmilk to last 24 hours at home. We considered ourselves lucky. The fear and anxiety about being able to feed my baby still stands out in my mind.
Pumping and sharing
Over the next few months, out of necessity, I became an “exclusively pumping” mother. My daughter, unable to latch, drank my pumped milk from a bottle. My body started to produce more milk than she needed in a day. In an effort to pay it forward and to put my extra milk to use, I became a human-milk donor. I underwent rigorous screening, including testing for infectious diseases such as HIV and hepatitis C. I was approved to donate to our local hospital’s milk bank, helping other families in the NICU feed their babies. Through informal connections on the internet, I also provide expressed milk to another mother in the community who is unable to lactate. To date, I’ve donated more than 1,500 oz of human milk (and counting).
The practice of human-milk donation dates back millennia with wet-nursing, when children were breastfed by someone other than their biological mothers: relatives, friends, or even strangers. The first milk bank in the United States opened in Boston in the early 20th century. In 1980, the World Health Organization and the United Nations Children’s Fund released a joint statement supporting the use of human-donor milk as the first alternative if the biological mother is unable to breastfeed. Donor milk is a safe option for families who cannot provide their own human milk to their children.
Human-milk banks
More than 30 nonprofit milk banks now operate in the United States. Because their mission is primarily to meet the needs of sick and hospitalized children rather than the general public, these milk banks are an impractical solution to the national formula shortage. Although families with healthy children can purchase donor milk with a prescription, supplies are scarce, and insurance doesn’t cover the cost.
Milk provided by formal human-milk banks is considered safe. Certain infections such as HIV and hepatitis can be transmitted through human milk. However, milk banks screen their donors and safely pasteurize and store donated breastmilk, following standard protocols. The risk of contracting an illness from banked donor milk is very low. The American Academy of Pediatrics recommends accepting donor milk only from a milk bank.
Informal human-milk donation
An increasingly popular alternative to formal human-milk banks is informal human-milk sharing. But many people, including health care professionals, hold misconceptions about how informal milk donation works. Today’s informal milk donation looks very different from age-old wet-nursing: Moms in support groups, often via social media, are requesting pumped milk from one another. (Note that this definition of “informal human-milk donation” does not include selling or purchasing human milk.)
Although the safety of sharing pumped human milk this way cannot be guaranteed, a harm-reduction approach is warranted, especially in view of the current formula scarcity.
I believe that medical professionals have a responsibility to raise awareness and dispel myths about donor breast milk. Many physicians acknowledge that informal milk sharing is common but rarely recommend it to patients. Whether they are donors or recipients, families who choose to participate need to be educated about how to go about the process as safely as possible.
Patients who are considering accepting informally donated human milk should ask key questions of the donor to gauge the risk of pathogens or other harmful substances being passed to their babies:
- What medications do you take?
- What supplements do you take?
- What recreational drugs do you take?
- Any recent travel?
- Any tattoos and if so, how recent?
- How much alcohol do you drink and how often?
- Have you been diagnosed with any infections?
- Any recent illness?
- How do you pump your breast milk?
- How do you store your breast milk?
- When was the available milk pumped?
We can help families by offering our medical expertise, allowing them to make an informed decision about whether to accept donated human milk. Clinicians can encourage patients and their families to use resources like the Infant Risk Center, which provides evidence-based information about medication safety and breast milk.
If your lactating patient is considering donating milk through informal channels to a family in need, encourage them to be open and honest about their medical history and lifestyle habits. If they cannot be transparent, they should not donate. A mutual level of respect and honesty can ensure the safety of those they hope to help. It is also important to counsel prospective milk donors to notify their milk recipients of any new illnesses, substance use, medications, travel, tattoos, or changes to their medical history.
Finally, encourage lactating patients who are able to do so to donate their extra milk to local nonprofit milk banks to increase the availability of screened, pasteurized breast milk in the community.
As a physician and mother, I hope that U.S. families will be less vulnerable to future formula shortages. Human milk is an ideal food source, but not everyone can lactate. Though not perfect, human milk donated outside of formal milk banks offers a safer alternative to diluting formula or feeding other unsuitable beverages to infants and children. As health care professionals, we need to counsel our patients about how to engage in this practice safely.
Dr. Mieses Malchuk is assistant professor in the department of family medicine at the University of North Carolina at Chapel Hill and a board-certified family physician and attending physician at UNC Health in Chapel Hill. She has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The latest on COVID-19 and the heart in children
The 2022 Pediatric Academic Societies meeting included an excellent session on the acute and delayed effects of COVID-19 on children’s hearts. Data on the risk for cardiac injury during acute COVID-19, return-to-play guidelines after COVID-19–related heart injury, and post–vaccine-associated myocarditis were reviewed.
COVID-induced cardiac injury
The risk for COVID-induced cardiac injury is directly associated with age. Recent Centers for Disease Control and Prevention data revealed a “myocarditis or pericarditis” rate in the range of 12-17 cases per 100,000 SARS-CoV-2 infections among male children aged 5-11 years (lower rates for females); the rate jumps to 50-65 cases per 100,000 infections among male children aged 12-17 years. So cardiac injury caused by acute COVID-19 appears rare, but the risk is clearly associated with male sex and adolescent age.
Return to play after COVID-19
Clinicians may be pressed by patients and parents for advice on return to play after illness with COVID-19. In July 2020, the American College of Cardiology published an algorithm that has been adjusted over time, most recently in 2022 by the American Academy of Pediatrics. These algorithms stratify recommendations by degree of illness. One rule of thumb: Patients with severe COVID-19 (ICU care or multisystem inflammatory syndrome in children [MIS-C]) have only one box on the algorithm, and that is to rest for 3-6 months and only return to usual activity after cardiac clearance. Moderate disease (defined as ≥ 4 days of fever > 100.4 °F; ≥ 1 week of myalgia, chills, lethargy, or any non-ICU hospital stay; and no evidence of MIS-C) require undergoing an ECG to look for cardiac dysfunction, followed by at least 10 days of rest if the ECG is negative or referral for cardiac evaluation if either ECG or exam by a pediatric cardiologist is abnormal.
Clinicians can perhaps be more permissible with patients who are younger or who have had less severe disease. For example, if a patient aged younger than 12 years is asymptomatic with routine activity at the time of evaluation, an ECG is not indicated. For patients aged 12-15 years who are asymptomatic at the time of evaluation but participate in a high-intensity sport, clinicians might consider obtaining an ECG. As few as 3 days of rest might be enough for select patients who are asymptomatic at presentation. For other patients, clinicians should work with parents to introduce activity gradually and make it clear to parents that any activity intolerance requires quick reevaluation. On existing athlete registries, no deaths that are attributable to post–COVID-19 cardiac effects have been confirmed in children; however, all data presented during the session were from prior to the Omicron variant surge in early 2022, so more information may be forthcoming.
Considerations for MIS-C
Among children experiencing MIS-C, 35% had ECG changes, 40% exhibited left ventricular systolic or diastolic dysfunction, and 30% had mitral regurgitation, meaning that a large percentage of patients with MIS-C show some degree of cardiac dysfunction. Unfortunately, we are still in the data-gathering phase for long-term outcomes. Functional parameters tend to improve within a week, and most patients will return to normal cardiac function by 3-4 months.
Return to play after MIS-C is quite different from that for acute COVID-19. Patients with MIS-C should be treated much like other patients with myocarditis with an expected return to play in 3-6 months and only after cardiac follow-up. Another good-to-remember recommendation is to delay COVID-19 vaccination for at least 90 days after an episode of MIS-C.
Vaccine-related myocarditis
Once again, older age appears to be a risk factor because most patients with postvaccine myocarditis have been in their mid-teens to early 20s, with events more likely after the second vaccine dose and also more likely in male children (4:1 ratio to female children). No deaths have occurred from postvaccination myocarditis in patients younger than 30 years. Still, many individuals have exhibited residual MRI enhancement in the cardiac tissue for some time after experiencing postvaccination myocarditis; it’s currently unclear whether that has clinical implications. By comparison, CDC data demonstrates convincingly that the risk for cardiac effects is much greater after acute COVID-19 than after COVID-19 vaccination, with risk ratios often higher than 20, depending on age and condition (for example, myocarditis vs. pericarditis). Data are still insufficient to determine whether clinicians should recommend or avoid COVID-19 vaccination in children with congenital heart disease.
In summary, administering COVID-19 vaccines requires a great deal of shared decision-making with parents, and the clinician’s role is to educate parents about all potential risks related to both the vaccine and COVID-19 illness. Research has consistently shown that acute COVID-19 myocarditis and myocarditis associated with MIS-C are much more likely to occur in unvaccinated youth and more likely than postvaccination myocarditis, regardless of age.
William T. Basco, Jr., MD, MS, is a professor of pediatrics at the Medical University of South Carolina, Charleston, and director of the division of general pediatrics. He is an active health services researcher and has published more than 60 manuscripts in the peer-reviewed literature.
A version of this article first appeared on Medscape.com.
The 2022 Pediatric Academic Societies meeting included an excellent session on the acute and delayed effects of COVID-19 on children’s hearts. Data on the risk for cardiac injury during acute COVID-19, return-to-play guidelines after COVID-19–related heart injury, and post–vaccine-associated myocarditis were reviewed.
COVID-induced cardiac injury
The risk for COVID-induced cardiac injury is directly associated with age. Recent Centers for Disease Control and Prevention data revealed a “myocarditis or pericarditis” rate in the range of 12-17 cases per 100,000 SARS-CoV-2 infections among male children aged 5-11 years (lower rates for females); the rate jumps to 50-65 cases per 100,000 infections among male children aged 12-17 years. So cardiac injury caused by acute COVID-19 appears rare, but the risk is clearly associated with male sex and adolescent age.
Return to play after COVID-19
Clinicians may be pressed by patients and parents for advice on return to play after illness with COVID-19. In July 2020, the American College of Cardiology published an algorithm that has been adjusted over time, most recently in 2022 by the American Academy of Pediatrics. These algorithms stratify recommendations by degree of illness. One rule of thumb: Patients with severe COVID-19 (ICU care or multisystem inflammatory syndrome in children [MIS-C]) have only one box on the algorithm, and that is to rest for 3-6 months and only return to usual activity after cardiac clearance. Moderate disease (defined as ≥ 4 days of fever > 100.4 °F; ≥ 1 week of myalgia, chills, lethargy, or any non-ICU hospital stay; and no evidence of MIS-C) require undergoing an ECG to look for cardiac dysfunction, followed by at least 10 days of rest if the ECG is negative or referral for cardiac evaluation if either ECG or exam by a pediatric cardiologist is abnormal.
Clinicians can perhaps be more permissible with patients who are younger or who have had less severe disease. For example, if a patient aged younger than 12 years is asymptomatic with routine activity at the time of evaluation, an ECG is not indicated. For patients aged 12-15 years who are asymptomatic at the time of evaluation but participate in a high-intensity sport, clinicians might consider obtaining an ECG. As few as 3 days of rest might be enough for select patients who are asymptomatic at presentation. For other patients, clinicians should work with parents to introduce activity gradually and make it clear to parents that any activity intolerance requires quick reevaluation. On existing athlete registries, no deaths that are attributable to post–COVID-19 cardiac effects have been confirmed in children; however, all data presented during the session were from prior to the Omicron variant surge in early 2022, so more information may be forthcoming.
Considerations for MIS-C
Among children experiencing MIS-C, 35% had ECG changes, 40% exhibited left ventricular systolic or diastolic dysfunction, and 30% had mitral regurgitation, meaning that a large percentage of patients with MIS-C show some degree of cardiac dysfunction. Unfortunately, we are still in the data-gathering phase for long-term outcomes. Functional parameters tend to improve within a week, and most patients will return to normal cardiac function by 3-4 months.
Return to play after MIS-C is quite different from that for acute COVID-19. Patients with MIS-C should be treated much like other patients with myocarditis with an expected return to play in 3-6 months and only after cardiac follow-up. Another good-to-remember recommendation is to delay COVID-19 vaccination for at least 90 days after an episode of MIS-C.
Vaccine-related myocarditis
Once again, older age appears to be a risk factor because most patients with postvaccine myocarditis have been in their mid-teens to early 20s, with events more likely after the second vaccine dose and also more likely in male children (4:1 ratio to female children). No deaths have occurred from postvaccination myocarditis in patients younger than 30 years. Still, many individuals have exhibited residual MRI enhancement in the cardiac tissue for some time after experiencing postvaccination myocarditis; it’s currently unclear whether that has clinical implications. By comparison, CDC data demonstrates convincingly that the risk for cardiac effects is much greater after acute COVID-19 than after COVID-19 vaccination, with risk ratios often higher than 20, depending on age and condition (for example, myocarditis vs. pericarditis). Data are still insufficient to determine whether clinicians should recommend or avoid COVID-19 vaccination in children with congenital heart disease.
In summary, administering COVID-19 vaccines requires a great deal of shared decision-making with parents, and the clinician’s role is to educate parents about all potential risks related to both the vaccine and COVID-19 illness. Research has consistently shown that acute COVID-19 myocarditis and myocarditis associated with MIS-C are much more likely to occur in unvaccinated youth and more likely than postvaccination myocarditis, regardless of age.
William T. Basco, Jr., MD, MS, is a professor of pediatrics at the Medical University of South Carolina, Charleston, and director of the division of general pediatrics. He is an active health services researcher and has published more than 60 manuscripts in the peer-reviewed literature.
A version of this article first appeared on Medscape.com.
The 2022 Pediatric Academic Societies meeting included an excellent session on the acute and delayed effects of COVID-19 on children’s hearts. Data on the risk for cardiac injury during acute COVID-19, return-to-play guidelines after COVID-19–related heart injury, and post–vaccine-associated myocarditis were reviewed.
COVID-induced cardiac injury
The risk for COVID-induced cardiac injury is directly associated with age. Recent Centers for Disease Control and Prevention data revealed a “myocarditis or pericarditis” rate in the range of 12-17 cases per 100,000 SARS-CoV-2 infections among male children aged 5-11 years (lower rates for females); the rate jumps to 50-65 cases per 100,000 infections among male children aged 12-17 years. So cardiac injury caused by acute COVID-19 appears rare, but the risk is clearly associated with male sex and adolescent age.
Return to play after COVID-19
Clinicians may be pressed by patients and parents for advice on return to play after illness with COVID-19. In July 2020, the American College of Cardiology published an algorithm that has been adjusted over time, most recently in 2022 by the American Academy of Pediatrics. These algorithms stratify recommendations by degree of illness. One rule of thumb: Patients with severe COVID-19 (ICU care or multisystem inflammatory syndrome in children [MIS-C]) have only one box on the algorithm, and that is to rest for 3-6 months and only return to usual activity after cardiac clearance. Moderate disease (defined as ≥ 4 days of fever > 100.4 °F; ≥ 1 week of myalgia, chills, lethargy, or any non-ICU hospital stay; and no evidence of MIS-C) require undergoing an ECG to look for cardiac dysfunction, followed by at least 10 days of rest if the ECG is negative or referral for cardiac evaluation if either ECG or exam by a pediatric cardiologist is abnormal.
Clinicians can perhaps be more permissible with patients who are younger or who have had less severe disease. For example, if a patient aged younger than 12 years is asymptomatic with routine activity at the time of evaluation, an ECG is not indicated. For patients aged 12-15 years who are asymptomatic at the time of evaluation but participate in a high-intensity sport, clinicians might consider obtaining an ECG. As few as 3 days of rest might be enough for select patients who are asymptomatic at presentation. For other patients, clinicians should work with parents to introduce activity gradually and make it clear to parents that any activity intolerance requires quick reevaluation. On existing athlete registries, no deaths that are attributable to post–COVID-19 cardiac effects have been confirmed in children; however, all data presented during the session were from prior to the Omicron variant surge in early 2022, so more information may be forthcoming.
Considerations for MIS-C
Among children experiencing MIS-C, 35% had ECG changes, 40% exhibited left ventricular systolic or diastolic dysfunction, and 30% had mitral regurgitation, meaning that a large percentage of patients with MIS-C show some degree of cardiac dysfunction. Unfortunately, we are still in the data-gathering phase for long-term outcomes. Functional parameters tend to improve within a week, and most patients will return to normal cardiac function by 3-4 months.
Return to play after MIS-C is quite different from that for acute COVID-19. Patients with MIS-C should be treated much like other patients with myocarditis with an expected return to play in 3-6 months and only after cardiac follow-up. Another good-to-remember recommendation is to delay COVID-19 vaccination for at least 90 days after an episode of MIS-C.
Vaccine-related myocarditis
Once again, older age appears to be a risk factor because most patients with postvaccine myocarditis have been in their mid-teens to early 20s, with events more likely after the second vaccine dose and also more likely in male children (4:1 ratio to female children). No deaths have occurred from postvaccination myocarditis in patients younger than 30 years. Still, many individuals have exhibited residual MRI enhancement in the cardiac tissue for some time after experiencing postvaccination myocarditis; it’s currently unclear whether that has clinical implications. By comparison, CDC data demonstrates convincingly that the risk for cardiac effects is much greater after acute COVID-19 than after COVID-19 vaccination, with risk ratios often higher than 20, depending on age and condition (for example, myocarditis vs. pericarditis). Data are still insufficient to determine whether clinicians should recommend or avoid COVID-19 vaccination in children with congenital heart disease.
In summary, administering COVID-19 vaccines requires a great deal of shared decision-making with parents, and the clinician’s role is to educate parents about all potential risks related to both the vaccine and COVID-19 illness. Research has consistently shown that acute COVID-19 myocarditis and myocarditis associated with MIS-C are much more likely to occur in unvaccinated youth and more likely than postvaccination myocarditis, regardless of age.
William T. Basco, Jr., MD, MS, is a professor of pediatrics at the Medical University of South Carolina, Charleston, and director of the division of general pediatrics. He is an active health services researcher and has published more than 60 manuscripts in the peer-reviewed literature.
A version of this article first appeared on Medscape.com.
Journalism or medicine: Why not both?
I had an early attraction to newspapers. As a child growing up in Jersey City, N.J., I delivered them door-to-door. I was editor-in-chief of my high school newspaper and worked as a copy boy and sports reporter on the daily Jersey Journal. At Princeton, I joined the University Press Club, working as a string reporter for the New York Herald Tribune, Philadelphia Inquirer, and Associated Press.
I thought I might become a journalist, but medicine was too strong a calling. During my GI elective as a senior medical resident at New York Hospital, I was able to work with some of the first commercial fiberoptic instruments, which presaged my academic career in endoscopic innovation. I was editor-in-chief of Gastrointestinal Endoscopy from 1988 to 1996, and have been the consulting editor for GI Endoscopy Clinics of North America since 1997.
As the first editor-in-chief of GI & Hepatology News, I had the opportunity to combine a background in peer review with my early newspaper experience. My vision for the new publication was to provide information curated and vetted by experts, in contrast to the torrent pouring down from the Internet that was (pertinent to our specialty) “indigestible.” I put in much effort selecting stories provided by Elsevier Global Medical News, especially in constructing the front page. AGA Institute provided strong support, allowing me to choose an editorial board covering all subspecialties. I wanted to highlight the excitement of researchers balanced by expert review and commentary. The digital version added search features, and I tried to promote the “browse factor” that would also encourage advertising, critical to the success of any newspaper. At the end of my term, I felt I had laid a strong foundation, and have been delighted to see the publication continue to thrive.
Charles Lightdale, MD, is professor of medicine at Columbia University Medical Center in New York. He disclosed having no conflicts of interest.
I had an early attraction to newspapers. As a child growing up in Jersey City, N.J., I delivered them door-to-door. I was editor-in-chief of my high school newspaper and worked as a copy boy and sports reporter on the daily Jersey Journal. At Princeton, I joined the University Press Club, working as a string reporter for the New York Herald Tribune, Philadelphia Inquirer, and Associated Press.
I thought I might become a journalist, but medicine was too strong a calling. During my GI elective as a senior medical resident at New York Hospital, I was able to work with some of the first commercial fiberoptic instruments, which presaged my academic career in endoscopic innovation. I was editor-in-chief of Gastrointestinal Endoscopy from 1988 to 1996, and have been the consulting editor for GI Endoscopy Clinics of North America since 1997.
As the first editor-in-chief of GI & Hepatology News, I had the opportunity to combine a background in peer review with my early newspaper experience. My vision for the new publication was to provide information curated and vetted by experts, in contrast to the torrent pouring down from the Internet that was (pertinent to our specialty) “indigestible.” I put in much effort selecting stories provided by Elsevier Global Medical News, especially in constructing the front page. AGA Institute provided strong support, allowing me to choose an editorial board covering all subspecialties. I wanted to highlight the excitement of researchers balanced by expert review and commentary. The digital version added search features, and I tried to promote the “browse factor” that would also encourage advertising, critical to the success of any newspaper. At the end of my term, I felt I had laid a strong foundation, and have been delighted to see the publication continue to thrive.
Charles Lightdale, MD, is professor of medicine at Columbia University Medical Center in New York. He disclosed having no conflicts of interest.
I had an early attraction to newspapers. As a child growing up in Jersey City, N.J., I delivered them door-to-door. I was editor-in-chief of my high school newspaper and worked as a copy boy and sports reporter on the daily Jersey Journal. At Princeton, I joined the University Press Club, working as a string reporter for the New York Herald Tribune, Philadelphia Inquirer, and Associated Press.
I thought I might become a journalist, but medicine was too strong a calling. During my GI elective as a senior medical resident at New York Hospital, I was able to work with some of the first commercial fiberoptic instruments, which presaged my academic career in endoscopic innovation. I was editor-in-chief of Gastrointestinal Endoscopy from 1988 to 1996, and have been the consulting editor for GI Endoscopy Clinics of North America since 1997.
As the first editor-in-chief of GI & Hepatology News, I had the opportunity to combine a background in peer review with my early newspaper experience. My vision for the new publication was to provide information curated and vetted by experts, in contrast to the torrent pouring down from the Internet that was (pertinent to our specialty) “indigestible.” I put in much effort selecting stories provided by Elsevier Global Medical News, especially in constructing the front page. AGA Institute provided strong support, allowing me to choose an editorial board covering all subspecialties. I wanted to highlight the excitement of researchers balanced by expert review and commentary. The digital version added search features, and I tried to promote the “browse factor” that would also encourage advertising, critical to the success of any newspaper. At the end of my term, I felt I had laid a strong foundation, and have been delighted to see the publication continue to thrive.
Charles Lightdale, MD, is professor of medicine at Columbia University Medical Center in New York. He disclosed having no conflicts of interest.