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Doing the Best They Can
Our dermatology department is composed of 25 doctors spread across 4 offices. It can be difficult to sustain cohesion so we have a few rituals to help hold us together. One is the morning huddle. This is a stand-up meeting lasting 3-5 minutes at 8:42 a.m. (just before the 8:45 a.m. patients). Led by our staff, huddle is a quick review of the priorities, issues, and celebrations across our department. While enthusiastically celebrating a staff member’s promotion one morning, a patient swung open the exam door and shouted, “What’s going on out here?! I’m sitting here waiting!” before slamming the door closed again. “Well, that was unnecessary,” our morning lead interjected as she went to reprimand him.
His behavior was easily recognizable to any doctor with children. It was an emotional outburst we call a tantrum. Although a graphic of tantrums by age would show a steep curve that drops precipitously after 4-years-old (please God, I hope), it persists throughout life. Even adults have tantrums. After? When I broke my pinky toe saving the family from flaming tornadoes a few weeks ago (I ran into the sofa), I flung the ice bag across the room in frustration. “You’ve a right to be mad,” my wife said returning the ice to where I was elevating my foot. She was spot on, it is understandable that I would be angry. It will be weeks before I can run again. And also my toe was broken. Both things were true.
“Two things are true” is a technique for managing tantrums in toddlers. I first learned of it from Dr. Becky Kennedy, a clinical psychologist specializing in family therapy. She has a popular podcast called “Good Inside” based on her book of the same name. Her approach is to use positive psychology with an emphasis on connecting with children to not only shape behavior, but also to help them learn to manage their emotions. I read her book to level up dad skills and realized many of her principles are applicable to various types of relationships. Instead of viewing behaviors as an end, she instead recommends using them as an opportunity to probe for understanding. Assume they are doing the best they can. When my 4-year-old obstinately refused to go to bed despite the usual colored night lights and bedtime rituals, it seemed she was being a typical tantrum-y toddler. The more I insisted — lights-out! the more she resisted. It wasn’t until I asked why that I learned she was worried that the trash truck was going to come overnight. What seemed like just a behavioral problem, time for bed, was actually an opportunity for her to be seen and for us to connect.
I was finishing up with a patient last week when my medical assistant interrupted to advise my next patient was leaving. I walked out to see her storm into the corridor heading for the exit. “I am sorry, you must be quite frustrated having to wait for me.” “Yes, you don’t respect my time,” she said loudly enough for everyone pretending to not notice. I coaxed her back into the room and sat down. After apologizing for her wait and explaining it was because an urgent patient had been added to my schedule, she calmed down and allowed me to continue. At her previous visit, I had biopsied a firm dermal papule on her upper abdomen that turned out to be metastatic breast cancer. She was treated years ago and believed she was in complete remission. Now she was alone, terrified, and wanted her full appointment with me. Because I was running late, she assumed I wouldn’t have the time for her. It was an opportunity for me to connect with her and help her feel safe. I would have missed that opportunity if I had labeled her as just another angry “Karen” brassly asserting herself.
Dr. Kennedy talks a lot in her book about taking the “Most generous interpretation” of whatever behavioral issue arises. Take the time to validate what they are feeling and empathize as best as we can. Acknowledge that it’s normal to be angry and also these are the truths we have to work with. Two truths commonly appear in these emotional episodes. One, the immutable facts, for example, insurance doesn’t cover that drug, and two, your right to be frustrated by that. Above all, remember you, the doctor, are good inside as is your discourteous patient, disaffected staff member or sometimes mendacious teenager. “All good decisions start with feeling secure and nothing feels more secure than being recognized for the good people we are,” says Dr. Kennedy. True I believe even if we sometimes slam the door.
Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].
Our dermatology department is composed of 25 doctors spread across 4 offices. It can be difficult to sustain cohesion so we have a few rituals to help hold us together. One is the morning huddle. This is a stand-up meeting lasting 3-5 minutes at 8:42 a.m. (just before the 8:45 a.m. patients). Led by our staff, huddle is a quick review of the priorities, issues, and celebrations across our department. While enthusiastically celebrating a staff member’s promotion one morning, a patient swung open the exam door and shouted, “What’s going on out here?! I’m sitting here waiting!” before slamming the door closed again. “Well, that was unnecessary,” our morning lead interjected as she went to reprimand him.
His behavior was easily recognizable to any doctor with children. It was an emotional outburst we call a tantrum. Although a graphic of tantrums by age would show a steep curve that drops precipitously after 4-years-old (please God, I hope), it persists throughout life. Even adults have tantrums. After? When I broke my pinky toe saving the family from flaming tornadoes a few weeks ago (I ran into the sofa), I flung the ice bag across the room in frustration. “You’ve a right to be mad,” my wife said returning the ice to where I was elevating my foot. She was spot on, it is understandable that I would be angry. It will be weeks before I can run again. And also my toe was broken. Both things were true.
“Two things are true” is a technique for managing tantrums in toddlers. I first learned of it from Dr. Becky Kennedy, a clinical psychologist specializing in family therapy. She has a popular podcast called “Good Inside” based on her book of the same name. Her approach is to use positive psychology with an emphasis on connecting with children to not only shape behavior, but also to help them learn to manage their emotions. I read her book to level up dad skills and realized many of her principles are applicable to various types of relationships. Instead of viewing behaviors as an end, she instead recommends using them as an opportunity to probe for understanding. Assume they are doing the best they can. When my 4-year-old obstinately refused to go to bed despite the usual colored night lights and bedtime rituals, it seemed she was being a typical tantrum-y toddler. The more I insisted — lights-out! the more she resisted. It wasn’t until I asked why that I learned she was worried that the trash truck was going to come overnight. What seemed like just a behavioral problem, time for bed, was actually an opportunity for her to be seen and for us to connect.
I was finishing up with a patient last week when my medical assistant interrupted to advise my next patient was leaving. I walked out to see her storm into the corridor heading for the exit. “I am sorry, you must be quite frustrated having to wait for me.” “Yes, you don’t respect my time,” she said loudly enough for everyone pretending to not notice. I coaxed her back into the room and sat down. After apologizing for her wait and explaining it was because an urgent patient had been added to my schedule, she calmed down and allowed me to continue. At her previous visit, I had biopsied a firm dermal papule on her upper abdomen that turned out to be metastatic breast cancer. She was treated years ago and believed she was in complete remission. Now she was alone, terrified, and wanted her full appointment with me. Because I was running late, she assumed I wouldn’t have the time for her. It was an opportunity for me to connect with her and help her feel safe. I would have missed that opportunity if I had labeled her as just another angry “Karen” brassly asserting herself.
Dr. Kennedy talks a lot in her book about taking the “Most generous interpretation” of whatever behavioral issue arises. Take the time to validate what they are feeling and empathize as best as we can. Acknowledge that it’s normal to be angry and also these are the truths we have to work with. Two truths commonly appear in these emotional episodes. One, the immutable facts, for example, insurance doesn’t cover that drug, and two, your right to be frustrated by that. Above all, remember you, the doctor, are good inside as is your discourteous patient, disaffected staff member or sometimes mendacious teenager. “All good decisions start with feeling secure and nothing feels more secure than being recognized for the good people we are,” says Dr. Kennedy. True I believe even if we sometimes slam the door.
Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].
Our dermatology department is composed of 25 doctors spread across 4 offices. It can be difficult to sustain cohesion so we have a few rituals to help hold us together. One is the morning huddle. This is a stand-up meeting lasting 3-5 minutes at 8:42 a.m. (just before the 8:45 a.m. patients). Led by our staff, huddle is a quick review of the priorities, issues, and celebrations across our department. While enthusiastically celebrating a staff member’s promotion one morning, a patient swung open the exam door and shouted, “What’s going on out here?! I’m sitting here waiting!” before slamming the door closed again. “Well, that was unnecessary,” our morning lead interjected as she went to reprimand him.
His behavior was easily recognizable to any doctor with children. It was an emotional outburst we call a tantrum. Although a graphic of tantrums by age would show a steep curve that drops precipitously after 4-years-old (please God, I hope), it persists throughout life. Even adults have tantrums. After? When I broke my pinky toe saving the family from flaming tornadoes a few weeks ago (I ran into the sofa), I flung the ice bag across the room in frustration. “You’ve a right to be mad,” my wife said returning the ice to where I was elevating my foot. She was spot on, it is understandable that I would be angry. It will be weeks before I can run again. And also my toe was broken. Both things were true.
“Two things are true” is a technique for managing tantrums in toddlers. I first learned of it from Dr. Becky Kennedy, a clinical psychologist specializing in family therapy. She has a popular podcast called “Good Inside” based on her book of the same name. Her approach is to use positive psychology with an emphasis on connecting with children to not only shape behavior, but also to help them learn to manage their emotions. I read her book to level up dad skills and realized many of her principles are applicable to various types of relationships. Instead of viewing behaviors as an end, she instead recommends using them as an opportunity to probe for understanding. Assume they are doing the best they can. When my 4-year-old obstinately refused to go to bed despite the usual colored night lights and bedtime rituals, it seemed she was being a typical tantrum-y toddler. The more I insisted — lights-out! the more she resisted. It wasn’t until I asked why that I learned she was worried that the trash truck was going to come overnight. What seemed like just a behavioral problem, time for bed, was actually an opportunity for her to be seen and for us to connect.
I was finishing up with a patient last week when my medical assistant interrupted to advise my next patient was leaving. I walked out to see her storm into the corridor heading for the exit. “I am sorry, you must be quite frustrated having to wait for me.” “Yes, you don’t respect my time,” she said loudly enough for everyone pretending to not notice. I coaxed her back into the room and sat down. After apologizing for her wait and explaining it was because an urgent patient had been added to my schedule, she calmed down and allowed me to continue. At her previous visit, I had biopsied a firm dermal papule on her upper abdomen that turned out to be metastatic breast cancer. She was treated years ago and believed she was in complete remission. Now she was alone, terrified, and wanted her full appointment with me. Because I was running late, she assumed I wouldn’t have the time for her. It was an opportunity for me to connect with her and help her feel safe. I would have missed that opportunity if I had labeled her as just another angry “Karen” brassly asserting herself.
Dr. Kennedy talks a lot in her book about taking the “Most generous interpretation” of whatever behavioral issue arises. Take the time to validate what they are feeling and empathize as best as we can. Acknowledge that it’s normal to be angry and also these are the truths we have to work with. Two truths commonly appear in these emotional episodes. One, the immutable facts, for example, insurance doesn’t cover that drug, and two, your right to be frustrated by that. Above all, remember you, the doctor, are good inside as is your discourteous patient, disaffected staff member or sometimes mendacious teenager. “All good decisions start with feeling secure and nothing feels more secure than being recognized for the good people we are,” says Dr. Kennedy. True I believe even if we sometimes slam the door.
Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].
The Sexual Revolution Has Been Great — For Men
During the month of September, Sexual Health Awareness Month, it may help to notice something: Men and their doctors have significantly more options to help with sexual function than do women and their clinicians. Moreover, .
Not convinced? Let’s take a quick tour.
The New Sexual Revolution and the Growing Anger
Around the time of the release of the book and movie Fifty Shades of Grey, Newsweek put the cultural sensation on its cover.
I bought the magazine at the airport and, while waiting for my plane, showed the story to a woman sitting next to me. “What do you think — is this the new ‘sexual revolution’?” I asked her.
She glanced at the cover and answered as accurately as if she had written the article: “In the ’60s, it became okay for women to have sex; now, it’s okay for women to demand good sex.”
I would add to that: Women are demanding good sex, and they want to define for themselves what “good” means.
That social revolution rages, still.
You would think that the demand would bring a corresponding response in clinical medicine. You would be wrong. Although efforts in some sectors are heroic, overall, the results are lagging the forward movement of women wanting better sex.
The Lag in Sexual Education
To examine the progression of the education of physicians regarding the treatment of female sexual dysfunction (FSD), Codispoti and colleagues examined the curricula of seven medical schools in and around Chicago. They found the following: Only one institution identified all anatomic components of the clitoris — one! Four of the seven discussed the physiology of the female orgasm. Only three of the seven highlighted the prevalence and epidemiology of FSD or the treatments for FSD. Only one of the seven explained how to do a genitourinary physical exam specific to assessing FSD.
When assessing obstetrics and gynecology clinical materials, sexual pleasure, arousal, and libido were not included anywhere in the curricula.
I have been teaching physicians about the therapies I developed (over 5000 clinicians in 50-plus countries over the past 14 years). During those sessions, I often stop the class and ask, “Who in here was taught how to retract the foreskin and examine the penis for phimosis?”
All hands will go up.
Then I will ask, “Who in here was taught in medical school how to retract the clitoral hood and examine the clitoris for phimosis?”
Not once has anyone raised a hand.
The Sex Remedies Gap
When I first published research offering support for using platelet-rich plasma to improve sexual function in women, women had not one drug approved by the US Food and Drug Administration (FDA) for the treatment of sexual dysfunction — none. Men had over 20. Today, men have a growing number of FDA-approved drugs for erectile dysfunction, including the “fils”; women have three.
Women have access to only one FDA-approved medication that primarily affects the genitalia: prasterone. This drug is indicated only for the treatment of pain in postmenopausal women. It does not directly enhance desire or improve orgasms. Said another way, although the incidence of sexual dysfunction is higher in premenopausal women than in other groups, they do not have a single approved medication designed to improve the function of their genitalia.
The other two of the three available drugs — flibanserin and bremelanotide — primarily affect the brain and could accurately be called psychoactive agents. They are available only for premenopausal women to improve desire. Flibanserin resulted in one extra sexual encounter per month on average, and patients are advised to avoid alcohol while using the drug. The other can make you vomit.
I do think all three of these treatments can be of great help to some women. I am not advising their disappearance. But in contrast to what is available to men, they are woefully inadequate.
Historical Perspective
In 1980, the medical establishment believed “most instances of acquired impotence are psychogenic.” Then, with the accidental discovery of the benefits of phosphodiesterase type 5 inhibitors, we realized that most cases of male sexual dysfunction involve the vasculature of the genitalia, not the neuroses of the brain. Yet, our two FDA-approved drugs for women with sexual dysfunction are designed to affect the brain. Women have nothing but off-label therapies to improve the function of the genitalia.
Despite the fact research supports the use of testosterone in women for both libido and orgasm, and despite the fact millions of women are treated with testosterone off-label for the benefit of sexual function, the only widely used FDA-approved class of drugs for women that affects testosterone — birth control pills, by blocking pituitary hormone production (the way they prevent pregnancy) — lowers the production of testosterone.
One might wonder, considering our expanded understanding of the endocrinology of both men and women, at the irony of why it is acceptable to lower the testosterone level of an adolescent girl knowingly, as if her development did not require the hormone (such would never be acceptable in an adolescent male unless sexual transitioning were the goal); yet, we are fearful of giving testosterone to grown women who can no longer make it.
Premenopausal Women: An Orphan Population
The concept of “orphan populations” can partially explain the gap in available therapies between men and women.
Women of childbearing age are risky to study; so, with testosterone, for example, it is safer and cheaper for pharmaceutical companies to prove the benefits for men and ride the profits from the off-label use for women. I don’t mean to condemn the manufacturers of testosterone, only to point out the phenomenon of why up to 30% of the prescriptions written by a primary care physician are off-label; off-label use is common among cardiologists (46%); up to 90% of children in the hospital receive at least one off-label drug; and approval of drugs for premenopausal women is more expensive than approval of drugs for men.
What Can Be Done?
The regrettable situation does not reflect evil intent on the part of regulators, educators, or physicians. But the gap between what women want and what medical education and the pharmaceutical-regulatory complex are providing is intolerably wide.
First, I would recommend a standard, required curriculum for the study of female sexual anatomy and function be established and widely adopted by medical schools. The reproductive system contains different components and a different purpose from the orgasm system, with modest overlap. Both systems should be taught in every medical school.
Second, physicians should be required to undergo a course in understanding their own sexuality. Research demonstrates doctors will avoid conversations about sex, and it seems to me this could be secondary to being uncomfortable with their own sexuality. After all, to talk with a patient about sex, you cannot be fearful of where the conversation may lead.
Third, the FDA might reconsider the requirements for the approval of drugs for FSD. Currently, to approve a drug for men, an objective finding — ie, an erection — can be sufficient. However, a higher bar, “satisfaction,” which is subjective, must be obtained with women.
Regenerative therapies have proved helpful but are not yet widely adopted; more grant money for the study of regenerative therapies would be a good start here.
Finally, by the definition of FSD, a woman must be psychologically distressed. The idea of sex is not pleasure alone. Sexual function affects family relationships, emotional health, confidence, even sleep, as well as the emotional well-being of the children who live in the house. Saying women are wonderfully and mysteriously made may be poetic, but it is not an excuse for not learning more and closing the gaps.
Dr. Runels is medical director of the Cellular Medicine Association, Fairhope, Alabama. He reported conflicts of interest with the Cellular Medicine Association, Runels Research Institute, Institute for Lichen Sclerosus, and Vulvar Health. A version of this article first appeared on Medscape.com.
During the month of September, Sexual Health Awareness Month, it may help to notice something: Men and their doctors have significantly more options to help with sexual function than do women and their clinicians. Moreover, .
Not convinced? Let’s take a quick tour.
The New Sexual Revolution and the Growing Anger
Around the time of the release of the book and movie Fifty Shades of Grey, Newsweek put the cultural sensation on its cover.
I bought the magazine at the airport and, while waiting for my plane, showed the story to a woman sitting next to me. “What do you think — is this the new ‘sexual revolution’?” I asked her.
She glanced at the cover and answered as accurately as if she had written the article: “In the ’60s, it became okay for women to have sex; now, it’s okay for women to demand good sex.”
I would add to that: Women are demanding good sex, and they want to define for themselves what “good” means.
That social revolution rages, still.
You would think that the demand would bring a corresponding response in clinical medicine. You would be wrong. Although efforts in some sectors are heroic, overall, the results are lagging the forward movement of women wanting better sex.
The Lag in Sexual Education
To examine the progression of the education of physicians regarding the treatment of female sexual dysfunction (FSD), Codispoti and colleagues examined the curricula of seven medical schools in and around Chicago. They found the following: Only one institution identified all anatomic components of the clitoris — one! Four of the seven discussed the physiology of the female orgasm. Only three of the seven highlighted the prevalence and epidemiology of FSD or the treatments for FSD. Only one of the seven explained how to do a genitourinary physical exam specific to assessing FSD.
When assessing obstetrics and gynecology clinical materials, sexual pleasure, arousal, and libido were not included anywhere in the curricula.
I have been teaching physicians about the therapies I developed (over 5000 clinicians in 50-plus countries over the past 14 years). During those sessions, I often stop the class and ask, “Who in here was taught how to retract the foreskin and examine the penis for phimosis?”
All hands will go up.
Then I will ask, “Who in here was taught in medical school how to retract the clitoral hood and examine the clitoris for phimosis?”
Not once has anyone raised a hand.
The Sex Remedies Gap
When I first published research offering support for using platelet-rich plasma to improve sexual function in women, women had not one drug approved by the US Food and Drug Administration (FDA) for the treatment of sexual dysfunction — none. Men had over 20. Today, men have a growing number of FDA-approved drugs for erectile dysfunction, including the “fils”; women have three.
Women have access to only one FDA-approved medication that primarily affects the genitalia: prasterone. This drug is indicated only for the treatment of pain in postmenopausal women. It does not directly enhance desire or improve orgasms. Said another way, although the incidence of sexual dysfunction is higher in premenopausal women than in other groups, they do not have a single approved medication designed to improve the function of their genitalia.
The other two of the three available drugs — flibanserin and bremelanotide — primarily affect the brain and could accurately be called psychoactive agents. They are available only for premenopausal women to improve desire. Flibanserin resulted in one extra sexual encounter per month on average, and patients are advised to avoid alcohol while using the drug. The other can make you vomit.
I do think all three of these treatments can be of great help to some women. I am not advising their disappearance. But in contrast to what is available to men, they are woefully inadequate.
Historical Perspective
In 1980, the medical establishment believed “most instances of acquired impotence are psychogenic.” Then, with the accidental discovery of the benefits of phosphodiesterase type 5 inhibitors, we realized that most cases of male sexual dysfunction involve the vasculature of the genitalia, not the neuroses of the brain. Yet, our two FDA-approved drugs for women with sexual dysfunction are designed to affect the brain. Women have nothing but off-label therapies to improve the function of the genitalia.
Despite the fact research supports the use of testosterone in women for both libido and orgasm, and despite the fact millions of women are treated with testosterone off-label for the benefit of sexual function, the only widely used FDA-approved class of drugs for women that affects testosterone — birth control pills, by blocking pituitary hormone production (the way they prevent pregnancy) — lowers the production of testosterone.
One might wonder, considering our expanded understanding of the endocrinology of both men and women, at the irony of why it is acceptable to lower the testosterone level of an adolescent girl knowingly, as if her development did not require the hormone (such would never be acceptable in an adolescent male unless sexual transitioning were the goal); yet, we are fearful of giving testosterone to grown women who can no longer make it.
Premenopausal Women: An Orphan Population
The concept of “orphan populations” can partially explain the gap in available therapies between men and women.
Women of childbearing age are risky to study; so, with testosterone, for example, it is safer and cheaper for pharmaceutical companies to prove the benefits for men and ride the profits from the off-label use for women. I don’t mean to condemn the manufacturers of testosterone, only to point out the phenomenon of why up to 30% of the prescriptions written by a primary care physician are off-label; off-label use is common among cardiologists (46%); up to 90% of children in the hospital receive at least one off-label drug; and approval of drugs for premenopausal women is more expensive than approval of drugs for men.
What Can Be Done?
The regrettable situation does not reflect evil intent on the part of regulators, educators, or physicians. But the gap between what women want and what medical education and the pharmaceutical-regulatory complex are providing is intolerably wide.
First, I would recommend a standard, required curriculum for the study of female sexual anatomy and function be established and widely adopted by medical schools. The reproductive system contains different components and a different purpose from the orgasm system, with modest overlap. Both systems should be taught in every medical school.
Second, physicians should be required to undergo a course in understanding their own sexuality. Research demonstrates doctors will avoid conversations about sex, and it seems to me this could be secondary to being uncomfortable with their own sexuality. After all, to talk with a patient about sex, you cannot be fearful of where the conversation may lead.
Third, the FDA might reconsider the requirements for the approval of drugs for FSD. Currently, to approve a drug for men, an objective finding — ie, an erection — can be sufficient. However, a higher bar, “satisfaction,” which is subjective, must be obtained with women.
Regenerative therapies have proved helpful but are not yet widely adopted; more grant money for the study of regenerative therapies would be a good start here.
Finally, by the definition of FSD, a woman must be psychologically distressed. The idea of sex is not pleasure alone. Sexual function affects family relationships, emotional health, confidence, even sleep, as well as the emotional well-being of the children who live in the house. Saying women are wonderfully and mysteriously made may be poetic, but it is not an excuse for not learning more and closing the gaps.
Dr. Runels is medical director of the Cellular Medicine Association, Fairhope, Alabama. He reported conflicts of interest with the Cellular Medicine Association, Runels Research Institute, Institute for Lichen Sclerosus, and Vulvar Health. A version of this article first appeared on Medscape.com.
During the month of September, Sexual Health Awareness Month, it may help to notice something: Men and their doctors have significantly more options to help with sexual function than do women and their clinicians. Moreover, .
Not convinced? Let’s take a quick tour.
The New Sexual Revolution and the Growing Anger
Around the time of the release of the book and movie Fifty Shades of Grey, Newsweek put the cultural sensation on its cover.
I bought the magazine at the airport and, while waiting for my plane, showed the story to a woman sitting next to me. “What do you think — is this the new ‘sexual revolution’?” I asked her.
She glanced at the cover and answered as accurately as if she had written the article: “In the ’60s, it became okay for women to have sex; now, it’s okay for women to demand good sex.”
I would add to that: Women are demanding good sex, and they want to define for themselves what “good” means.
That social revolution rages, still.
You would think that the demand would bring a corresponding response in clinical medicine. You would be wrong. Although efforts in some sectors are heroic, overall, the results are lagging the forward movement of women wanting better sex.
The Lag in Sexual Education
To examine the progression of the education of physicians regarding the treatment of female sexual dysfunction (FSD), Codispoti and colleagues examined the curricula of seven medical schools in and around Chicago. They found the following: Only one institution identified all anatomic components of the clitoris — one! Four of the seven discussed the physiology of the female orgasm. Only three of the seven highlighted the prevalence and epidemiology of FSD or the treatments for FSD. Only one of the seven explained how to do a genitourinary physical exam specific to assessing FSD.
When assessing obstetrics and gynecology clinical materials, sexual pleasure, arousal, and libido were not included anywhere in the curricula.
I have been teaching physicians about the therapies I developed (over 5000 clinicians in 50-plus countries over the past 14 years). During those sessions, I often stop the class and ask, “Who in here was taught how to retract the foreskin and examine the penis for phimosis?”
All hands will go up.
Then I will ask, “Who in here was taught in medical school how to retract the clitoral hood and examine the clitoris for phimosis?”
Not once has anyone raised a hand.
The Sex Remedies Gap
When I first published research offering support for using platelet-rich plasma to improve sexual function in women, women had not one drug approved by the US Food and Drug Administration (FDA) for the treatment of sexual dysfunction — none. Men had over 20. Today, men have a growing number of FDA-approved drugs for erectile dysfunction, including the “fils”; women have three.
Women have access to only one FDA-approved medication that primarily affects the genitalia: prasterone. This drug is indicated only for the treatment of pain in postmenopausal women. It does not directly enhance desire or improve orgasms. Said another way, although the incidence of sexual dysfunction is higher in premenopausal women than in other groups, they do not have a single approved medication designed to improve the function of their genitalia.
The other two of the three available drugs — flibanserin and bremelanotide — primarily affect the brain and could accurately be called psychoactive agents. They are available only for premenopausal women to improve desire. Flibanserin resulted in one extra sexual encounter per month on average, and patients are advised to avoid alcohol while using the drug. The other can make you vomit.
I do think all three of these treatments can be of great help to some women. I am not advising their disappearance. But in contrast to what is available to men, they are woefully inadequate.
Historical Perspective
In 1980, the medical establishment believed “most instances of acquired impotence are psychogenic.” Then, with the accidental discovery of the benefits of phosphodiesterase type 5 inhibitors, we realized that most cases of male sexual dysfunction involve the vasculature of the genitalia, not the neuroses of the brain. Yet, our two FDA-approved drugs for women with sexual dysfunction are designed to affect the brain. Women have nothing but off-label therapies to improve the function of the genitalia.
Despite the fact research supports the use of testosterone in women for both libido and orgasm, and despite the fact millions of women are treated with testosterone off-label for the benefit of sexual function, the only widely used FDA-approved class of drugs for women that affects testosterone — birth control pills, by blocking pituitary hormone production (the way they prevent pregnancy) — lowers the production of testosterone.
One might wonder, considering our expanded understanding of the endocrinology of both men and women, at the irony of why it is acceptable to lower the testosterone level of an adolescent girl knowingly, as if her development did not require the hormone (such would never be acceptable in an adolescent male unless sexual transitioning were the goal); yet, we are fearful of giving testosterone to grown women who can no longer make it.
Premenopausal Women: An Orphan Population
The concept of “orphan populations” can partially explain the gap in available therapies between men and women.
Women of childbearing age are risky to study; so, with testosterone, for example, it is safer and cheaper for pharmaceutical companies to prove the benefits for men and ride the profits from the off-label use for women. I don’t mean to condemn the manufacturers of testosterone, only to point out the phenomenon of why up to 30% of the prescriptions written by a primary care physician are off-label; off-label use is common among cardiologists (46%); up to 90% of children in the hospital receive at least one off-label drug; and approval of drugs for premenopausal women is more expensive than approval of drugs for men.
What Can Be Done?
The regrettable situation does not reflect evil intent on the part of regulators, educators, or physicians. But the gap between what women want and what medical education and the pharmaceutical-regulatory complex are providing is intolerably wide.
First, I would recommend a standard, required curriculum for the study of female sexual anatomy and function be established and widely adopted by medical schools. The reproductive system contains different components and a different purpose from the orgasm system, with modest overlap. Both systems should be taught in every medical school.
Second, physicians should be required to undergo a course in understanding their own sexuality. Research demonstrates doctors will avoid conversations about sex, and it seems to me this could be secondary to being uncomfortable with their own sexuality. After all, to talk with a patient about sex, you cannot be fearful of where the conversation may lead.
Third, the FDA might reconsider the requirements for the approval of drugs for FSD. Currently, to approve a drug for men, an objective finding — ie, an erection — can be sufficient. However, a higher bar, “satisfaction,” which is subjective, must be obtained with women.
Regenerative therapies have proved helpful but are not yet widely adopted; more grant money for the study of regenerative therapies would be a good start here.
Finally, by the definition of FSD, a woman must be psychologically distressed. The idea of sex is not pleasure alone. Sexual function affects family relationships, emotional health, confidence, even sleep, as well as the emotional well-being of the children who live in the house. Saying women are wonderfully and mysteriously made may be poetic, but it is not an excuse for not learning more and closing the gaps.
Dr. Runels is medical director of the Cellular Medicine Association, Fairhope, Alabama. He reported conflicts of interest with the Cellular Medicine Association, Runels Research Institute, Institute for Lichen Sclerosus, and Vulvar Health. A version of this article first appeared on Medscape.com.
Burnout and Vacations
How many weeks of vacation do you take each year? Does it feel like enough? What prevents you from taking more time off? Is it a contractual obligation to your employer? Or a concern about the lack of income while your are away? Is it the difficulty of finding coverage for your patient care responsibilities? How much of it is the dread of facing your unattended or poorly attended EHR box when you return?
A recent survey of more than 3000 US physicians found that almost 60% took 3 weeks or less vacation per year? The investigators also learned that 70% of the respondents did patient-related tasks while they were on vacation and less than half had full EHR coverage while they were away. Not surprisingly, providers who expressed concerns about finding someone to cover clinical responsibilities and financial concerns were less likely to take more than 3 weeks’ vacation.
As one might hope, taking more than 3 weeks’ vacation and having full EHR coverage were associated with decreased rates of burnout. On the other hand, spending more than 30 minutes per day doing patient-related work while on vacation was associated with higher rates of burnout.
In their conclusion, the authors suggest that if we hope to reduce physician burnout, employers should introduce system-level initiatives to ensure that physicians take adequate vacation and have adequate coverage for their clinical responsibilities — including EHR inbox management.
I will readily admit that I was one of those physicians who took less than 3 weeks of vacation and can’t recall ever taking more than 2 weeks. Since most of our vacations were staycations, I would usually round on the newborns first thing in the morning when I was in town to keep the flow of new patients coming into the practice.
I’m sure there was some collateral damage to my family, but our children continue to reassure me that they weren’t envious of their peers who went away on “real” vacations. As adults two of them take their families on the kind of vacations that make me envious. The third has married someone who shares, what I might call, a “robust commitment” to showing up in the office. But they seem to be a happy couple.
At the root of my vacation style was an egotistical delusion that there weren’t any clinicians in the community who could look after my patients as well as I did. Unfortunately, I had done little to discourage those patients who shared my distorted view.
I was lucky to have spent nearly all my career without the added burden of an EHR inbox. However, in the lead up to our infrequent vacations, the rush to tie up the loose ends of those patients for whom we had not achieved diagnostic closure was stressful and time consuming. Luckily, as a primary care pediatrician most of their problems were short lived. But, leaving the ship battened down could be exhausting.
I can fully understand why the physicians who are taking less than 3 weeks’ vacation and continue to be burdened by patient-related tasks while they are “away” are more likely to experience burnout. However, I wonder why I seemed to have been resistant considering my vacation style, which the authors of the above-mentioned article feel would have placed me at high risk.
I think the answer may lie in my commitment to making decisions that allowed me to maintain equilibrium in my life. In other words, if there were things in my day-to-day activities that were so taxing or distasteful that I am counting the hours and days until I can escape them, then I needed to make the necessary changes promptly and not count on a vacation to repair the accumulating damage. That may have required cutting back some responsibilities or it may have meant that I needed to be in better mental and physical shape to be able to maintain that equilibrium. Maybe it was more sleep, more exercise, less television, not investing as much in time-wasting meetings. This doesn’t mean that I didn’t have bad days. Stuff happens. But if I was putting together two or three bad days a week, something had to change. A vacation wasn’t going solve the inherent or systemic problems that are making day-to-day life so intolerable that I needed to escape for some respite.
In full disclosure, I will share that at age 55 I took a leave of 2 1/2 months and with my wife and another couple bicycled across America. This was a goal I had harbored since childhood and in anticipation over several decades had banked considerable coverage equity by doing extra coverage for other providers to minimize my guilt feelings at being away. This was not an escape from I job I didn’t enjoy going to everyday. It was an exercise in goal fulfillment.
I think the authors of this recent study should be applauded for providing some numbers to support the obvious. However,
Encouraging a clinician to take a bit more vacation may help. But, having someone to properly manage the EHR inbox would do a lot more. If your coverage is telling everyone to “Wait until Dr. Away has returned” it is only going to make things worse.
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].
How many weeks of vacation do you take each year? Does it feel like enough? What prevents you from taking more time off? Is it a contractual obligation to your employer? Or a concern about the lack of income while your are away? Is it the difficulty of finding coverage for your patient care responsibilities? How much of it is the dread of facing your unattended or poorly attended EHR box when you return?
A recent survey of more than 3000 US physicians found that almost 60% took 3 weeks or less vacation per year? The investigators also learned that 70% of the respondents did patient-related tasks while they were on vacation and less than half had full EHR coverage while they were away. Not surprisingly, providers who expressed concerns about finding someone to cover clinical responsibilities and financial concerns were less likely to take more than 3 weeks’ vacation.
As one might hope, taking more than 3 weeks’ vacation and having full EHR coverage were associated with decreased rates of burnout. On the other hand, spending more than 30 minutes per day doing patient-related work while on vacation was associated with higher rates of burnout.
In their conclusion, the authors suggest that if we hope to reduce physician burnout, employers should introduce system-level initiatives to ensure that physicians take adequate vacation and have adequate coverage for their clinical responsibilities — including EHR inbox management.
I will readily admit that I was one of those physicians who took less than 3 weeks of vacation and can’t recall ever taking more than 2 weeks. Since most of our vacations were staycations, I would usually round on the newborns first thing in the morning when I was in town to keep the flow of new patients coming into the practice.
I’m sure there was some collateral damage to my family, but our children continue to reassure me that they weren’t envious of their peers who went away on “real” vacations. As adults two of them take their families on the kind of vacations that make me envious. The third has married someone who shares, what I might call, a “robust commitment” to showing up in the office. But they seem to be a happy couple.
At the root of my vacation style was an egotistical delusion that there weren’t any clinicians in the community who could look after my patients as well as I did. Unfortunately, I had done little to discourage those patients who shared my distorted view.
I was lucky to have spent nearly all my career without the added burden of an EHR inbox. However, in the lead up to our infrequent vacations, the rush to tie up the loose ends of those patients for whom we had not achieved diagnostic closure was stressful and time consuming. Luckily, as a primary care pediatrician most of their problems were short lived. But, leaving the ship battened down could be exhausting.
I can fully understand why the physicians who are taking less than 3 weeks’ vacation and continue to be burdened by patient-related tasks while they are “away” are more likely to experience burnout. However, I wonder why I seemed to have been resistant considering my vacation style, which the authors of the above-mentioned article feel would have placed me at high risk.
I think the answer may lie in my commitment to making decisions that allowed me to maintain equilibrium in my life. In other words, if there were things in my day-to-day activities that were so taxing or distasteful that I am counting the hours and days until I can escape them, then I needed to make the necessary changes promptly and not count on a vacation to repair the accumulating damage. That may have required cutting back some responsibilities or it may have meant that I needed to be in better mental and physical shape to be able to maintain that equilibrium. Maybe it was more sleep, more exercise, less television, not investing as much in time-wasting meetings. This doesn’t mean that I didn’t have bad days. Stuff happens. But if I was putting together two or three bad days a week, something had to change. A vacation wasn’t going solve the inherent or systemic problems that are making day-to-day life so intolerable that I needed to escape for some respite.
In full disclosure, I will share that at age 55 I took a leave of 2 1/2 months and with my wife and another couple bicycled across America. This was a goal I had harbored since childhood and in anticipation over several decades had banked considerable coverage equity by doing extra coverage for other providers to minimize my guilt feelings at being away. This was not an escape from I job I didn’t enjoy going to everyday. It was an exercise in goal fulfillment.
I think the authors of this recent study should be applauded for providing some numbers to support the obvious. However,
Encouraging a clinician to take a bit more vacation may help. But, having someone to properly manage the EHR inbox would do a lot more. If your coverage is telling everyone to “Wait until Dr. Away has returned” it is only going to make things worse.
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].
How many weeks of vacation do you take each year? Does it feel like enough? What prevents you from taking more time off? Is it a contractual obligation to your employer? Or a concern about the lack of income while your are away? Is it the difficulty of finding coverage for your patient care responsibilities? How much of it is the dread of facing your unattended or poorly attended EHR box when you return?
A recent survey of more than 3000 US physicians found that almost 60% took 3 weeks or less vacation per year? The investigators also learned that 70% of the respondents did patient-related tasks while they were on vacation and less than half had full EHR coverage while they were away. Not surprisingly, providers who expressed concerns about finding someone to cover clinical responsibilities and financial concerns were less likely to take more than 3 weeks’ vacation.
As one might hope, taking more than 3 weeks’ vacation and having full EHR coverage were associated with decreased rates of burnout. On the other hand, spending more than 30 minutes per day doing patient-related work while on vacation was associated with higher rates of burnout.
In their conclusion, the authors suggest that if we hope to reduce physician burnout, employers should introduce system-level initiatives to ensure that physicians take adequate vacation and have adequate coverage for their clinical responsibilities — including EHR inbox management.
I will readily admit that I was one of those physicians who took less than 3 weeks of vacation and can’t recall ever taking more than 2 weeks. Since most of our vacations were staycations, I would usually round on the newborns first thing in the morning when I was in town to keep the flow of new patients coming into the practice.
I’m sure there was some collateral damage to my family, but our children continue to reassure me that they weren’t envious of their peers who went away on “real” vacations. As adults two of them take their families on the kind of vacations that make me envious. The third has married someone who shares, what I might call, a “robust commitment” to showing up in the office. But they seem to be a happy couple.
At the root of my vacation style was an egotistical delusion that there weren’t any clinicians in the community who could look after my patients as well as I did. Unfortunately, I had done little to discourage those patients who shared my distorted view.
I was lucky to have spent nearly all my career without the added burden of an EHR inbox. However, in the lead up to our infrequent vacations, the rush to tie up the loose ends of those patients for whom we had not achieved diagnostic closure was stressful and time consuming. Luckily, as a primary care pediatrician most of their problems were short lived. But, leaving the ship battened down could be exhausting.
I can fully understand why the physicians who are taking less than 3 weeks’ vacation and continue to be burdened by patient-related tasks while they are “away” are more likely to experience burnout. However, I wonder why I seemed to have been resistant considering my vacation style, which the authors of the above-mentioned article feel would have placed me at high risk.
I think the answer may lie in my commitment to making decisions that allowed me to maintain equilibrium in my life. In other words, if there were things in my day-to-day activities that were so taxing or distasteful that I am counting the hours and days until I can escape them, then I needed to make the necessary changes promptly and not count on a vacation to repair the accumulating damage. That may have required cutting back some responsibilities or it may have meant that I needed to be in better mental and physical shape to be able to maintain that equilibrium. Maybe it was more sleep, more exercise, less television, not investing as much in time-wasting meetings. This doesn’t mean that I didn’t have bad days. Stuff happens. But if I was putting together two or three bad days a week, something had to change. A vacation wasn’t going solve the inherent or systemic problems that are making day-to-day life so intolerable that I needed to escape for some respite.
In full disclosure, I will share that at age 55 I took a leave of 2 1/2 months and with my wife and another couple bicycled across America. This was a goal I had harbored since childhood and in anticipation over several decades had banked considerable coverage equity by doing extra coverage for other providers to minimize my guilt feelings at being away. This was not an escape from I job I didn’t enjoy going to everyday. It was an exercise in goal fulfillment.
I think the authors of this recent study should be applauded for providing some numbers to support the obvious. However,
Encouraging a clinician to take a bit more vacation may help. But, having someone to properly manage the EHR inbox would do a lot more. If your coverage is telling everyone to “Wait until Dr. Away has returned” it is only going to make things worse.
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].
Not Keeping Up With the Joneses
Dr. Jones and Dr. Joans are neurologists in town. I don’t know either one particularly well.
I don’t know their backstory, either, but they seem to have some intense competition going on.
Technically all of us neuros in the area compete with each other, but it’s pretty friendly. There are plenty of patients, and we all get along on the occasions we run into each other at the hospital or Costco or a meeting. Occasionally we call to bounce a case off each other. None of us advertise.
But Jones and Joans have kicked it up a notch. One got an EEG machine, the other got an EEG machine. A few weeks later one got a balance testing gadget, then the other got the same thing. One invested in all kinds of fancy devices to detect concussions, and shortly afterward so did the other one. Within a few months each bought their own Doppler equipment and hired an ultrasound tech. One took out a glossy ad in a local magazine, the next month so had the other. Both point out that they’ve been named on different “best doctor” lists. I assume it’s only a matter of time before each invests in their own MRI.
This kind of thing requires a lot of money to support, so both have jumped into the world of medical liens and hired NPs and PAs to increase patient volume.
I’m sure they both make more money than I ever will, and they can have it.
I don’t need that kind of complexity in my life. I have my own EMG/NCV machine, and beyond that I send all the testing (and complicated EMG/NCVs) to other facilities. I don’t want to figure out how to make payments on all those new gadgets, or hire staff to run them, or learn all the new codes I’d need (I do all my own coding, anyway), or decide if the advertising will pay for itself, or deal with liens.
I’m not even sure I want to be that busy. Obviously, I don’t want to be empty, but I also like having some degree of sanity. Time to review tests, type up notes, return calls ... all the things you have to do on the fly between patients, because if you don’t get them done at the office then you have to do them when you get home. Believe me, I already have enough going on there.
I have no desire to advertise that I’m the best neurologist in town (though I believe I’m the best in my building, since there isn’t another one) or to be the busiest, or to be involved in a game of one-upmanship with the nice group down the street.
If Drs. Jones and Joans want to do that, fine. More power to them.
For me, I’ve chosen simplicity in my practice, and prefer it.
I’m willing to trade that for money.
Dr. Block has a solo neurology practice in Scottsdale, Arizona.
Dr. Jones and Dr. Joans are neurologists in town. I don’t know either one particularly well.
I don’t know their backstory, either, but they seem to have some intense competition going on.
Technically all of us neuros in the area compete with each other, but it’s pretty friendly. There are plenty of patients, and we all get along on the occasions we run into each other at the hospital or Costco or a meeting. Occasionally we call to bounce a case off each other. None of us advertise.
But Jones and Joans have kicked it up a notch. One got an EEG machine, the other got an EEG machine. A few weeks later one got a balance testing gadget, then the other got the same thing. One invested in all kinds of fancy devices to detect concussions, and shortly afterward so did the other one. Within a few months each bought their own Doppler equipment and hired an ultrasound tech. One took out a glossy ad in a local magazine, the next month so had the other. Both point out that they’ve been named on different “best doctor” lists. I assume it’s only a matter of time before each invests in their own MRI.
This kind of thing requires a lot of money to support, so both have jumped into the world of medical liens and hired NPs and PAs to increase patient volume.
I’m sure they both make more money than I ever will, and they can have it.
I don’t need that kind of complexity in my life. I have my own EMG/NCV machine, and beyond that I send all the testing (and complicated EMG/NCVs) to other facilities. I don’t want to figure out how to make payments on all those new gadgets, or hire staff to run them, or learn all the new codes I’d need (I do all my own coding, anyway), or decide if the advertising will pay for itself, or deal with liens.
I’m not even sure I want to be that busy. Obviously, I don’t want to be empty, but I also like having some degree of sanity. Time to review tests, type up notes, return calls ... all the things you have to do on the fly between patients, because if you don’t get them done at the office then you have to do them when you get home. Believe me, I already have enough going on there.
I have no desire to advertise that I’m the best neurologist in town (though I believe I’m the best in my building, since there isn’t another one) or to be the busiest, or to be involved in a game of one-upmanship with the nice group down the street.
If Drs. Jones and Joans want to do that, fine. More power to them.
For me, I’ve chosen simplicity in my practice, and prefer it.
I’m willing to trade that for money.
Dr. Block has a solo neurology practice in Scottsdale, Arizona.
Dr. Jones and Dr. Joans are neurologists in town. I don’t know either one particularly well.
I don’t know their backstory, either, but they seem to have some intense competition going on.
Technically all of us neuros in the area compete with each other, but it’s pretty friendly. There are plenty of patients, and we all get along on the occasions we run into each other at the hospital or Costco or a meeting. Occasionally we call to bounce a case off each other. None of us advertise.
But Jones and Joans have kicked it up a notch. One got an EEG machine, the other got an EEG machine. A few weeks later one got a balance testing gadget, then the other got the same thing. One invested in all kinds of fancy devices to detect concussions, and shortly afterward so did the other one. Within a few months each bought their own Doppler equipment and hired an ultrasound tech. One took out a glossy ad in a local magazine, the next month so had the other. Both point out that they’ve been named on different “best doctor” lists. I assume it’s only a matter of time before each invests in their own MRI.
This kind of thing requires a lot of money to support, so both have jumped into the world of medical liens and hired NPs and PAs to increase patient volume.
I’m sure they both make more money than I ever will, and they can have it.
I don’t need that kind of complexity in my life. I have my own EMG/NCV machine, and beyond that I send all the testing (and complicated EMG/NCVs) to other facilities. I don’t want to figure out how to make payments on all those new gadgets, or hire staff to run them, or learn all the new codes I’d need (I do all my own coding, anyway), or decide if the advertising will pay for itself, or deal with liens.
I’m not even sure I want to be that busy. Obviously, I don’t want to be empty, but I also like having some degree of sanity. Time to review tests, type up notes, return calls ... all the things you have to do on the fly between patients, because if you don’t get them done at the office then you have to do them when you get home. Believe me, I already have enough going on there.
I have no desire to advertise that I’m the best neurologist in town (though I believe I’m the best in my building, since there isn’t another one) or to be the busiest, or to be involved in a game of one-upmanship with the nice group down the street.
If Drs. Jones and Joans want to do that, fine. More power to them.
For me, I’ve chosen simplicity in my practice, and prefer it.
I’m willing to trade that for money.
Dr. Block has a solo neurology practice in Scottsdale, Arizona.
Once-Weekly Insulin: A Game-Changer for Primary Care
Presented at the European Association for the Study of Diabetes (EASD) 2024 congress in Madrid, the QWINT-2 study established that. Study participants were, however, receiving noninsulin glucose-lowering agents, including glucagon-like peptide 1 (GLP-1) receptor agonists.
Slightly higher rates of mild to moderate hypoglycemia were noted with efsitora compared with degludec, but no significant differences in severe hypoglycemia were observed. Nor was there any difference in weight gain between groups, and adverse events were balanced between study arms.
This study positions insulin efsitora alongside once-weekly insulin icodec as a novel long-acting insulin therapy. In the ONWARDS 3 trial, icodec was noninferior to once-daily degludec, in terms of A1c reduction. It also had an adverse effect profile like that of efsitora with respect to hypoglycemia and weight change.
So, what are the implications of a once-weekly insulin for primary care?
“Game-changer” is an overused term, but from the perspective of primary care, it applies to once-weekly insulin.
I initiate basal insulin much less frequently these days, given the multitude of noninsulin options now available to me in primary care, particularly the GLP-1 receptor agonists and the dual GLP-1/glucose-dependent insulinotropic polypeptide receptor agonists. The American Diabetes Association/EASD 2022 consensus report also reminds me that GLP-1 receptor agonists should be considered in all individuals with T2D before insulin, unless they are contraindicated. GLP-1 receptor agonists are insulin-sparing agents with a lower injection burden and a lower risk for hypoglycemia. They also promote significant weight loss compared with basal insulin.
But progressive beta-cell decline and insulin deficiency are among the key pathophysiologic abnormalities in T2D. Eventually, many patients with T2D, despite lifestyle interventions and medication adherence, do require insulin.
Understandably, many of my patients have reservations about commencing insulin. Significant stigma about starting insulin persists, because others often perceive insulin use as a failure to manage T2D. Patients frequently fear injections, and many are worried about how insulin therapy, specifically the risk for hypoglycemia, will affect their daily activities such as driving.
Clinicians often experience therapeutic inertia, hesitating to escalate therapy to insulin because of a lack of confidence and competence, which often results from inadequate education. Lengthy referral-to-treatment waiting times are common in the United Kingdom, and there is concern about the workload implications associated with insulin initiation.
Workload is a particular concern for my community nursing colleagues, who must visit some of my more frail and functionally dependent patients daily to administer their insulin.
In addition, the delivery of high-quality diabetes care in nursing homes, particularly for patients requiring insulin, has been a perennial challenge in the UK, again because of a lack of confidence and competence due to an absence of education for nursing and ancillary staff.
Moreover, it is not appropriate to switch many of these frail patients to noninsulin therapies because of their insulinopenia, as well as the significant weight (and sometimes muscle) loss associated with GLP-1 receptor agonists. Also, sodium-glucose cotransporter 2 inhibitors are associated with a risk for volume depletion and diabetic ketoacidosis.
I believe that the availability of a once-weekly insulin will help overcome many of the above barriers.
From a patient’s viewpoint, simplification of insulin therapy with once-weekly insulin will substantially reduce the number of injections required (from 365 to 52 over 1 year). This change will improve compliance and concordance even in patients with injection anxiety. These results will hopefully translate into improved glycemic control and a lower risk for the complications of T2D. Real-world evidence for these outcomes is not yet available, however. Also, the reduced amount of insulin consumables that once-weekly dosing requires will also help improve the environmental footprint of insulin therapy.
From a clinician’s viewpoint, once-weekly insulin may seem less daunting and could reduce therapeutic inertia, thus facilitating earlier initiation of insulin therapy and reducing the risk for complications of T2D. Although education remains pivotal, this ease of dosing may be more acceptable to many clinicians because it has less of an effect on workload. This dosing could even save time because it requires less intensive follow-up than daily basal insulin does.
My community nurse colleagues were ecstatic when I mentioned that once-weekly basal insulin was on the horizon. This formulation could reduce the number of weekly home visits from 7 to just 1, thus freeing up considerable healthcare resources. And if once-weekly insulin is coupled with continuous glucose monitoring, then remote review of glucose data can further streamline and optimize the management of T2D in frail older patients. I am sure that my nursing-home colleagues will be equally enthusiastic about simplifying insulin regimens and monitoring.
Finally, an unanswered question is how I manage “sick days” for patients on weekly insulin dosing. Of course, the golden rule of never stopping insulin during intercurrent illness must be followed, but is any dose titration required for once-weekly insulin? I suspect not, but do I need to consider adding a once-daily basal insulin or rapid-acting insulin to mitigate the glucose counterregulatory hormone response during acute illness? Initially, I will be asking specialist diabetes teams for further advice on managing sick days.
In conclusion, once-weekly dosing of insulin is a game-changer for primary care and could finally be the driver to quash therapeutic inertia and address common patient barriers when escalation to insulin is required.
Dr. Fernando, general practitioner partner, North Berwick Health Centre, North Berwick, Scotland, disclosed ties with Amarin, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Dexcom, Daiichi Sankyo, Lilly, Menarini, Novartis, Novo Nordisk, Roche Diagnostics, Embecta, Roche Diabetes Care, and Sanofi.
A version of this article appeared on Medscape.com.
Presented at the European Association for the Study of Diabetes (EASD) 2024 congress in Madrid, the QWINT-2 study established that. Study participants were, however, receiving noninsulin glucose-lowering agents, including glucagon-like peptide 1 (GLP-1) receptor agonists.
Slightly higher rates of mild to moderate hypoglycemia were noted with efsitora compared with degludec, but no significant differences in severe hypoglycemia were observed. Nor was there any difference in weight gain between groups, and adverse events were balanced between study arms.
This study positions insulin efsitora alongside once-weekly insulin icodec as a novel long-acting insulin therapy. In the ONWARDS 3 trial, icodec was noninferior to once-daily degludec, in terms of A1c reduction. It also had an adverse effect profile like that of efsitora with respect to hypoglycemia and weight change.
So, what are the implications of a once-weekly insulin for primary care?
“Game-changer” is an overused term, but from the perspective of primary care, it applies to once-weekly insulin.
I initiate basal insulin much less frequently these days, given the multitude of noninsulin options now available to me in primary care, particularly the GLP-1 receptor agonists and the dual GLP-1/glucose-dependent insulinotropic polypeptide receptor agonists. The American Diabetes Association/EASD 2022 consensus report also reminds me that GLP-1 receptor agonists should be considered in all individuals with T2D before insulin, unless they are contraindicated. GLP-1 receptor agonists are insulin-sparing agents with a lower injection burden and a lower risk for hypoglycemia. They also promote significant weight loss compared with basal insulin.
But progressive beta-cell decline and insulin deficiency are among the key pathophysiologic abnormalities in T2D. Eventually, many patients with T2D, despite lifestyle interventions and medication adherence, do require insulin.
Understandably, many of my patients have reservations about commencing insulin. Significant stigma about starting insulin persists, because others often perceive insulin use as a failure to manage T2D. Patients frequently fear injections, and many are worried about how insulin therapy, specifically the risk for hypoglycemia, will affect their daily activities such as driving.
Clinicians often experience therapeutic inertia, hesitating to escalate therapy to insulin because of a lack of confidence and competence, which often results from inadequate education. Lengthy referral-to-treatment waiting times are common in the United Kingdom, and there is concern about the workload implications associated with insulin initiation.
Workload is a particular concern for my community nursing colleagues, who must visit some of my more frail and functionally dependent patients daily to administer their insulin.
In addition, the delivery of high-quality diabetes care in nursing homes, particularly for patients requiring insulin, has been a perennial challenge in the UK, again because of a lack of confidence and competence due to an absence of education for nursing and ancillary staff.
Moreover, it is not appropriate to switch many of these frail patients to noninsulin therapies because of their insulinopenia, as well as the significant weight (and sometimes muscle) loss associated with GLP-1 receptor agonists. Also, sodium-glucose cotransporter 2 inhibitors are associated with a risk for volume depletion and diabetic ketoacidosis.
I believe that the availability of a once-weekly insulin will help overcome many of the above barriers.
From a patient’s viewpoint, simplification of insulin therapy with once-weekly insulin will substantially reduce the number of injections required (from 365 to 52 over 1 year). This change will improve compliance and concordance even in patients with injection anxiety. These results will hopefully translate into improved glycemic control and a lower risk for the complications of T2D. Real-world evidence for these outcomes is not yet available, however. Also, the reduced amount of insulin consumables that once-weekly dosing requires will also help improve the environmental footprint of insulin therapy.
From a clinician’s viewpoint, once-weekly insulin may seem less daunting and could reduce therapeutic inertia, thus facilitating earlier initiation of insulin therapy and reducing the risk for complications of T2D. Although education remains pivotal, this ease of dosing may be more acceptable to many clinicians because it has less of an effect on workload. This dosing could even save time because it requires less intensive follow-up than daily basal insulin does.
My community nurse colleagues were ecstatic when I mentioned that once-weekly basal insulin was on the horizon. This formulation could reduce the number of weekly home visits from 7 to just 1, thus freeing up considerable healthcare resources. And if once-weekly insulin is coupled with continuous glucose monitoring, then remote review of glucose data can further streamline and optimize the management of T2D in frail older patients. I am sure that my nursing-home colleagues will be equally enthusiastic about simplifying insulin regimens and monitoring.
Finally, an unanswered question is how I manage “sick days” for patients on weekly insulin dosing. Of course, the golden rule of never stopping insulin during intercurrent illness must be followed, but is any dose titration required for once-weekly insulin? I suspect not, but do I need to consider adding a once-daily basal insulin or rapid-acting insulin to mitigate the glucose counterregulatory hormone response during acute illness? Initially, I will be asking specialist diabetes teams for further advice on managing sick days.
In conclusion, once-weekly dosing of insulin is a game-changer for primary care and could finally be the driver to quash therapeutic inertia and address common patient barriers when escalation to insulin is required.
Dr. Fernando, general practitioner partner, North Berwick Health Centre, North Berwick, Scotland, disclosed ties with Amarin, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Dexcom, Daiichi Sankyo, Lilly, Menarini, Novartis, Novo Nordisk, Roche Diagnostics, Embecta, Roche Diabetes Care, and Sanofi.
A version of this article appeared on Medscape.com.
Presented at the European Association for the Study of Diabetes (EASD) 2024 congress in Madrid, the QWINT-2 study established that. Study participants were, however, receiving noninsulin glucose-lowering agents, including glucagon-like peptide 1 (GLP-1) receptor agonists.
Slightly higher rates of mild to moderate hypoglycemia were noted with efsitora compared with degludec, but no significant differences in severe hypoglycemia were observed. Nor was there any difference in weight gain between groups, and adverse events were balanced between study arms.
This study positions insulin efsitora alongside once-weekly insulin icodec as a novel long-acting insulin therapy. In the ONWARDS 3 trial, icodec was noninferior to once-daily degludec, in terms of A1c reduction. It also had an adverse effect profile like that of efsitora with respect to hypoglycemia and weight change.
So, what are the implications of a once-weekly insulin for primary care?
“Game-changer” is an overused term, but from the perspective of primary care, it applies to once-weekly insulin.
I initiate basal insulin much less frequently these days, given the multitude of noninsulin options now available to me in primary care, particularly the GLP-1 receptor agonists and the dual GLP-1/glucose-dependent insulinotropic polypeptide receptor agonists. The American Diabetes Association/EASD 2022 consensus report also reminds me that GLP-1 receptor agonists should be considered in all individuals with T2D before insulin, unless they are contraindicated. GLP-1 receptor agonists are insulin-sparing agents with a lower injection burden and a lower risk for hypoglycemia. They also promote significant weight loss compared with basal insulin.
But progressive beta-cell decline and insulin deficiency are among the key pathophysiologic abnormalities in T2D. Eventually, many patients with T2D, despite lifestyle interventions and medication adherence, do require insulin.
Understandably, many of my patients have reservations about commencing insulin. Significant stigma about starting insulin persists, because others often perceive insulin use as a failure to manage T2D. Patients frequently fear injections, and many are worried about how insulin therapy, specifically the risk for hypoglycemia, will affect their daily activities such as driving.
Clinicians often experience therapeutic inertia, hesitating to escalate therapy to insulin because of a lack of confidence and competence, which often results from inadequate education. Lengthy referral-to-treatment waiting times are common in the United Kingdom, and there is concern about the workload implications associated with insulin initiation.
Workload is a particular concern for my community nursing colleagues, who must visit some of my more frail and functionally dependent patients daily to administer their insulin.
In addition, the delivery of high-quality diabetes care in nursing homes, particularly for patients requiring insulin, has been a perennial challenge in the UK, again because of a lack of confidence and competence due to an absence of education for nursing and ancillary staff.
Moreover, it is not appropriate to switch many of these frail patients to noninsulin therapies because of their insulinopenia, as well as the significant weight (and sometimes muscle) loss associated with GLP-1 receptor agonists. Also, sodium-glucose cotransporter 2 inhibitors are associated with a risk for volume depletion and diabetic ketoacidosis.
I believe that the availability of a once-weekly insulin will help overcome many of the above barriers.
From a patient’s viewpoint, simplification of insulin therapy with once-weekly insulin will substantially reduce the number of injections required (from 365 to 52 over 1 year). This change will improve compliance and concordance even in patients with injection anxiety. These results will hopefully translate into improved glycemic control and a lower risk for the complications of T2D. Real-world evidence for these outcomes is not yet available, however. Also, the reduced amount of insulin consumables that once-weekly dosing requires will also help improve the environmental footprint of insulin therapy.
From a clinician’s viewpoint, once-weekly insulin may seem less daunting and could reduce therapeutic inertia, thus facilitating earlier initiation of insulin therapy and reducing the risk for complications of T2D. Although education remains pivotal, this ease of dosing may be more acceptable to many clinicians because it has less of an effect on workload. This dosing could even save time because it requires less intensive follow-up than daily basal insulin does.
My community nurse colleagues were ecstatic when I mentioned that once-weekly basal insulin was on the horizon. This formulation could reduce the number of weekly home visits from 7 to just 1, thus freeing up considerable healthcare resources. And if once-weekly insulin is coupled with continuous glucose monitoring, then remote review of glucose data can further streamline and optimize the management of T2D in frail older patients. I am sure that my nursing-home colleagues will be equally enthusiastic about simplifying insulin regimens and monitoring.
Finally, an unanswered question is how I manage “sick days” for patients on weekly insulin dosing. Of course, the golden rule of never stopping insulin during intercurrent illness must be followed, but is any dose titration required for once-weekly insulin? I suspect not, but do I need to consider adding a once-daily basal insulin or rapid-acting insulin to mitigate the glucose counterregulatory hormone response during acute illness? Initially, I will be asking specialist diabetes teams for further advice on managing sick days.
In conclusion, once-weekly dosing of insulin is a game-changer for primary care and could finally be the driver to quash therapeutic inertia and address common patient barriers when escalation to insulin is required.
Dr. Fernando, general practitioner partner, North Berwick Health Centre, North Berwick, Scotland, disclosed ties with Amarin, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Dexcom, Daiichi Sankyo, Lilly, Menarini, Novartis, Novo Nordisk, Roche Diagnostics, Embecta, Roche Diabetes Care, and Sanofi.
A version of this article appeared on Medscape.com.
Abnormal TSH: Forget it or Fret it?
If you’re like most primary care clinicians, your email inbox is flooded with messages from patients with questions about lab results. A common query: Should I be worried about an abnormal value on a test of thyroid-stimulating hormone (TSH)?
For guidance, this news organization spoke with Angela Leung, MD, associate professor of medicine in the Division of Endocrinology, Diabetes & Metabolism at the UCLA David Geffen School of Medicine and an endocrinologist at UCLA and the VA Greater Los Angeles Healthcare System, and Karen Tsai, MD, assistant clinical professor of endocrinology at City of Hope Comprehensive Cancer Center in Duarte, California. The following interview has been edited for length and clarity.
Question: Why do you usually start by measuring TSH levels?
Dr. Leung: We need to measure the thyroid status in a way that integrates more information about the long-term thyroid status and not small changes in thyroid hormone levels. TSH is made by the pituitary gland in the brain, which integrates information about the signals of high and low levels from each of the different thyroid hormones.
Now we can measure the actual thyroid hormones — primarily we’re talking about T3 and T4 — but if we do that, we are relying on a single snapshot in the bloodstream at that moment. The levels might change throughout the day in response to ongoing metabolism and outside stresses. So we usually start by measuring the TSH level, which is a good representation of the compilation of all those things over the past 30 days or so.
Question: How do you describe a low TSH result to patients?
Dr. Leung: Whenever we encounter a low TSH level, we want to repeat the test because it is a dynamic test, and it can change in response to several factors. If it is indeed low, we’re thinking that perhaps there’s a little bit of extra thyroid hormone in the body. It can be either temporary or more chronic, but that higher amount of thyroid hormone is telling the pituitary gland in the brain to start making less. So TSH levels go low when we need less thyroid hormone.
Question: What are some of the reasons for a low TSH level?
Dr. Leung: One of the most common situations for a temporarily low TSH level I see is what we call nonthyroidal illness, like a common cold or just being under the weather. Other things that can artifactually lower the TSH level could be the use of steroids, such as prednisone for asthma or some sort of a rheumatologic condition. Also, the TSH level could be low if a person has been recently exposed to very high amounts of iodine, such as iodinated contrast needed for a CT scan.
If the TSH level remains persistently low, usually in the presence of high thyroid hormone (T3 and/or T4) levels, the most common reason for hyperthyroidism is Graves disease, in which there are autoantibodies — measurable in the blood — that can stimulate the thyroid gland in the neck to make extra thyroid hormone.
Question: And what does an elevated TSH level mean?
Dr. Leung: Again, we want to confirm that it is elevated. We need at least two tests to confirm a high TSH level. A persistently elevated TSH level is a signal there might be low thyroid hormone levels in the body, which could be transient or more longer lasting.
Question: What are some of the most common causes of an elevated TSH level?
Dr. Leung: If the TSH level is confirmed high and the thyroid hormone levels are low, the most common cause of hypothyroidism here in the United States is Hashimoto thyroiditis.
Globally, iodine deficiency is the most common reason for hypothyroidism and may be a problem in parts of the globe where there are endemically low iodine levels in soil, crops, and the food supply like not having enough iodized salt. The thyroid is reliant on having enough iodine as a micronutrient to make thyroid hormone. If it doesn’t, the thyroid really can’t make thyroid hormone. It’s important to also remember, though, that having too much iodine can result in hypo- or hyperthyroidism.
Dr. Tsai: I take a glance at their medication list. Some of the patients are on methimazole or levothyroxine, and those medications should be adjusted first to normalize the TSH level. Other medications like lithium and amiodarone can also cause elevated TSH levels. We are also seeing a lot of patients on cancer therapies, such as tyrosine kinase inhibitors or immunotherapy, that can cause an elevated TSH level.
Question: If the repeat TSH test shows that TSH levels are still elevated, what comes next in your workup?
Dr. Tsai: If there’s not a real clear-cut diagnosis, I’ll order the thyroid peroxidase antibody and the thyroglobulin antibody, although thyroid peroxidase antibody, which is indicative of autoimmune thyroid disease, alone is usually sufficient to make that diagnosis.
Question: Should clinicians follow thyroid antibodies over time?
Dr. Tsai: I usually don’t repeat the antibody tests. In those circumstances where patients who were diagnosed 50-60 years ago and perhaps it is unknown if they had the thyroid antibodies measured at the time and now they’re saying, “Do I actually have Hashimoto’s?” or “Do I really need to continue this for the rest of my life?” I do repeat antibody tests to help gauge if the patient’s levothyroxine can be stopped.
Question: How important is it to follow T4 or T3 levels?
Dr. Tsai: T4 and T3 levels can help differentiate overt thyroid dysfunction — where T3 and/or T4 levels will be abnormal — from subclinical thyroid dysfunction — where T3 and T4 levels would be normal. In general, although we do not fully appreciate the best metric to monitor hypo- or hyperthyroidism, because some patients with a normal TSH level still may have symptoms of thyroid dysfunction, these peripheral thyroid hormone levels are usually the most helpful at the time of initial diagnosis.
Question: What are your criteria for initiating treatment for hypothyroidism?
Dr. Tsai: If the TSH level > 10 mIU/L, I recommend levothyroxine hormone replacement. A lot of published data support clinical benefit in this group.
There is a gray area in those patients who have a TSH level higher than the upper limit of the reference range but less than 10. If the patient doesn’t have overt hypothyroid symptoms, I discuss the findings with the patient but don’t really feel eager to treat. I recommend checking the levels again in 6 months to see where that TSH goes, and if it worsens or becomes greater than 10 mIU/L, I then recommend levothyroxine hormone replacement.
It is also important to note that a TSH level of 5-7 may be an acceptable range for older patients, and they do not require levothyroxine.
The other category is patients whose TSH level is greater than the upper limit of the normal reference range but less than 10 and with overt hypothyroid symptoms such as fatigue, unintentional weight gain, constipation, or cold intolerance. In these patients, it is worthwhile to try a low dose of levothyroxine (25-50 mcg/d) and repeat TSH and free T4 tests in 6-8 weeks and see if the TSH level normalizes.
Dr. Leung: When you look at subclinical hypothyroidism, the situation of an isolated high TSH level in the setting of normal T4 levels, if the TSH level is mildly elevated in the 5-7 mIU/L range, there’s a 60% chance that it will normalize within 6 months.
Going back to Karen’s point, a lot of people are started and maintained on low doses of thyroid hormone forever and ever. A recent study on levothyroxine use found half of the prescriptions were unnecessary.
Question: In an era where many patients obtain much of their health information from TikTok, what’s your approach with patients with a normal TSH level who feel that they should have more testing or start treatment?
Dr. Tsai: Fatigue is one of the common referrals we get into our endocrinology practice, and everyone is convinced that their thyroid is the culprit. It is important to note, however, that fatigue can be due to different diseases such as anemia, depression, sleep disorders, or a recent viral illness.
TSH tests are readily available and cheap. I don’t mind ordering the lab test again if it helps give the patient some reassurance. I also find that patients are relieved once they hear from their endocrinologist that their thyroid is unlikely to be the cause of their fatigue.
Some other endocrine causes we may consider additionally working up include adrenal insufficiency, vitamin D deficiency, and diabetes. A comprehensive metabolic panel and complete blood count is part of my workup to rule out any gross electrolyte abnormalities or any new diagnosis of anemia, liver disease, or chronic kidney disease.
Question: What are your criteria for recommending that someone see an endocrinologist?
Dr. Tsai: Our primary care colleagues can do a workup and interpretation of thyroid function tests in most cases. In the situations where the thyroid function test results are discordant (ie, elevated TSH and elevated free T4 levels or low TSH and low free T4 levels) or difficult to interpret, it would be appropriate to refer the patient to an endocrinologist.
One of the common referrals that we do get from the community is a patient’s thyroid function tests going from hyperthyroid to hypothyroid without a clear explanation or the patient is suboptimally controlled with levothyroxine or methimazole. In those circumstances, it would be worthwhile to send to an endocrinologist try to discern an underlying cause or for optimization of medication.
Dr. Leung and Dr. Tsai had no financial disclosures.
A version of this article appeared on Medscape.com.
If you’re like most primary care clinicians, your email inbox is flooded with messages from patients with questions about lab results. A common query: Should I be worried about an abnormal value on a test of thyroid-stimulating hormone (TSH)?
For guidance, this news organization spoke with Angela Leung, MD, associate professor of medicine in the Division of Endocrinology, Diabetes & Metabolism at the UCLA David Geffen School of Medicine and an endocrinologist at UCLA and the VA Greater Los Angeles Healthcare System, and Karen Tsai, MD, assistant clinical professor of endocrinology at City of Hope Comprehensive Cancer Center in Duarte, California. The following interview has been edited for length and clarity.
Question: Why do you usually start by measuring TSH levels?
Dr. Leung: We need to measure the thyroid status in a way that integrates more information about the long-term thyroid status and not small changes in thyroid hormone levels. TSH is made by the pituitary gland in the brain, which integrates information about the signals of high and low levels from each of the different thyroid hormones.
Now we can measure the actual thyroid hormones — primarily we’re talking about T3 and T4 — but if we do that, we are relying on a single snapshot in the bloodstream at that moment. The levels might change throughout the day in response to ongoing metabolism and outside stresses. So we usually start by measuring the TSH level, which is a good representation of the compilation of all those things over the past 30 days or so.
Question: How do you describe a low TSH result to patients?
Dr. Leung: Whenever we encounter a low TSH level, we want to repeat the test because it is a dynamic test, and it can change in response to several factors. If it is indeed low, we’re thinking that perhaps there’s a little bit of extra thyroid hormone in the body. It can be either temporary or more chronic, but that higher amount of thyroid hormone is telling the pituitary gland in the brain to start making less. So TSH levels go low when we need less thyroid hormone.
Question: What are some of the reasons for a low TSH level?
Dr. Leung: One of the most common situations for a temporarily low TSH level I see is what we call nonthyroidal illness, like a common cold or just being under the weather. Other things that can artifactually lower the TSH level could be the use of steroids, such as prednisone for asthma or some sort of a rheumatologic condition. Also, the TSH level could be low if a person has been recently exposed to very high amounts of iodine, such as iodinated contrast needed for a CT scan.
If the TSH level remains persistently low, usually in the presence of high thyroid hormone (T3 and/or T4) levels, the most common reason for hyperthyroidism is Graves disease, in which there are autoantibodies — measurable in the blood — that can stimulate the thyroid gland in the neck to make extra thyroid hormone.
Question: And what does an elevated TSH level mean?
Dr. Leung: Again, we want to confirm that it is elevated. We need at least two tests to confirm a high TSH level. A persistently elevated TSH level is a signal there might be low thyroid hormone levels in the body, which could be transient or more longer lasting.
Question: What are some of the most common causes of an elevated TSH level?
Dr. Leung: If the TSH level is confirmed high and the thyroid hormone levels are low, the most common cause of hypothyroidism here in the United States is Hashimoto thyroiditis.
Globally, iodine deficiency is the most common reason for hypothyroidism and may be a problem in parts of the globe where there are endemically low iodine levels in soil, crops, and the food supply like not having enough iodized salt. The thyroid is reliant on having enough iodine as a micronutrient to make thyroid hormone. If it doesn’t, the thyroid really can’t make thyroid hormone. It’s important to also remember, though, that having too much iodine can result in hypo- or hyperthyroidism.
Dr. Tsai: I take a glance at their medication list. Some of the patients are on methimazole or levothyroxine, and those medications should be adjusted first to normalize the TSH level. Other medications like lithium and amiodarone can also cause elevated TSH levels. We are also seeing a lot of patients on cancer therapies, such as tyrosine kinase inhibitors or immunotherapy, that can cause an elevated TSH level.
Question: If the repeat TSH test shows that TSH levels are still elevated, what comes next in your workup?
Dr. Tsai: If there’s not a real clear-cut diagnosis, I’ll order the thyroid peroxidase antibody and the thyroglobulin antibody, although thyroid peroxidase antibody, which is indicative of autoimmune thyroid disease, alone is usually sufficient to make that diagnosis.
Question: Should clinicians follow thyroid antibodies over time?
Dr. Tsai: I usually don’t repeat the antibody tests. In those circumstances where patients who were diagnosed 50-60 years ago and perhaps it is unknown if they had the thyroid antibodies measured at the time and now they’re saying, “Do I actually have Hashimoto’s?” or “Do I really need to continue this for the rest of my life?” I do repeat antibody tests to help gauge if the patient’s levothyroxine can be stopped.
Question: How important is it to follow T4 or T3 levels?
Dr. Tsai: T4 and T3 levels can help differentiate overt thyroid dysfunction — where T3 and/or T4 levels will be abnormal — from subclinical thyroid dysfunction — where T3 and T4 levels would be normal. In general, although we do not fully appreciate the best metric to monitor hypo- or hyperthyroidism, because some patients with a normal TSH level still may have symptoms of thyroid dysfunction, these peripheral thyroid hormone levels are usually the most helpful at the time of initial diagnosis.
Question: What are your criteria for initiating treatment for hypothyroidism?
Dr. Tsai: If the TSH level > 10 mIU/L, I recommend levothyroxine hormone replacement. A lot of published data support clinical benefit in this group.
There is a gray area in those patients who have a TSH level higher than the upper limit of the reference range but less than 10. If the patient doesn’t have overt hypothyroid symptoms, I discuss the findings with the patient but don’t really feel eager to treat. I recommend checking the levels again in 6 months to see where that TSH goes, and if it worsens or becomes greater than 10 mIU/L, I then recommend levothyroxine hormone replacement.
It is also important to note that a TSH level of 5-7 may be an acceptable range for older patients, and they do not require levothyroxine.
The other category is patients whose TSH level is greater than the upper limit of the normal reference range but less than 10 and with overt hypothyroid symptoms such as fatigue, unintentional weight gain, constipation, or cold intolerance. In these patients, it is worthwhile to try a low dose of levothyroxine (25-50 mcg/d) and repeat TSH and free T4 tests in 6-8 weeks and see if the TSH level normalizes.
Dr. Leung: When you look at subclinical hypothyroidism, the situation of an isolated high TSH level in the setting of normal T4 levels, if the TSH level is mildly elevated in the 5-7 mIU/L range, there’s a 60% chance that it will normalize within 6 months.
Going back to Karen’s point, a lot of people are started and maintained on low doses of thyroid hormone forever and ever. A recent study on levothyroxine use found half of the prescriptions were unnecessary.
Question: In an era where many patients obtain much of their health information from TikTok, what’s your approach with patients with a normal TSH level who feel that they should have more testing or start treatment?
Dr. Tsai: Fatigue is one of the common referrals we get into our endocrinology practice, and everyone is convinced that their thyroid is the culprit. It is important to note, however, that fatigue can be due to different diseases such as anemia, depression, sleep disorders, or a recent viral illness.
TSH tests are readily available and cheap. I don’t mind ordering the lab test again if it helps give the patient some reassurance. I also find that patients are relieved once they hear from their endocrinologist that their thyroid is unlikely to be the cause of their fatigue.
Some other endocrine causes we may consider additionally working up include adrenal insufficiency, vitamin D deficiency, and diabetes. A comprehensive metabolic panel and complete blood count is part of my workup to rule out any gross electrolyte abnormalities or any new diagnosis of anemia, liver disease, or chronic kidney disease.
Question: What are your criteria for recommending that someone see an endocrinologist?
Dr. Tsai: Our primary care colleagues can do a workup and interpretation of thyroid function tests in most cases. In the situations where the thyroid function test results are discordant (ie, elevated TSH and elevated free T4 levels or low TSH and low free T4 levels) or difficult to interpret, it would be appropriate to refer the patient to an endocrinologist.
One of the common referrals that we do get from the community is a patient’s thyroid function tests going from hyperthyroid to hypothyroid without a clear explanation or the patient is suboptimally controlled with levothyroxine or methimazole. In those circumstances, it would be worthwhile to send to an endocrinologist try to discern an underlying cause or for optimization of medication.
Dr. Leung and Dr. Tsai had no financial disclosures.
A version of this article appeared on Medscape.com.
If you’re like most primary care clinicians, your email inbox is flooded with messages from patients with questions about lab results. A common query: Should I be worried about an abnormal value on a test of thyroid-stimulating hormone (TSH)?
For guidance, this news organization spoke with Angela Leung, MD, associate professor of medicine in the Division of Endocrinology, Diabetes & Metabolism at the UCLA David Geffen School of Medicine and an endocrinologist at UCLA and the VA Greater Los Angeles Healthcare System, and Karen Tsai, MD, assistant clinical professor of endocrinology at City of Hope Comprehensive Cancer Center in Duarte, California. The following interview has been edited for length and clarity.
Question: Why do you usually start by measuring TSH levels?
Dr. Leung: We need to measure the thyroid status in a way that integrates more information about the long-term thyroid status and not small changes in thyroid hormone levels. TSH is made by the pituitary gland in the brain, which integrates information about the signals of high and low levels from each of the different thyroid hormones.
Now we can measure the actual thyroid hormones — primarily we’re talking about T3 and T4 — but if we do that, we are relying on a single snapshot in the bloodstream at that moment. The levels might change throughout the day in response to ongoing metabolism and outside stresses. So we usually start by measuring the TSH level, which is a good representation of the compilation of all those things over the past 30 days or so.
Question: How do you describe a low TSH result to patients?
Dr. Leung: Whenever we encounter a low TSH level, we want to repeat the test because it is a dynamic test, and it can change in response to several factors. If it is indeed low, we’re thinking that perhaps there’s a little bit of extra thyroid hormone in the body. It can be either temporary or more chronic, but that higher amount of thyroid hormone is telling the pituitary gland in the brain to start making less. So TSH levels go low when we need less thyroid hormone.
Question: What are some of the reasons for a low TSH level?
Dr. Leung: One of the most common situations for a temporarily low TSH level I see is what we call nonthyroidal illness, like a common cold or just being under the weather. Other things that can artifactually lower the TSH level could be the use of steroids, such as prednisone for asthma or some sort of a rheumatologic condition. Also, the TSH level could be low if a person has been recently exposed to very high amounts of iodine, such as iodinated contrast needed for a CT scan.
If the TSH level remains persistently low, usually in the presence of high thyroid hormone (T3 and/or T4) levels, the most common reason for hyperthyroidism is Graves disease, in which there are autoantibodies — measurable in the blood — that can stimulate the thyroid gland in the neck to make extra thyroid hormone.
Question: And what does an elevated TSH level mean?
Dr. Leung: Again, we want to confirm that it is elevated. We need at least two tests to confirm a high TSH level. A persistently elevated TSH level is a signal there might be low thyroid hormone levels in the body, which could be transient or more longer lasting.
Question: What are some of the most common causes of an elevated TSH level?
Dr. Leung: If the TSH level is confirmed high and the thyroid hormone levels are low, the most common cause of hypothyroidism here in the United States is Hashimoto thyroiditis.
Globally, iodine deficiency is the most common reason for hypothyroidism and may be a problem in parts of the globe where there are endemically low iodine levels in soil, crops, and the food supply like not having enough iodized salt. The thyroid is reliant on having enough iodine as a micronutrient to make thyroid hormone. If it doesn’t, the thyroid really can’t make thyroid hormone. It’s important to also remember, though, that having too much iodine can result in hypo- or hyperthyroidism.
Dr. Tsai: I take a glance at their medication list. Some of the patients are on methimazole or levothyroxine, and those medications should be adjusted first to normalize the TSH level. Other medications like lithium and amiodarone can also cause elevated TSH levels. We are also seeing a lot of patients on cancer therapies, such as tyrosine kinase inhibitors or immunotherapy, that can cause an elevated TSH level.
Question: If the repeat TSH test shows that TSH levels are still elevated, what comes next in your workup?
Dr. Tsai: If there’s not a real clear-cut diagnosis, I’ll order the thyroid peroxidase antibody and the thyroglobulin antibody, although thyroid peroxidase antibody, which is indicative of autoimmune thyroid disease, alone is usually sufficient to make that diagnosis.
Question: Should clinicians follow thyroid antibodies over time?
Dr. Tsai: I usually don’t repeat the antibody tests. In those circumstances where patients who were diagnosed 50-60 years ago and perhaps it is unknown if they had the thyroid antibodies measured at the time and now they’re saying, “Do I actually have Hashimoto’s?” or “Do I really need to continue this for the rest of my life?” I do repeat antibody tests to help gauge if the patient’s levothyroxine can be stopped.
Question: How important is it to follow T4 or T3 levels?
Dr. Tsai: T4 and T3 levels can help differentiate overt thyroid dysfunction — where T3 and/or T4 levels will be abnormal — from subclinical thyroid dysfunction — where T3 and T4 levels would be normal. In general, although we do not fully appreciate the best metric to monitor hypo- or hyperthyroidism, because some patients with a normal TSH level still may have symptoms of thyroid dysfunction, these peripheral thyroid hormone levels are usually the most helpful at the time of initial diagnosis.
Question: What are your criteria for initiating treatment for hypothyroidism?
Dr. Tsai: If the TSH level > 10 mIU/L, I recommend levothyroxine hormone replacement. A lot of published data support clinical benefit in this group.
There is a gray area in those patients who have a TSH level higher than the upper limit of the reference range but less than 10. If the patient doesn’t have overt hypothyroid symptoms, I discuss the findings with the patient but don’t really feel eager to treat. I recommend checking the levels again in 6 months to see where that TSH goes, and if it worsens or becomes greater than 10 mIU/L, I then recommend levothyroxine hormone replacement.
It is also important to note that a TSH level of 5-7 may be an acceptable range for older patients, and they do not require levothyroxine.
The other category is patients whose TSH level is greater than the upper limit of the normal reference range but less than 10 and with overt hypothyroid symptoms such as fatigue, unintentional weight gain, constipation, or cold intolerance. In these patients, it is worthwhile to try a low dose of levothyroxine (25-50 mcg/d) and repeat TSH and free T4 tests in 6-8 weeks and see if the TSH level normalizes.
Dr. Leung: When you look at subclinical hypothyroidism, the situation of an isolated high TSH level in the setting of normal T4 levels, if the TSH level is mildly elevated in the 5-7 mIU/L range, there’s a 60% chance that it will normalize within 6 months.
Going back to Karen’s point, a lot of people are started and maintained on low doses of thyroid hormone forever and ever. A recent study on levothyroxine use found half of the prescriptions were unnecessary.
Question: In an era where many patients obtain much of their health information from TikTok, what’s your approach with patients with a normal TSH level who feel that they should have more testing or start treatment?
Dr. Tsai: Fatigue is one of the common referrals we get into our endocrinology practice, and everyone is convinced that their thyroid is the culprit. It is important to note, however, that fatigue can be due to different diseases such as anemia, depression, sleep disorders, or a recent viral illness.
TSH tests are readily available and cheap. I don’t mind ordering the lab test again if it helps give the patient some reassurance. I also find that patients are relieved once they hear from their endocrinologist that their thyroid is unlikely to be the cause of their fatigue.
Some other endocrine causes we may consider additionally working up include adrenal insufficiency, vitamin D deficiency, and diabetes. A comprehensive metabolic panel and complete blood count is part of my workup to rule out any gross electrolyte abnormalities or any new diagnosis of anemia, liver disease, or chronic kidney disease.
Question: What are your criteria for recommending that someone see an endocrinologist?
Dr. Tsai: Our primary care colleagues can do a workup and interpretation of thyroid function tests in most cases. In the situations where the thyroid function test results are discordant (ie, elevated TSH and elevated free T4 levels or low TSH and low free T4 levels) or difficult to interpret, it would be appropriate to refer the patient to an endocrinologist.
One of the common referrals that we do get from the community is a patient’s thyroid function tests going from hyperthyroid to hypothyroid without a clear explanation or the patient is suboptimally controlled with levothyroxine or methimazole. In those circumstances, it would be worthwhile to send to an endocrinologist try to discern an underlying cause or for optimization of medication.
Dr. Leung and Dr. Tsai had no financial disclosures.
A version of this article appeared on Medscape.com.
What We Know About Salmon Sperm in Dermatology
It may not have an aesthetic-sounding appeal to most people, but salmon sperm is indeed one of the novel ingredients featured in products for human skin. These products also reportedly enhance and promote skin regeneration.1 This column will focus on the innovative approach to skin care involving purified polynucleotides derived from salmon sperm.
The Properties and Activities of PDRNs, PNs
PDRNs contain DNA fragments primarily derived from Pacific or chum salmon (Oncorhynchus keta), and salmon trout (Oncorhynchus mykiss) sperm cells.2 Through preclinical and clinical trials, PDRN has demonstrated a wide range of salutary functions, including antiallodynic, antiapoptotic, anti-inflammatory, antimelanogenetic, antiosteonecrotic, antiosteoporotic, antiulcerative, bone-regenerative, tissue damage–preventive, and wound-healing activities through adenosine A2A receptor and salvage pathways activation. Indeed, PDRNs have been shown in vitro to spur the proliferation of preadipocytes and, in vivo, to be effective in treating wounds and ulcers.3,4 In particular, atrophic, hypertrophic, surgical, and various acne scars have been treated with such injections.2,5,6 PDRN is thought to affect cutaneous health more directly by facilitating angiogenesis, cellular functions, especially fibroblast stimulation, collagen production, soft-tissue regeneration, and skin revitalization. Further, it has been used successfully to treat hyperpigmentation.7
PNs, derived from the same fish species as PDRNs, have been used effectively to ameliorate skin elasticity, hydration, pore size, thickness, wrinkles, as well as pigmentation and, specifically, in treating periorbital rhytides and postsurgical scars.5,6,8 Beyond skin rejuvenation, PNs have been recognized for effectiveness in treating stretch marks and achieving vulvovaginal revitalization; guidelines for its use have been established and implemented in recent years.6,9,10 In South Korea, PNs have become a popular treatment for facial erythema even though preclinical and clinical data are sparse.11 Nevertheless, the use of these novel substances is thought to foster tissue regeneration and a more natural rejuvenation than achieved through more traditional fillers.6
Skin Rejuvenation
Park and colleagues conducted a small study with five patients in 2016 in which long-chain polynucleotide filler was used for skin rejuvenation. Over a 2-week period, five Korean women received four injections of the filler (0.05 mL) on one side of the face. No adverse side effects were reported. In the patients in their 30s, pore and skin thickness significantly improved with treatment. For patients in their 40s, observable improvements were noted in melanin, sagging, skin tone, and wrinkles. Despite the small study size, the investigators concluded that this intradermal injection material is a safe and effective product for skin rejuvenation therapy.1 The product is also available in Europe and reportedly spurs the regeneration of damaged tissues and yields a more natural appearance.1
A Hybrid HA-PN Filler
Given that the most common filling agent, hyaluronic acid (HA), is associated with multiple side effects, JH Kim and colleagues set out in 2020 to compare HA with a new HA-PN dermal filler that has displayed notable biocompatibility and promoted tissue regeneration. The investigators observed that the combination filler provoked greater cell migration in a wound healing assay and was more effective in promoting collagen production in human and mouse fibroblasts. To their knowledge, this was the first study showing the efficacy, safety, and durability of a hybrid HA-PN filler. They concluded that fillers containing both HA and PN were more effective than HA alone in suppressing cutaneous aging and may represent the next step in the evolution of dermal filling agents.12
Most Recent Findings
In August 2023, MJ Kim and colleagues became the first to report on the successful use of PNs derived from fish sperm as a volumizing treatment for fat atrophy in vivo (in the temple in one case, and the cheek in the other). Injections were made into the subcutaneous layer to treat iatrogenic volume loss resulting from lipolysis injections. In one case, a depression in the left temple of a 53-year-old female lipolysis patient was treated with a series of 1 cc PN injections in a 20 mg/mL concentration. At 1 month after the final series of injections (four treatments), significant clinical improvement was observed, with the result (barely visible depression) maintained at 11 months and 21 months after the last treatment. The second patient, a 34-year-old female, presented with two depressed areas on the left cheek 2 months after steroid injections for two acne lesions. A series of PN filler injections also with a concentration of 20 mg/mL was administered (four treatments) at 1-month intervals. Significant improvement was seen 2 months after the last treatment, with maintenance of complete healing noted at 5 months and 12 months after the final treatment. No adverse effects were reported in either case. The investigators concluded that long-chain PN fillers appear to be effective in treating depressions in the skin, but more data, particularly from controlled studies, is necessary to determine the safety and efficacy as a lone therapeutic approach for soft-tissue depression.6
A month later, Lee and colleagues reported on the results of their survey of clinicians in South Korea who use PNs in clinical practice. The goal was to understand current practices and perceptions of effectiveness in treating facial erythema. Of the 557 physicians who participated, 84.4% used PNs for facial erythema provoked by inflammatory facial dermatosis, 66.4% for facial erythema induced by repeated laser/microneedle radiofrequency, and 47.4% for facial erythema caused by steroid overuse. In these same classifications, 88.1%, 90%, and 83.7%, respectively, found PNs to be “highly effective” or “effective.” Survey respondents also characterized PNs as imparting wound healing/regeneration (95.8%), skin barrier protection (92.2%), hydration (90.5%), vascular stabilization (81.0%), and anti-inflammatory activity (79.5%).11
Conclusion
The use of salmon sperm cells is an example of the recent trend toward a cellular approach in which cutaneous components are activated with the intention of stimulating tissue regeneration. It is commonly used in Brazil and my Brazilian patients seem to know all about it. This innovative outlook is intriguing as are a spate of recently reported results. Nevertheless, much more evidence is required to ascertain safety and effectiveness in large sample sizes and, ideally, to establish maintenance of corrections over longer periods whether these ingredients are used in filling agents or topical formulations.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as a e-commerce solution. Write to her at [email protected].
References
1. Park KY et al. Dermatol Ther. 2016 Jan;29(1):37-40. .
2. Kim TH et al. Mar Drugs. 2021 May 22;19(6):296.
3. Raposio E et al. Cell Prolif. 2008 Oct;41(5):739-54.
4. Veronesi F et al. J Cell Physiol. 2017 Sep;232(9):2299-2307.
5. Kim JH et al. Lasers Surg Med. 2018 Mar 25.
6. Kim MJ et al. Skin Res Technol. 2023 Aug;29(8):e13439.
7. Khan A et al. Chinese Journal of Plastic and Reconstructive Surgery. 2022 Dec;4(4):187-193.
8. Lee YJ et al. J Dermatolog Treat. 2022 Feb;33(1):254-260.
9. De Caridi G et al. Int Wound J. 2016 Oct;13(5):754-8.
10. Cavallini M et al. J Cosmet Dermatol. 2021 Mar;20(3):922-928.
11. Lee D. Skin Res Technol. 2023 Sep;29(9):e13466. doi: 10.1111/srt.13466.
12. Kim JH et al. Sci Rep. 2020 Mar 20;10(1):5127. .
It may not have an aesthetic-sounding appeal to most people, but salmon sperm is indeed one of the novel ingredients featured in products for human skin. These products also reportedly enhance and promote skin regeneration.1 This column will focus on the innovative approach to skin care involving purified polynucleotides derived from salmon sperm.
The Properties and Activities of PDRNs, PNs
PDRNs contain DNA fragments primarily derived from Pacific or chum salmon (Oncorhynchus keta), and salmon trout (Oncorhynchus mykiss) sperm cells.2 Through preclinical and clinical trials, PDRN has demonstrated a wide range of salutary functions, including antiallodynic, antiapoptotic, anti-inflammatory, antimelanogenetic, antiosteonecrotic, antiosteoporotic, antiulcerative, bone-regenerative, tissue damage–preventive, and wound-healing activities through adenosine A2A receptor and salvage pathways activation. Indeed, PDRNs have been shown in vitro to spur the proliferation of preadipocytes and, in vivo, to be effective in treating wounds and ulcers.3,4 In particular, atrophic, hypertrophic, surgical, and various acne scars have been treated with such injections.2,5,6 PDRN is thought to affect cutaneous health more directly by facilitating angiogenesis, cellular functions, especially fibroblast stimulation, collagen production, soft-tissue regeneration, and skin revitalization. Further, it has been used successfully to treat hyperpigmentation.7
PNs, derived from the same fish species as PDRNs, have been used effectively to ameliorate skin elasticity, hydration, pore size, thickness, wrinkles, as well as pigmentation and, specifically, in treating periorbital rhytides and postsurgical scars.5,6,8 Beyond skin rejuvenation, PNs have been recognized for effectiveness in treating stretch marks and achieving vulvovaginal revitalization; guidelines for its use have been established and implemented in recent years.6,9,10 In South Korea, PNs have become a popular treatment for facial erythema even though preclinical and clinical data are sparse.11 Nevertheless, the use of these novel substances is thought to foster tissue regeneration and a more natural rejuvenation than achieved through more traditional fillers.6
Skin Rejuvenation
Park and colleagues conducted a small study with five patients in 2016 in which long-chain polynucleotide filler was used for skin rejuvenation. Over a 2-week period, five Korean women received four injections of the filler (0.05 mL) on one side of the face. No adverse side effects were reported. In the patients in their 30s, pore and skin thickness significantly improved with treatment. For patients in their 40s, observable improvements were noted in melanin, sagging, skin tone, and wrinkles. Despite the small study size, the investigators concluded that this intradermal injection material is a safe and effective product for skin rejuvenation therapy.1 The product is also available in Europe and reportedly spurs the regeneration of damaged tissues and yields a more natural appearance.1
A Hybrid HA-PN Filler
Given that the most common filling agent, hyaluronic acid (HA), is associated with multiple side effects, JH Kim and colleagues set out in 2020 to compare HA with a new HA-PN dermal filler that has displayed notable biocompatibility and promoted tissue regeneration. The investigators observed that the combination filler provoked greater cell migration in a wound healing assay and was more effective in promoting collagen production in human and mouse fibroblasts. To their knowledge, this was the first study showing the efficacy, safety, and durability of a hybrid HA-PN filler. They concluded that fillers containing both HA and PN were more effective than HA alone in suppressing cutaneous aging and may represent the next step in the evolution of dermal filling agents.12
Most Recent Findings
In August 2023, MJ Kim and colleagues became the first to report on the successful use of PNs derived from fish sperm as a volumizing treatment for fat atrophy in vivo (in the temple in one case, and the cheek in the other). Injections were made into the subcutaneous layer to treat iatrogenic volume loss resulting from lipolysis injections. In one case, a depression in the left temple of a 53-year-old female lipolysis patient was treated with a series of 1 cc PN injections in a 20 mg/mL concentration. At 1 month after the final series of injections (four treatments), significant clinical improvement was observed, with the result (barely visible depression) maintained at 11 months and 21 months after the last treatment. The second patient, a 34-year-old female, presented with two depressed areas on the left cheek 2 months after steroid injections for two acne lesions. A series of PN filler injections also with a concentration of 20 mg/mL was administered (four treatments) at 1-month intervals. Significant improvement was seen 2 months after the last treatment, with maintenance of complete healing noted at 5 months and 12 months after the final treatment. No adverse effects were reported in either case. The investigators concluded that long-chain PN fillers appear to be effective in treating depressions in the skin, but more data, particularly from controlled studies, is necessary to determine the safety and efficacy as a lone therapeutic approach for soft-tissue depression.6
A month later, Lee and colleagues reported on the results of their survey of clinicians in South Korea who use PNs in clinical practice. The goal was to understand current practices and perceptions of effectiveness in treating facial erythema. Of the 557 physicians who participated, 84.4% used PNs for facial erythema provoked by inflammatory facial dermatosis, 66.4% for facial erythema induced by repeated laser/microneedle radiofrequency, and 47.4% for facial erythema caused by steroid overuse. In these same classifications, 88.1%, 90%, and 83.7%, respectively, found PNs to be “highly effective” or “effective.” Survey respondents also characterized PNs as imparting wound healing/regeneration (95.8%), skin barrier protection (92.2%), hydration (90.5%), vascular stabilization (81.0%), and anti-inflammatory activity (79.5%).11
Conclusion
The use of salmon sperm cells is an example of the recent trend toward a cellular approach in which cutaneous components are activated with the intention of stimulating tissue regeneration. It is commonly used in Brazil and my Brazilian patients seem to know all about it. This innovative outlook is intriguing as are a spate of recently reported results. Nevertheless, much more evidence is required to ascertain safety and effectiveness in large sample sizes and, ideally, to establish maintenance of corrections over longer periods whether these ingredients are used in filling agents or topical formulations.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as a e-commerce solution. Write to her at [email protected].
References
1. Park KY et al. Dermatol Ther. 2016 Jan;29(1):37-40. .
2. Kim TH et al. Mar Drugs. 2021 May 22;19(6):296.
3. Raposio E et al. Cell Prolif. 2008 Oct;41(5):739-54.
4. Veronesi F et al. J Cell Physiol. 2017 Sep;232(9):2299-2307.
5. Kim JH et al. Lasers Surg Med. 2018 Mar 25.
6. Kim MJ et al. Skin Res Technol. 2023 Aug;29(8):e13439.
7. Khan A et al. Chinese Journal of Plastic and Reconstructive Surgery. 2022 Dec;4(4):187-193.
8. Lee YJ et al. J Dermatolog Treat. 2022 Feb;33(1):254-260.
9. De Caridi G et al. Int Wound J. 2016 Oct;13(5):754-8.
10. Cavallini M et al. J Cosmet Dermatol. 2021 Mar;20(3):922-928.
11. Lee D. Skin Res Technol. 2023 Sep;29(9):e13466. doi: 10.1111/srt.13466.
12. Kim JH et al. Sci Rep. 2020 Mar 20;10(1):5127. .
It may not have an aesthetic-sounding appeal to most people, but salmon sperm is indeed one of the novel ingredients featured in products for human skin. These products also reportedly enhance and promote skin regeneration.1 This column will focus on the innovative approach to skin care involving purified polynucleotides derived from salmon sperm.
The Properties and Activities of PDRNs, PNs
PDRNs contain DNA fragments primarily derived from Pacific or chum salmon (Oncorhynchus keta), and salmon trout (Oncorhynchus mykiss) sperm cells.2 Through preclinical and clinical trials, PDRN has demonstrated a wide range of salutary functions, including antiallodynic, antiapoptotic, anti-inflammatory, antimelanogenetic, antiosteonecrotic, antiosteoporotic, antiulcerative, bone-regenerative, tissue damage–preventive, and wound-healing activities through adenosine A2A receptor and salvage pathways activation. Indeed, PDRNs have been shown in vitro to spur the proliferation of preadipocytes and, in vivo, to be effective in treating wounds and ulcers.3,4 In particular, atrophic, hypertrophic, surgical, and various acne scars have been treated with such injections.2,5,6 PDRN is thought to affect cutaneous health more directly by facilitating angiogenesis, cellular functions, especially fibroblast stimulation, collagen production, soft-tissue regeneration, and skin revitalization. Further, it has been used successfully to treat hyperpigmentation.7
PNs, derived from the same fish species as PDRNs, have been used effectively to ameliorate skin elasticity, hydration, pore size, thickness, wrinkles, as well as pigmentation and, specifically, in treating periorbital rhytides and postsurgical scars.5,6,8 Beyond skin rejuvenation, PNs have been recognized for effectiveness in treating stretch marks and achieving vulvovaginal revitalization; guidelines for its use have been established and implemented in recent years.6,9,10 In South Korea, PNs have become a popular treatment for facial erythema even though preclinical and clinical data are sparse.11 Nevertheless, the use of these novel substances is thought to foster tissue regeneration and a more natural rejuvenation than achieved through more traditional fillers.6
Skin Rejuvenation
Park and colleagues conducted a small study with five patients in 2016 in which long-chain polynucleotide filler was used for skin rejuvenation. Over a 2-week period, five Korean women received four injections of the filler (0.05 mL) on one side of the face. No adverse side effects were reported. In the patients in their 30s, pore and skin thickness significantly improved with treatment. For patients in their 40s, observable improvements were noted in melanin, sagging, skin tone, and wrinkles. Despite the small study size, the investigators concluded that this intradermal injection material is a safe and effective product for skin rejuvenation therapy.1 The product is also available in Europe and reportedly spurs the regeneration of damaged tissues and yields a more natural appearance.1
A Hybrid HA-PN Filler
Given that the most common filling agent, hyaluronic acid (HA), is associated with multiple side effects, JH Kim and colleagues set out in 2020 to compare HA with a new HA-PN dermal filler that has displayed notable biocompatibility and promoted tissue regeneration. The investigators observed that the combination filler provoked greater cell migration in a wound healing assay and was more effective in promoting collagen production in human and mouse fibroblasts. To their knowledge, this was the first study showing the efficacy, safety, and durability of a hybrid HA-PN filler. They concluded that fillers containing both HA and PN were more effective than HA alone in suppressing cutaneous aging and may represent the next step in the evolution of dermal filling agents.12
Most Recent Findings
In August 2023, MJ Kim and colleagues became the first to report on the successful use of PNs derived from fish sperm as a volumizing treatment for fat atrophy in vivo (in the temple in one case, and the cheek in the other). Injections were made into the subcutaneous layer to treat iatrogenic volume loss resulting from lipolysis injections. In one case, a depression in the left temple of a 53-year-old female lipolysis patient was treated with a series of 1 cc PN injections in a 20 mg/mL concentration. At 1 month after the final series of injections (four treatments), significant clinical improvement was observed, with the result (barely visible depression) maintained at 11 months and 21 months after the last treatment. The second patient, a 34-year-old female, presented with two depressed areas on the left cheek 2 months after steroid injections for two acne lesions. A series of PN filler injections also with a concentration of 20 mg/mL was administered (four treatments) at 1-month intervals. Significant improvement was seen 2 months after the last treatment, with maintenance of complete healing noted at 5 months and 12 months after the final treatment. No adverse effects were reported in either case. The investigators concluded that long-chain PN fillers appear to be effective in treating depressions in the skin, but more data, particularly from controlled studies, is necessary to determine the safety and efficacy as a lone therapeutic approach for soft-tissue depression.6
A month later, Lee and colleagues reported on the results of their survey of clinicians in South Korea who use PNs in clinical practice. The goal was to understand current practices and perceptions of effectiveness in treating facial erythema. Of the 557 physicians who participated, 84.4% used PNs for facial erythema provoked by inflammatory facial dermatosis, 66.4% for facial erythema induced by repeated laser/microneedle radiofrequency, and 47.4% for facial erythema caused by steroid overuse. In these same classifications, 88.1%, 90%, and 83.7%, respectively, found PNs to be “highly effective” or “effective.” Survey respondents also characterized PNs as imparting wound healing/regeneration (95.8%), skin barrier protection (92.2%), hydration (90.5%), vascular stabilization (81.0%), and anti-inflammatory activity (79.5%).11
Conclusion
The use of salmon sperm cells is an example of the recent trend toward a cellular approach in which cutaneous components are activated with the intention of stimulating tissue regeneration. It is commonly used in Brazil and my Brazilian patients seem to know all about it. This innovative outlook is intriguing as are a spate of recently reported results. Nevertheless, much more evidence is required to ascertain safety and effectiveness in large sample sizes and, ideally, to establish maintenance of corrections over longer periods whether these ingredients are used in filling agents or topical formulations.
Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as a e-commerce solution. Write to her at [email protected].
References
1. Park KY et al. Dermatol Ther. 2016 Jan;29(1):37-40. .
2. Kim TH et al. Mar Drugs. 2021 May 22;19(6):296.
3. Raposio E et al. Cell Prolif. 2008 Oct;41(5):739-54.
4. Veronesi F et al. J Cell Physiol. 2017 Sep;232(9):2299-2307.
5. Kim JH et al. Lasers Surg Med. 2018 Mar 25.
6. Kim MJ et al. Skin Res Technol. 2023 Aug;29(8):e13439.
7. Khan A et al. Chinese Journal of Plastic and Reconstructive Surgery. 2022 Dec;4(4):187-193.
8. Lee YJ et al. J Dermatolog Treat. 2022 Feb;33(1):254-260.
9. De Caridi G et al. Int Wound J. 2016 Oct;13(5):754-8.
10. Cavallini M et al. J Cosmet Dermatol. 2021 Mar;20(3):922-928.
11. Lee D. Skin Res Technol. 2023 Sep;29(9):e13466. doi: 10.1111/srt.13466.
12. Kim JH et al. Sci Rep. 2020 Mar 20;10(1):5127. .
A 71-year-old White female developed erosions after hip replacement surgery 2 months prior to presentation
The patient had been diagnosed with pemphigus vulgaris (PV) 1 year prior to presentation with erosions on the axilla. Biopsy at that time revealed intraepithelial acantholytic blistering with areas of suprabasilar and subcorneal clefting. Direct immunofluorescence was positive for linear/granular IgG deposition throughout the epithelial cell surfaces, as well as linear/granular C3 deposits of the lower two thirds of the epithelial strata, consistent for pemphigus vulgaris.
There is likely a genetic predisposition. Medications that may induce pemphigus include penicillamine, nifedipine, or captopril.
Clinically, PV presents with flaccid blistering lesions that may be cutaneous and/or mucosal. Bullae can progress to erosions and crusting, which then heal with pigment alteration but not scarring. The most commonly affected sites are the mouth, intertriginous areas, face, and neck. Mucosal lesions can involve the lips, esophagus, conjunctiva, and genitals.
Biopsy for histology and direct immunofluorescence is important in distinguishing between PV and other blistering disorders. Up to 75% of patients with active disease also have a positive indirect immunofluorescence with circulating IgG.
There are numerous reports in the literature of PV occurring in previous surgical scars, and areas of friction or trauma. This so-called Koebner’s phenomenon is seen more commonly in several dermatologic conditions, such as psoriasis, lichen planus, verruca vulgaris, and vitiligo.
Treatment for PV is generally immunosuppressive. Systemic therapy usually begins with prednisone and then is transitioned to a steroid sparing agent such as mycophenolate mofetil. Other steroid sparing agents include azathioprine, methotrexate, cyclophosphamide, and intravenous immunoglobulin. Secondary infections are possible and should be treated. Topical therapies aimed at reducing pain, especially in mucosal lesions, can be beneficial.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
Cerottini JP et al. Eur J Dermatol. 2000 Oct-Nov;10(7):546-7.
Reichert-Penetrat S et al. Eur J Dermatol. 1998 Jan-Feb;8(1):60-2.
Saini P et al. Skinmed. 2020 Aug 1;18(4):252-253.
The patient had been diagnosed with pemphigus vulgaris (PV) 1 year prior to presentation with erosions on the axilla. Biopsy at that time revealed intraepithelial acantholytic blistering with areas of suprabasilar and subcorneal clefting. Direct immunofluorescence was positive for linear/granular IgG deposition throughout the epithelial cell surfaces, as well as linear/granular C3 deposits of the lower two thirds of the epithelial strata, consistent for pemphigus vulgaris.
There is likely a genetic predisposition. Medications that may induce pemphigus include penicillamine, nifedipine, or captopril.
Clinically, PV presents with flaccid blistering lesions that may be cutaneous and/or mucosal. Bullae can progress to erosions and crusting, which then heal with pigment alteration but not scarring. The most commonly affected sites are the mouth, intertriginous areas, face, and neck. Mucosal lesions can involve the lips, esophagus, conjunctiva, and genitals.
Biopsy for histology and direct immunofluorescence is important in distinguishing between PV and other blistering disorders. Up to 75% of patients with active disease also have a positive indirect immunofluorescence with circulating IgG.
There are numerous reports in the literature of PV occurring in previous surgical scars, and areas of friction or trauma. This so-called Koebner’s phenomenon is seen more commonly in several dermatologic conditions, such as psoriasis, lichen planus, verruca vulgaris, and vitiligo.
Treatment for PV is generally immunosuppressive. Systemic therapy usually begins with prednisone and then is transitioned to a steroid sparing agent such as mycophenolate mofetil. Other steroid sparing agents include azathioprine, methotrexate, cyclophosphamide, and intravenous immunoglobulin. Secondary infections are possible and should be treated. Topical therapies aimed at reducing pain, especially in mucosal lesions, can be beneficial.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
Cerottini JP et al. Eur J Dermatol. 2000 Oct-Nov;10(7):546-7.
Reichert-Penetrat S et al. Eur J Dermatol. 1998 Jan-Feb;8(1):60-2.
Saini P et al. Skinmed. 2020 Aug 1;18(4):252-253.
The patient had been diagnosed with pemphigus vulgaris (PV) 1 year prior to presentation with erosions on the axilla. Biopsy at that time revealed intraepithelial acantholytic blistering with areas of suprabasilar and subcorneal clefting. Direct immunofluorescence was positive for linear/granular IgG deposition throughout the epithelial cell surfaces, as well as linear/granular C3 deposits of the lower two thirds of the epithelial strata, consistent for pemphigus vulgaris.
There is likely a genetic predisposition. Medications that may induce pemphigus include penicillamine, nifedipine, or captopril.
Clinically, PV presents with flaccid blistering lesions that may be cutaneous and/or mucosal. Bullae can progress to erosions and crusting, which then heal with pigment alteration but not scarring. The most commonly affected sites are the mouth, intertriginous areas, face, and neck. Mucosal lesions can involve the lips, esophagus, conjunctiva, and genitals.
Biopsy for histology and direct immunofluorescence is important in distinguishing between PV and other blistering disorders. Up to 75% of patients with active disease also have a positive indirect immunofluorescence with circulating IgG.
There are numerous reports in the literature of PV occurring in previous surgical scars, and areas of friction or trauma. This so-called Koebner’s phenomenon is seen more commonly in several dermatologic conditions, such as psoriasis, lichen planus, verruca vulgaris, and vitiligo.
Treatment for PV is generally immunosuppressive. Systemic therapy usually begins with prednisone and then is transitioned to a steroid sparing agent such as mycophenolate mofetil. Other steroid sparing agents include azathioprine, methotrexate, cyclophosphamide, and intravenous immunoglobulin. Secondary infections are possible and should be treated. Topical therapies aimed at reducing pain, especially in mucosal lesions, can be beneficial.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].
References
Cerottini JP et al. Eur J Dermatol. 2000 Oct-Nov;10(7):546-7.
Reichert-Penetrat S et al. Eur J Dermatol. 1998 Jan-Feb;8(1):60-2.
Saini P et al. Skinmed. 2020 Aug 1;18(4):252-253.
Myth of the Month: Vitamin C vs the Common Cold
Case: A 38-year-old presents for acute onset runny nose, cough, and fever for the last 3 days. Her children at home have a similar presentation. She believes that she has been managing her symptoms well with Tylenol and rest. The patient is up to date on her COVID and flu shots and was wondering if there was anything else she could have done to prevent her symptoms. She saw a commercial about vitamin C supplements boosting the immune system and was wondering about their efficacy. How would you respond?
Studies of Vitamin C
Linus Pauling, FRS, did a summary of four relatively small published studies of vitamin C and concluded that vitamin C supplementation helped prevent and lessen colds.1 He mentioned a placebo-controlled study of vitamin C with viral inoculation which did not show any effect. His overall conclusion of efficacy for vitamin C led to the widespread belief that vitamin C was a proven effective therapy to prevent and treat the common cold. Since then, multiple trials and studies have examined the effect of vitamin C on the prevention and treatment of colds.
The Cochrane Review conducted a meta-analysis comparing 29 placebo-controlled trials involving 11,306 participants.2 Criteria included vitamin C supplementation of 0.2 g-1 g/day to study its efficacy in preventing the common cold. The analysis showed that supplemental vitamin C did not significantly reduce the incidence of colds. However, there was a statistically significant 8% reduction in adults and 14% in children in the duration of colds. In terms of treatment, there was no evidence of vitamin C’s efficacy.
A 2001 study conducted a small double-blind, randomized control trial to evaluate large doses of vitamin C as treatment for the common cold.3 Volunteers were divided and instructed to take varying doses ranging from 1 to 3 g of vitamin C vs a placebo at the onset of cold-like symptoms. Subjects were expected to assess the duration and severity of their cold. The data showed no significant difference in the severity or duration of cold symptoms between small or large vitamin C doses or placebo.
A more recent meta-analysis by Hemilä and Chalker looked at 10 placebo-controlled trials of vitamin C for the prevention and treatment of colds.4 The analysis showed a small 15% reduction in more severe cold symptoms.
Summary
While vitamin C is safe, there is no evidence for its ability to prevent the common cold. Although the Cochrane review and more a recent meta-analysis by Hemilä and Chalker demonstrated statistical significance in shortening the duration of symptoms, it was a minimal reduction with little clinical significance. .
Ms. Ibabao is a fourth year medical student at the University of Washington School of Medicine; Dr. Paauw is Professor of Medicine, Rathmann Family Foundation Endowed Chair Patient-centered Clinical Education, at the University of Washington School of Medicine, Seattle. They have no conflicts of interest.
References
1. Pauling L. The significance of the evidence about ascorbic acid and the common cold. Proc Natl Acad Sci USA. 1971;68:2678-2671.
2. Hemilä H, Chalker E. Vitamin C for preventing and treating the common cold. Cochrane Database of Systematic Reviews. 2013;1(1).
3. Audera C et al. Mega‐dose vitamin C in treatment of the common cold: a randomised controlled trial. Med J Australia. 2001;175(7):359-362.
4. Hemilä H, Chalker E. Vitamin C reduces the severity of common colds: a meta-analysis. BMC Public Health. 2023;23:2468.
Case: A 38-year-old presents for acute onset runny nose, cough, and fever for the last 3 days. Her children at home have a similar presentation. She believes that she has been managing her symptoms well with Tylenol and rest. The patient is up to date on her COVID and flu shots and was wondering if there was anything else she could have done to prevent her symptoms. She saw a commercial about vitamin C supplements boosting the immune system and was wondering about their efficacy. How would you respond?
Studies of Vitamin C
Linus Pauling, FRS, did a summary of four relatively small published studies of vitamin C and concluded that vitamin C supplementation helped prevent and lessen colds.1 He mentioned a placebo-controlled study of vitamin C with viral inoculation which did not show any effect. His overall conclusion of efficacy for vitamin C led to the widespread belief that vitamin C was a proven effective therapy to prevent and treat the common cold. Since then, multiple trials and studies have examined the effect of vitamin C on the prevention and treatment of colds.
The Cochrane Review conducted a meta-analysis comparing 29 placebo-controlled trials involving 11,306 participants.2 Criteria included vitamin C supplementation of 0.2 g-1 g/day to study its efficacy in preventing the common cold. The analysis showed that supplemental vitamin C did not significantly reduce the incidence of colds. However, there was a statistically significant 8% reduction in adults and 14% in children in the duration of colds. In terms of treatment, there was no evidence of vitamin C’s efficacy.
A 2001 study conducted a small double-blind, randomized control trial to evaluate large doses of vitamin C as treatment for the common cold.3 Volunteers were divided and instructed to take varying doses ranging from 1 to 3 g of vitamin C vs a placebo at the onset of cold-like symptoms. Subjects were expected to assess the duration and severity of their cold. The data showed no significant difference in the severity or duration of cold symptoms between small or large vitamin C doses or placebo.
A more recent meta-analysis by Hemilä and Chalker looked at 10 placebo-controlled trials of vitamin C for the prevention and treatment of colds.4 The analysis showed a small 15% reduction in more severe cold symptoms.
Summary
While vitamin C is safe, there is no evidence for its ability to prevent the common cold. Although the Cochrane review and more a recent meta-analysis by Hemilä and Chalker demonstrated statistical significance in shortening the duration of symptoms, it was a minimal reduction with little clinical significance. .
Ms. Ibabao is a fourth year medical student at the University of Washington School of Medicine; Dr. Paauw is Professor of Medicine, Rathmann Family Foundation Endowed Chair Patient-centered Clinical Education, at the University of Washington School of Medicine, Seattle. They have no conflicts of interest.
References
1. Pauling L. The significance of the evidence about ascorbic acid and the common cold. Proc Natl Acad Sci USA. 1971;68:2678-2671.
2. Hemilä H, Chalker E. Vitamin C for preventing and treating the common cold. Cochrane Database of Systematic Reviews. 2013;1(1).
3. Audera C et al. Mega‐dose vitamin C in treatment of the common cold: a randomised controlled trial. Med J Australia. 2001;175(7):359-362.
4. Hemilä H, Chalker E. Vitamin C reduces the severity of common colds: a meta-analysis. BMC Public Health. 2023;23:2468.
Case: A 38-year-old presents for acute onset runny nose, cough, and fever for the last 3 days. Her children at home have a similar presentation. She believes that she has been managing her symptoms well with Tylenol and rest. The patient is up to date on her COVID and flu shots and was wondering if there was anything else she could have done to prevent her symptoms. She saw a commercial about vitamin C supplements boosting the immune system and was wondering about their efficacy. How would you respond?
Studies of Vitamin C
Linus Pauling, FRS, did a summary of four relatively small published studies of vitamin C and concluded that vitamin C supplementation helped prevent and lessen colds.1 He mentioned a placebo-controlled study of vitamin C with viral inoculation which did not show any effect. His overall conclusion of efficacy for vitamin C led to the widespread belief that vitamin C was a proven effective therapy to prevent and treat the common cold. Since then, multiple trials and studies have examined the effect of vitamin C on the prevention and treatment of colds.
The Cochrane Review conducted a meta-analysis comparing 29 placebo-controlled trials involving 11,306 participants.2 Criteria included vitamin C supplementation of 0.2 g-1 g/day to study its efficacy in preventing the common cold. The analysis showed that supplemental vitamin C did not significantly reduce the incidence of colds. However, there was a statistically significant 8% reduction in adults and 14% in children in the duration of colds. In terms of treatment, there was no evidence of vitamin C’s efficacy.
A 2001 study conducted a small double-blind, randomized control trial to evaluate large doses of vitamin C as treatment for the common cold.3 Volunteers were divided and instructed to take varying doses ranging from 1 to 3 g of vitamin C vs a placebo at the onset of cold-like symptoms. Subjects were expected to assess the duration and severity of their cold. The data showed no significant difference in the severity or duration of cold symptoms between small or large vitamin C doses or placebo.
A more recent meta-analysis by Hemilä and Chalker looked at 10 placebo-controlled trials of vitamin C for the prevention and treatment of colds.4 The analysis showed a small 15% reduction in more severe cold symptoms.
Summary
While vitamin C is safe, there is no evidence for its ability to prevent the common cold. Although the Cochrane review and more a recent meta-analysis by Hemilä and Chalker demonstrated statistical significance in shortening the duration of symptoms, it was a minimal reduction with little clinical significance. .
Ms. Ibabao is a fourth year medical student at the University of Washington School of Medicine; Dr. Paauw is Professor of Medicine, Rathmann Family Foundation Endowed Chair Patient-centered Clinical Education, at the University of Washington School of Medicine, Seattle. They have no conflicts of interest.
References
1. Pauling L. The significance of the evidence about ascorbic acid and the common cold. Proc Natl Acad Sci USA. 1971;68:2678-2671.
2. Hemilä H, Chalker E. Vitamin C for preventing and treating the common cold. Cochrane Database of Systematic Reviews. 2013;1(1).
3. Audera C et al. Mega‐dose vitamin C in treatment of the common cold: a randomised controlled trial. Med J Australia. 2001;175(7):359-362.
4. Hemilä H, Chalker E. Vitamin C reduces the severity of common colds: a meta-analysis. BMC Public Health. 2023;23:2468.
Treating Family: Ethicist Discusses Whether It’s Appropriate
This transcript has been edited for clarity.
There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.
He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.
This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.
The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.
By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.
If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.
I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.
It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.
All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.
You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.
What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.
It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”
Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.
Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.
At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.
At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”
Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.
Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.
He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.
This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.
The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.
By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.
If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.
I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.
It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.
All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.
You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.
What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.
It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”
Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.
Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.
At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.
At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”
Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.
Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.
He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.
This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.
The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.
By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.
If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.
I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.
It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.
All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.
You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.
What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.
It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”
Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.
Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.
At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.
At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”
Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.
Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.
A version of this article first appeared on Medscape.com.